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| | Epidemiology
- mean age 33 yrs
- 75% males
Predisposing factors
- degenerative disease of spine
- spinal canal stenosis
- ankylosing spondylitis
- Down's syndrome
- Klippel-Feil syndrome
- Arnold-Chiari malformation
- metastatic CA
- osteomyelitis
- rheumatoid arthritis
Pathophysiology
Primary injury
Results from focal injuries (eg avulsion, contusion,
laceration and intraparenchymal haemorrhage) and diffuse lesions (eg concussive
and diffuse axonal injury). Further mechanical disruption can result from
external compression or angulation and ischaemic damage from occlusion of
arterial supply
Secondary injury
Results from:
- Cellular hypoxia
- Oligaemia
- Immediately after an acute spinal cord injury major reduction in blood
flow occurs at the level of the lesion. Becomes progressively worse over
the first few hours if left untreated. Pathophysiology underlying this
ischaemia is unclear but involves both systemic and local effects.
Putative local mechanisms include vasospasm, endothelial swelling or
damage, haemorrhage causing obstruction of small blood vessels, loss of
autoregulation and impaired venous drainage.
- Systemic
hypotension can cause further decreases in spinal cord blood flow but
induced hypertension may not necesssarily reverse the ischaemia. It may
instead cause marked hyperaemia in adjacent parts of the spinal cord
- Pattern
of decreased perfusion within the spinal cord differs. Central grey
matter, along with adjacent white matter is more severely affected than
peripheral white matter.
- White
matter perfusion typically decreases within 5 minutes of injury and
begins to return to normal within 15 mins. Thereafter remains near
normal during first 24 hours
- Central
grey matter perfusion remains low for at least first 24 hours
- Oedema due to an
injury-induced neurochemical cascade
Exacerbated by hypotension
Site of injury
Most likely to occur at sites of maximum mobility
- Adults C6
- Children <8 yrs old C2
Clinical features
- "level" of cord lesion is conventionally the most caudal location
with normal motor and sensory function
- spinal shock may mimic a complete cord lesion with total loss of motor and
sensory function distal to injury. However if lesion is incomplete some function
will return
- 99% of patients with a complete lesion over 24 h will not show functional
recovery
- patients with partial lesion may regain substantial or even normal
neurological function even though the initial neurological deficit may be severe
- presence of bulbocavernous reflex (contraction of anal sphincter on pinching
penile shaft) or anal-cutaneous reflex (contraction of anus in response to
stroking of perianal skin) indicates sacral sparing and a more favourable
prognosis
Central spinal cord syndrome
- most frequently seen after spinal injury with acute hyperextension of neck
in older patients who have varying degrees of congenital or acquired cervival
spine stenosis due to spondylosis
- motor deficit more marked in upper than lower limbs and most profound in
intrinsic muscles of hands
- extent of sensory deficit varies as does degree of bowel and bladder
dysfunction
- although spontaneous improvement in neurological function is the rule
residual neurological deficit is common. Appears to be related to severity of
initial injury
Anatomy of cervical cord
Effect of central cord lesion
Brown-Sequard
- ipsilateral weakness and dorsal column loss
- contralateral pain and temperature deficit
- usually due to penetrating injury
Brown-Sequard lesion
Spinal shock
- direct force applied to the spinal cord results in a physiological block to
conduction
- areflexia, loss of sensation and flaccid paralysis below lesion
- flaccid bladder with retention of urine, lax anal sphincter
- CV complications include bradycardia and hypotension
- diagnosis of exclusion
Anterior cord syndrome
Complete loss of motor below the lesion and loss of light touch sensation but
preservation posterior column function.
Posterior cord syndrome
Rare condition. Results in loss of position sense
Cauda equina lesions
- due to lumbar fracture
- loss of bowel and bladder functions, with paresis of LMN type.
- sensory loss may be patchy plus radicular pain exacerbated by straight leg
raising.
Root loss
eg in C5/6 unilateral facet joint dislocation.
Investigations
NB
- spinal cord injury without radiographic abnormality not uncommon in adults
and frequent in children, Occurs in both thoracic and cervical spine
- if you see one fracture look for another approximately 15% of patients
have more than one fracture
Plain XR
- Indications for screening XR. History of trauma and:
- patient has received sedation or analgesia
- drowsy or intoxicated
- neurological signs
- neck pain
- other painful injury that may mask neck pain, particularly fractures
- additional indications (not evidence based):
- extremes of age
- mechanism of injury highly suggestive of cervical spine injury
- significant facial trauma
-
Lateral cervical spine
AP cervical spine useful for facet injuries, lower spinous process
fractures, anterior subluxations and pillar fractures -
Peg view: essential for evaluation of the odontoid process and C1/C2
relationship
-
Supine oblique view
- Flexion and extension views
- utility controversial
- indicated if stability is uncertain after plain films and CTs have been
obtained. Some advocate taking these views under fluoroscopy in patients who are at high risk of
cervical spine injury who are unconscious before removing neck collar but
risk of causing neurological injury.
- contraindicated in patients with subluxations identified on routine films
and in patients with a neurological deficit or neural structures that are
compressed by #s or soft tissue
- usually extension of cervical spine results in improved alignment of #s and
reduction of subluxations. Therefore first film should be an extension view
followed by images in neutral position
- physician should be in attendance while films are taken
- if awake patient should move his own neck without force or assistance
- if patient has parasthesiae of trunk or limbs or if there is an obvious
change in alignment of spinal column between flexion and neutral films no
further films should be obtained. Otherwise obtain flexion film. If this is
still no change in alignment the spine is probably stable
CT
- indications:
- subluxations or fractures that can be seen
on plain films
- neurological injuries but no apparent abnormalities on plain
films
- severe neck or back pain and normal plain films
- head injury: ? routinely CT C1-C3 (plain films most likely to miss upper cervical spine injuries)
- may miss odontoid #s and other abnormalities that are parallel to axial
image
- better than MRI for bony injuries
CT
showing T4 fracture
MRI
Better for cord and ligamentous injury
Clearing cervical spine in obtunded patient
- normal 3-view cervical spine series
- normal CT of C1-C2
Stability
- Anterior column = anterior 2/3 of the vertebral body, disc, and annulus, and
the anterior longitudinal ligament)
- Middle column = posterior 1/3 of the vertebral body, disc, annulus, and the
posterior longitudinal ligament
- Posterior column = pedicles, laminae, facets, capsule, and the interspinous
and supraspinous ligament
- injury is said to be stable if only one of the columns is involved.
- damage to two or more columns or risking neurological injury (ie damage to
the middle column) ̃ unstable.
Classification of cervical spine fractures
Details
Management
Aim is to prevent extension of primary injury, to reduce secondary injury and
to treat complications
Complications
Respiratory dysfunction
- degree depends on level of lesion. Lesions above C8 result in limited
expiratory function. Lesions above C3 result in total loss of ventilatory
function. Lesions at C3-5 result in similar levels of inspiratory dysfunction
but higher lesions have a greater respiratory complication rate
- leading cause of death, mainly due to pneumonia
- as
spinal shock resolves and the paralysis of the intercostal muscles becomes
spastic the chest wall becomes rigid and no longer collapses with
inspiration, resulting in an improvement in ventilatory (predominantly
inspiratory) function.
- In
the initial phase decreased tidal volumes can be compensated for by an
increase in respiratory rate. However the relatively high proportion of
minute ventilation that is dead space ventilation means that this
respiratory pattern is inefficient. In addition progressive atelectasis
results in increasing shunting and oxygenation failure. The decision to
intubate and ventilate the patient requires clinical judgement. On the one
hand 1/3 of patients with a cervical spine injury will require intubation,
many in the first 24 h. On the other hand intubation is associated with many
adverse effects, particularly nosocomial pneumonia
- Avoid suxamethonium if patient requires intubation between 3 days and 6 months
as it may precipitate hyperkalaemia
- Wean
patient in upright position
- In
the upright position the paralysed abdominal muscles allow the abdominal
contents to descend. This results in the diaphragm being in an
inefficient starting position for contraction
- In
the supine position the abdominal contents push the diaphragm into a
more efficient position for contraction
Haemodynamic instability
- Spinal
shock
- NB
Does not occur in low thoracic and lumbar spine lesions and is always
a diagnosis of exclusion
- Usually persist for weeks to months
- As
hypotension is due to a combination of peripheral vasodilatation and
bradycardia the appropriate treatment is fluid resuscitation followed by
an agent that has vasoconstrictor and chronotropic effects such as
epinephrine. The appropriate target blood pressure, in terms of spinal
perfusion, is not clear but at the very least mean arterial pressure
should be raised to a level that is associated with adequate urine
output and resolution of any other signs of inadequate tissue perfusion
- Arrhythmias
- Bradycardia
most common
- Supraventricular
and ventricular tachycardias may occur
- Most
common in first 14 days after injury
- More
common and severe in more severely injured patients
- ~50% with lesion above T7 demonstrate episodes of hypertension,
bradycardia, hypertonicity and cutaneous changes (either pallor or
vasodilatation) triggered by cutaneous, proprioceptive or visceral irritation
(often an overdistended bladder or rectum). Due to a loss of inhibition from
above. Sudden increase in BP stimulates a vagal response which can produce
bradycardia, heart block and vasodilatation above level of injury.
- Management:
good bladder and bowel care and alpha blockade when episode occurs
Visceral dysfunction
- bladder dysfunction: urinary catheter necessary in acute phase but after
2-3 weeks intermittent catheterisation preferable
- gastric stasis and ileus
- constipation. Gentle faecal disimpaction may be necessary in early stages
Venous thromboembolism
- high risk
- twice the risk of trauma patients without a spinal fracture
- spinal cord injury increases risk threefold
- risk of bleeding with anticoagulation and mechanical devices are not
sufficient prophylaxis on their own
- studies have shown that risk of DVT in first 72 hours is quite low so a
reasonable compromise seems to be to use a mechanical device alone in first
72 h and then subsequently to add low molecular weight heparin
Miscellaneous
- pressure sores. Greatly increase cost and morbidity
- poikilothermia in patients with lesion above T1
- hyponatraemia common in first week
Prognosis
Because of the possibility of spinal shock it is
difficult to assess prognosis prior to 72 hours. At 72h patients can be assessed
using the ASIA impairment scale. Patients are classified into classes A to E
depending on their motor and sensory function.
Bulbocavernosus reflex one of first reflexes to recover
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Description
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A
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Complete; no sensory or motor function preserved in
S4-S5
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B
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Incomplete; sensory but not motor function preserved
below neurological level and extending through S4-S5
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C
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Incomplete; motor function preserved below
neurological level. Most key muscles have < grade 3 power
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D
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Incomplete: motor function preserved below
neurological level. Most key muscles have > grade 3 power
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E
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Normal
motor and sensory function
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-
complete cord lesion at 72 h: 10-15% improve. Only 3%
improve to attain class D
-
class B at 72 h: 54% will improve to a lesser
degree of weakness
-
class C and D at 72 h: 86% will achieve useful motor
function below the level of the lesion
Further
reading
P. A. Ball. Critical care of spinal cord injury. Spine 26 (24 Suppl):S27-S30,
2001.
M. G. Fehlings. Editorial: recommendations regarding the use of
methylprednisolone in acute spinal cord injury. Spine 26 (24 Suppl):S56-S57,
2001
M. G. Fehlings, L. H. Sekhon, and C. Tator. The role and timing of
decompression in acute spinal cord injury: what do we know? What should we do?
Spine 26 (24 Suppl):S101-S110, 2001.
© Charles Gomersall and Ross Calcroft September 1999, Charles
Gomersall December 2002, March 2003, June 2003 |
