SPINAL CORD INJURY
SPINAL CORD INJURYDR. DAVIS KURIAN
Normal spine 3 columns
Anterior ant 2/3 of vertebral body, anterior longitudinal
ligament.Middle post 1/3 of the body, post longitudinal ligament,
post component of annulus fibrosisPosterior laminae, facets,
spinous process and interspinous ligament.
Two or more columns disturbed spinal injury results
Careful assessment required.
Failure to immobilise, investgiate and manage leads to worsening
of the existing cord injury or creating a new one.
Blunt trauma accounts for the majority of cord trauma: 40% from
motor vehicle collisions, 20% from falls, and the remainder due to
physical violence.
Usual sites include C5-C6 and T12-L1
Spinal cord injury at midthoracic levels is less common
-rotational stabilization provided by the rib cage and intercostal
musculature.
PATHOPHYSIOLOGY:
Primary neural damage- due to initial insult.
Secondary neural injury d/t:mechanical disruption
hypoxiahypotensionedemahaemorrhage into cordhyper/hypoglycemia
Includes sensory or motor deficits or both.
Incomplete deficits may be worse on one side, improve rapdily in
the first minutes and hours following injury
Complete deficits more obvious, little improvement seen.
Cervical spine injury -> quadriplegia and significant
hypotension seen (vasodilatation and loss of cardiac inotropy).
Lower cord normalises gradually normal vascular tone
returns.
Autonomic hyperreflexia in 85% with complete injury above T5
(excess sympathetic stimulus, absence of damping effect of
brain).
MECHANISMS:
DistractionCompressionTorsionPenetration.
Distraction in hyperextension (eg. Hanging), significant impact
on the head or face
Compression of the bony spine directly compromise the spinal
canal and spinal cord.
Torsion falls, high energy vehicle collisions can tear the
spinal cord tissue
Penetration in gun shot or stab injury
Usually radiographically visible injury to the bony spine and
concomitant disruption of the muscles, ligaments, and soft tissues
that support it are seen.
SCIWORA (spinal cord injury without radiographic abnormality) is
more common in children and is presumably the result of temporary
hyperdistraction or torsion of the neck insufficient to disrupt the
bony skeleton
TYPES OF INJURY:
Complete cord lesion: - motor, sensory and autonomic functions
are lost below the level of lesion.
Incomplete cord lesion includes 4 syndromes
Anterior cord syndrome :- Due to ischemia (eg. aortic injury)
blood supply from anterior spinal artery is distrupted.
Damage to cortico-spinal and spinothalamic tracts paralysis,
abnormal touch, pain and temperature sensation.
Posterior columns unaffected vibration and joint position senses
preserved.
Central cord syndrome :-
Central gray matter is damaged.
Paralysis with variable sensory loss UL>LL (upper limb fibres
close to centre).
Bladder dysfunction present as urinary retention.
Brown Sequard syndrome: -
Hemisection of the cord
Usually in penetrating trauma
Ipsilateral paralysis and loss of vibration and joint position
sense, with contralateral loss of pain and temperature
sensation.
Cauda equina syndrome:
Presents with loss of bowel and baldder function with LMN signs
on lower limbs.
Sensory signs unpredictable.
Assessing sensory level:-
Cervical :C5 deltoidC6 thumbC7 middle fingerC8 little finger
Thoracic :T4 nippleT8 xiphoidT10 umbilicusT12 symphysis
Lumbosacral:
L4 medial legL5 first/second toesS1 lateral footS4-5
perianal.
Assessing motor level:Cervical/thoracic:C5 biceps flexionC6
wrist extensionC7 elbow extensionC8 middle finger extnT1 little
finger abduction
Lumbosacral:L2 hip flexionL3 Knee extensionL4 - ankle
dorsiflexionL5 big toe extensionS1 big toe/ankle plantar
flexion
PROBLEMS:
AIRWAY:
Airway reflexes are lost and gastric stasis can have
aspiration.
BREATHING:
Above C4 diaphragm is paralysed apnea.
T2-T12 innervates intercostal muscles fractures above
diaphragmatic breathing limited expansion, decreased TV and FRC,
impaired cough, inc RV. Dec muscle power pneumonia is common.
ARDS and pulmonary emboli also occur
CIRCULATION:
Damage above T2 sympathteic innervation of heart lost loss of
reflex tachycardia, impaired LV function and risk of severe
bradycardia and asystole following unopposed vagal stimulation.
NEUROLOGICAL:
Spinal shock ms flaccidity and areflexia duration is
variable.
Following a/c phase of spinal shock majority of patients with
lesion above T7 autonomic dysreflexia (mass spinal reflex when area
below the lesion is stimulated) develops severe bradycardia,
hypertension, flushing and sweating above the lesion triggered by
distended bladder or bowel, pressure sores etc
TEMPERATURE:
Hypothermia due to peripheral vasodialatation.
BIOCHEMICAL AND ENDOCRINE:
Increased ADH water retentionGlucose intoleranceNG tube
hypokalemic metabolic alkalosisHypoventilation respiratory
acidosisOsteoporosis and hypercalcemia
SKIN pressure sores
THROMBOELASTOGRAM DVT and embolism.
MUSCULOSKELETAL muscle spasms and contractures.
PSYCHOLOGICAL reactive depression
MANAGEMENT:
PRIMARY SURVEY & RESUSCITATION:
Look for other injuries
Immobilise, minimise secondary causes of injury like hypoxia and
hyperperfusion before transferring the patient.
AIRWAY WITH CERVICAL SPINE CONTROL
MILSLow GCS- intubate at the earliest maintaining MILSSch can be
safely used.
FOB requires experienced hands.
BREATHING :
Sufficient oxygen and ventilation.
CIRCULATION:
Maintain adequate BP fluids alone/ fluids with pressors r/o
haemorrhage.
MAP >85mm Hg for 7 days after injury.
Hypotension with bradycardia is seen
SECONDARY SURVEY AND DIAGNOSIS
HISTORY
Mechanism of injuryPatient usually unconscious- so reliable
history not always possible.
EXAMINATION
Log roll tenderness and step off deformity
Other signs :
Flaccid anal sphincterAreflexiaDiaphragmatic
breathingHypotension without tachycardiaPriapism
Surgical decompression and stabilisation of spinal fractures
indicated when vertebral body loses >50% of normal height or
spinal canal narrowed >30% original diameter
INVESTIGATIONS/CLEARING THE SPINE IN TRAUMA PATIENTS:
X ray of cervical spine lateral occiput to T1, AP-C2-T1, open
mouth view- lateral masses of C1 and odontoid process.
Axial CT if radiological visibility is limited.
Life threatening injuries first priority.
Flexion and extension views in patients with normal radiographs
but has neck pain.
Patient with neurological deficit attributable to cervical spine
injury surgical subspeciality consult, MRI limited use in acute
phase, but gives definitive indication of severity of cord
injury.
DEFINITIVE CARE:
Early referral to a spinal injuries unit for early fixation.
AIRWAY:
Tracheostomy after cervical spine fixation for prolonged
ventilation.
BREATHING :
Insiduous worseing can occur hence close monitoring of
ventilation.
Early intubation to avoid late complications.
Suxamethonium avoided after the first 24 hrs for a year
following injury to avoid hyperkalemia.
CIRCULATION:IBP & CVP usually sufficient.
MINIMISING SECONDARY INJURY :
Avoid hypotension, hypoxia, hyper/hypothermia
Steroids methylprednisolone 30mg/kg over 15 min followed 45 min
later by cont infusion @ 5.4mg/kg/hr within 3 hrs of injury for 23
hrs and for 48 hrs if started 3-8 hrs after injury
AUTONOMIC DYSREFLEXIA
Good bowel and bladder care.
GIT
Early enteral feeding- maintains gut mucosa integrity. PEG- for
long term if swallowing inadequate.
SKIN
Prevent bed sores
THROMBOEMBOLISM:
Compression stockings, calf compression devices, s/c LMW heparin
for a minimum of 8 weeks.
PSYCHOLOGICAL
Important for good outcome, to avoid reactive depression.
INTRAOPERATIVE MANAGEMENT:
Challenge for anaesthesiologist :intubation for a known C spine
injurymost commonly by FOB nasal sinusitis later on, oral route
preferred.
Other methods : blind nasal, use of an illuminated stylet,
intubating LMA or bullard laryngoscope.
The clinician is advised to use the instrument and method which
he/she is familiar.
Whatever the method used the goal must be definitive tracheal
intubation with minimal cervical spine movement.
Quadriplegic and paraplegic patients hemodynamic instability due
to spinal shock.
Bleeding is minimal in spine surgeries but occur during iliac
crest bone harvesting.
Pressors should be continued, ABP monitored. Increased dose of
pressors to be assessed based on response to fluid therapy.
Thoracic and lumbar # bleed more.
Cases of other injuries with known spine injury management
guidelines are the same.
Remember that like a patient with traumatic brain injury, spinal
cord injured patient will also have impaired autoregulation hence
close monitoring of perfusion in the involved area is
essential.
SPINAL CORD INJURIES IN CHILDREN
Low incidence due to mobility of spine in children that can
dissipate force over larger area.
Management same as that in adults.
Infants and children less than 8 yrs- may need padding under
back for neutral position for immobilisation of spine.
SCIWORA:
Spinal cord injury without radiological abnormality.
Almost exclusively in children
