K.K.

Bansal
A comma OR a full stop ?
Manjunath Kalmani: Was a
software engineer. Paralyzed
from neck down. Spinal cord
injury level C4 when he got
injured in a car accident , in
April 2002, slowly injury level
became C2 complete. On
ventilator 100%.

Presently in Safdarjung
Hospital, New Delhi.
Introduction
INTRODUCTION:
 Leading cause of morbidity and mortality in youth
 Both physical and emotional aspects of spinal cord injury are
devastating.
 
OCCURRENCE:
 Approximate 20,000 new cases of SCI are added every year in
India - Sinha DK. Manual of Patna. Model for the care of Spinal cord injury patients. Patna:
SPARSH. 2000; 9-13.
 60-70% of them are illiterate, poor villagers. Most sustain this
injury by fall from unprotected roofs, trees or fall into
uncovered wells, which infact are preventable causes
 No definite treatment till date; the effect of initial trauma is
irreversible.
 High cost of medical treatment and supporting those
permanently disabled
Epidemiology
Age Group Causes
Young RTA
Atheletic events

Middle aged Industrial accidents

Old Fall

Urban areas Violence, e.g. Gunshot

Rural areas Diving

Age and sex distribution

Singh R. et al. Traumatic Spinal Cord Injuries in Haryana: An Epidemiological Study.

Indian Journal of Community Medicine, Vol. 28, No. 4 (2003-10 - 2003-12)
Mode of injury

Singh R. et al. Traumatic Spinal Cord Injuries in Haryana: An Epidemiological Study.

Indian Journal of Community Medicine, Vol. 28, No. 4 (2003-10 - 2003-12)
Being young…
Also means… Seeking risk…
Anatomy
Designation of lesion level
Three column model of Denis

Denis F. The three-column spine and its significance in the classification of acute thoracolumbar spinal
injuries. Spine 1983;8:817.
Definition :

Spinal cord injury is an insult to the spinal cord resulting in

the change , either temporary or permanent, in its
motor, sensory or autonomic function.

Terminology :

 Tetraplegia (quadriplegia) – injury to spinal cord in the cervical region

with associated loss of muscle strength in all 4 extremities.

 Paraplegia – injury in the spinal cord in the thoracic, lumbar, or sacral

segments with associated loss of muscle strength in both lower limbs.

 Pentaplegia - involving respiratory muscle i.e. Diaphragm also

Pathophysiology of Spinal Cord Injury
 Primary Injury –
Anatomical- Mechanical shearing of axons and blood
vessels
Physiological- so called concussion which is
uncommon and totally reversible within 2-4 wk.

 Secondary Injury –
Microvascular and neuronal injury due to a cascade
of pathophysiological events that exacerbate
primary injury
(Potential target of pharmacological treatment)
Primary mechanism of SCI
Mechanical force Mechanism of injury

Impact + compression Burst #, # dislocation, disc

rupture
Impact alone Hyperextension

Distraction Hyperflexion

Laceration, transection Burst #, laminar #, #

dislocation, missile
Secondary mechanisms
Systemic effects (spinal shock)
 Heart rate – bradycardia
 BP – hypotension
 Peripheral resistance – decreased
 Cardiac output – decreased
 Catecholamines – decreased
Local vascular damage of cord micro-circulation
 Mechanical disruption of capillary
 Haemorrhage – gray matter
 Loss of microcirculation – mechanical, thrombosis, vasospasm
 Reduction of cord blood flow – thrombosis, vasospasm
 Loss of autoregulation
Secondary mechanisms
Biochemical changes
 Excitotoxicity – glutamate
 Neurotransmitter accumulation – norad., dopamine
 Arachidonic acid release
 Free radical production
 Prostaglandin production
 Lipid peroxidation
Electrolyte shifts
 Increased intracellular calcium and sodium
 Increased extracellular potassium
Oedema
Decreased ATP production
PRIMARY LESIONS
4 types of lesions usually found :
 Contusion -23%, moderate contusive forces, leave
continuity of cord, centrally located hematomyelia,
becoming stable cyst
 Cord maceration -32%, massive compression, severe
destruction of almost all nervous tissue, pial breach,
subsequent connective tissue scarring
 Cord laceration -27%, open injury e.g. gun shot, torn
cord parenchyma
 Solid cord injury –18%, overall form of cord retained,
confined to white matter esp. corticospinal tract –
diffuse axonal disruption, grey matter not affected
Bunge RP, et al. Observation on pathology of human spinal cord injury. A review and classification
of 22 new cases with details from a case of chronic cord compression with extensive focal demyelination.
Adv Neurol 1993; 59: 75-89.
MECHANISM OF SCI

Flexion Injury Vertical Compression

Injury

Flexion-rotation Injury Hyperextension injury

 Risk Associated with Level of Injury

Intercostal Muscles Accessory Muscles C1-7

T1-11

Diaphragm Abdominal Muscles

C3-5 T6-12
 CLASSIFICATION OF
INJURY: either
quadriplegia or
paraplegia with
 Complete Lesions- no
sensory or motor
function below the
lesion
 Incomplete Lesions-
preservation of some
sensory or motor
function below lesion.
May present as one of
the following
Complete injury- worst prognosis
Incomplete injury-
With no motor function- poor recovery
With some motor function- good recovery

Other factors responsible- age, sex, rectal tone,

reflexes, medical & surgical treatment,
neurological status and initial strength of
muscles.
CLINICAL MANIFESTATIONS:
DIRECT
SPINAL SHOCK –common to all pts
Pain in the neck or back
Motor / sensory impairments
Impaired temperature control
Respiratory impairment
Spasticity
Bowel & Bladder dysfunction
Sexual dysfunction
 INDIRECT
Pressure sores
Contractures
Deep vein thrombosis (DVT)
Pain
Osteoporosis & Renal calculi
SPINAL SHOCK
It is a state of transient physiological reflex depression
of cord function below the level of injury with associated
loss of all sensorimotor and autonomic functions.
Spinal shock manifested by triad of hypotension,
bradycardia, and hypothermia
Neurogenic shock is due to combination of
1. Decresed sympathetic tone
2. Unopposed cardiac vagotonia
3. Possible secondary changes in heart

Kiss ZHT, et al. Neurogenic shock. In Geller ER (ed). Shock and Resuscitation.
New York: Mc Graw Hill, 1993, pp 421-440
Syndromes assoc. with SCI
Central cord syndrome
Often associated with a
cervical region injury
leading to weakness
greater in the upper
limbs than in lower
limbs with sacral
sensory sparing
Seen after
hyperextension injury
Anterior cord syndrome
Often associated with
lesions causing
variable loss of motor
function and senstivity
to pain and
temperature, while
proprioception is
preserved.
Seen in hyperflexion
injury
Poor prognosis
 Brown-sequard
syndrome
Hemisection lesion of the
cord, causing a
ipsilateral proprioceptive
and motor loss with
contralateral loss of
senstivity to pain and
temperature
Seen after penetrating injury
Better prognosis
Conus medullaris syndrome –assoc. with injury
leading toto the sacral cord and lumbar nerve roots
areflexic bladder, bowel, and lower limbs, while the
sacral segments occasionally may show preserved
reflexes( bulbocavernous and micturition reflexes)
Cauda equina syndrome is due to the injury to
lumbosacral nerve roots below L3 vertebrae leading to
areflexic bladder, bowel and lower limb.
Posterior cord syndrome –damage in post. column
leading to preservation of motor function and loss of
sensory function below injury level.
MANAGEMENT
 Goals :
1. Preservation of life –by primary management as A B
C
2. Preservation of function –by protecting the spine by
external support e.g collar,spine-board,sand
bags,traction etc.
3. Restoration of the function –by decompression,
fusion/fixation and finally by rehablitation.
At the site of accident
Assume every pt of trauma has SCI until
radiography of entire length proves
otherwise
↓
Until then the head & neck must be
stabilized with rigid collar of appropriate
size with sandbags on each side with
forehead tape on spinal board
↓
Spine immobilisation and log rolling
↓
Transfer to hospital
At emergency
Airway – clear airway , avoid excessive suction( as it
may stimulate vagal reflex-aggravate pre-existing
bradycardia & precipitate cardiac arrest),
tracheostomy if needed.
Avoid hyperextension of the neck, which will prevent
worsening of canal stenosis as well as exacerbating
motion of fractured segments or dislocations.
Breathing – oxygen support ,ventilator
Circulation – maintain B.P >110/70 (establishment of
adequate intravenous line). General support of
patient’s cardiovascular function is important to
optimize spinal cord perfusion and prevent ischemic
secondary injury.
The use of vasopressors, such as dopamine and
neosynephrine, is useful in reversing the effects of
neurogenic shock.
Spine immobilisation and positioning
 Avoid spinal rotaion
during resuscitation and
transfer.
 If pt comes within 8 hrs
of injury—start steroid
infusion
(methylprednisolone)
 Complete history &
neurological
examination –rule out
any other ass. Injury
and see for local
bruising, tenderness
and deformity of spine
 Shift to radiology
High Dose Methylprednisolone (MP) Therapy for
Acute Spinal Cord Injury

MP acts through microvascular and neuroprotective effects

Inhibition of post-traumatic lipid peroxidation appears to

be the principal neuroprotective mechanism

Glucocorticoid receptor-mediated anti-inflammatory

effects play only a minor role in comparison to lipid
antioxidant effects

Early treatment is required since lipid peroxidation

develops rapidly and is irreversible
Indication and duration of treatment
For acute non-penetrating SCI (<3 hours after
injury), MP should be given for 24 hours
For acute non-penetrating SCI (after 3 hours,
within 8 hours), MP should be given for 48 hrs
For acute non-penetrating SCI (>8 hours after
injury), MP should not be used.
For acute penetrating SCI, MP is not
recommended
Recommended Dosage and Administration for
Acute Spinal Cord Injury

STEP ONE: Initial bolus:

30 mg/kg of body weight
given over 15 mins. (45 mins
pause)

STEP TWO: 23-hour infusion:

5.4 mg/kg/hour of body weight
Investigations

X-ray spine – AP and lateral views of suspected

injured areas of spine.
X-ray chest
X-ray abdomen/ultrasonography
C.T is done only when MRI is not available.
MRI is mainstay of further treatment
Definitive management
Occipital condyle fractures
I. Hard cervical collar
or cervicothoracic
brace for 6-8 wks.
II. Halo vest for 12
wks.
III. Posterior occipital to
C2 arthrodesis or
Bohlman wire
technique and
posterior occipital
cervical fusion wit
atlanto-occipital
reconstruction plate.
Hard cervical collar Cervicothoracic brace
Halo vest
Atlanto-occipital dislocations
I. Cervical traction +
decompression + halo
vest

Internal fixation
II. Cervical traction is
contraindicated
III. Same as I
Atlas fractures (C1)
A. Cervical orthotic
device for 8-12
wks
B. Same as A
C. Halo vest
D. Collar
immobilization
Axis fractures (C2)
I. Cervical collar
II. Halo vest for 12
wks. In case of
unstable #,
posterior C1-C2
fusion with
atlanto axial
wiring or
transarticular
screw fixation.
III. Halo vest for 12
wks
Traumatic spondylolisthesis
I. Cervical collar
II. Reduction + halo vest
III. Same as II
Subaxial Fractures
Compression # - cervical collar
Burst # - operative fixation or halo vest
Teardrop # - halo vest or anterior decompression and
plating + a posterior procedure
Unilateral facet dislocation – closed reduction with
cervical traction + halo vest or open reduction
followed by fixation.
Bilateral facet dislocation – same as above
Hyperextension injuries – surgical stabilization
Clay Shoveler’s # - cervical collar
SCIWORA
Spinal cord injury without radiographic abnormality
 Most common in 1 – 16 yrs.
24 hours of steroids given although no hard data exists
Treatment: Bedrest, C-Collar until normal flex/ext,
halo vest for 1-3wks, discontinue if flex/ext X-rays
normal at 3 months
No sport participation for 3 monthss
Compression #
Universal segmental
fixation system or
Harrington
distraction rod system
Thoracolumbar
orthosis for 3 mths
Surgical stabilization
Occipito-Cervico-Thoracic
Spinal Fixation System
Burst #
Universal segmental
fixation system or
Harrington distraction
rod system
Thoracolumbar
orthosis for 3 mths
Anterior
decompression and
fusion
Laminectomy
Seat belt type injuries
Osseous injuries – bracing devices
Ligamentous injuries – posterior fusion and
compressive instrumentation
Fracture dislocations
Posterior fixation
and fusion and
decompression
(if needed)
Bed rest for 6-10
wks
Prevention
Prevention education -
Schools
University sports centre
Driving schools
Collaboration work –
with state deptt.
with law enforsement agencies
Epidemiological studies
Technical maintainance
Safety equipments (driving,work,sports)
Complications and mx
 Respiratory -regular chest physiotherapy, regular
monitoring of SPO2, vital capacity, Arterial blood
gases(ABG)----Tracheostomy & Ventilatory
support ,if required .
 Urological – bladder drainage facilitated by
intermittent or indwelling catheterization and avoid
UTI
 GIT- SCI is accompanied by paralytic ileus-so IVF
for first 48 hrs and avoid acute peptic ulceration by
giving antacids.
 Skin & Pressure areas- turn the pt every 2 hrly to
prevent pressure sores and nursing care requires use of
pillows to separate limbs, maintain alignment of spine
and prevent contractures.
Cx spine--- neck rolls---maintain Cx lordosis
D/L spine--- pillow----maintain lumber lordosis
Foot drop---vertical pillow—prevent equinous
contracture
 Thrombo- Embolism- regular limb
physiotherapy,stockings and heparin therapy.
 Joints & Limbs —joints movement prevent stiffness &
contractures. Use splints to keep tetraplegic pt in
functional position
Mulitidisciplinary approach to
neurological rehabilitation
Medical personnel
Rehabilitation nurse
Physiotherapist
Occupational therapist
Speech and language
therapist
Social workers
Dieticians
Clinical psychologists
THANK YOU