Traumatic spinal cord injury

Introduction to Traumatic SCI

1. TRAUMATIC SPINAL
CORD INJURY

2. 2Traumatic SCI

3. ETIOLOGY
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Traumatic SCI

4. 1.Tetraplegia :
Complete paralysis of all four extremities and trunk including
respiratory muscles
Results from lesion in cervical cord
2.Paraplegia :
Complete paralysis of all or part of trunk and both lower
extremities.
Results from lesion in thoracic or lumbar spinal cord or cauda
equina
CLASSIFICATION
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Traumatic SCI

5. DESIGNATION OF LESION
LEVEL
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Traumatic SCI

6. DESIGNATION OF LESION LEVEL
American Spinal Cord Injury Association (ASIA)
created International Standards Of Neurological
Classification Of Spinal Cord Injury ( ISNCSCI)
Provides a standardized examination method
Allows better communication between and among professionals
Provides guidance for establishing the prognosis
Important tool for clinical research trials
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Traumatic SCI

7. DESIGNATION OF LESION LEVEL
Neurological level: most caudal level of the spinal
cord with normal motor and sensory function on both
the left and right side of the body.
Motor level : most caudal segment of the spinal cord
with normal motor functions bilaterally.
Sensory level : most caudal segment of the spinal
cord with normal sensory functions (light touch and
pin prick) bilaterally.
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Traumatic SCI

8. DESIGNATION OF LESION LEVEL
Complete injury : no sensory or motor functions in
the lowest sacral segments (S4, S5)
Incomplete injury: having motor or sensory function
below the neurological level including sensory and
motor functions at S4 and S5
Zones of partial preservation: motor/sensory function below
the level of lesion present, but does not have function at S4
and S5.
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Traumatic SCI

9. CLINICAL SYNDROMES
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Traumatic SCI

10. BROWN SEQUARD SYNDROME
Causes :
Fracture dislocation of the vertebral
column
Bullet or stab wound
Expanding tumor
Clinical features :
Ipsilateral LMN paralysis at the level
of lesion
Ipsilateral UMN paralysis below the
level of lesion
Ipsilateral band of cutaneous
anesthesia at the level
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Traumatic SCI

11. BROWN SEQUARD SYNDROME
Ipsilateral loss of tactile
discrimination, vibration
and proprioception below
the level
Contralateral loss of pain
and temperature below
the level
Contralateral but not
complete loss of touch
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Traumatic SCI

12. ANTERIOR CORD SYNDROME
Causes :
Cord contusion during vertebral fracture
or dislocation (flexion injuries)
Injury to anterior spinal artery or its
feeder artery
Herniated IV disc
Clinical features :
Bil LMN paralysis at the level of lesion
Bil UMN paralysis below the level of
lesion
Bil loss of pain, temperature and light
touch below the level
Tactile discrimination, vibration and
proprioception preserved
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Traumatic SCI

13. CENTRAL CORD SYNDROME
Causes :
Hyperextension injuries
Congenital or degenerative
narrowing of the spinal canal
Clinical features :
Bil LMN paralysis at the level of
lesion
Bil UMN paralysis below the level of
lesion (U.L > L.L)
Sacral sparing
Bil loss of pain, temperature, light
touch and pressure (U.L > L.L).
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Traumatic SCI

14. POSTERIOR CORD SYNDROME
Rare syndrome
Preservation of motor
function, sense of pain
and light touch.
Loss of proprioception
and discrimination below
the level of lesion.
Wide based steppage gait
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Traumatic SCI

15. CAUDA EQUINA SYNDROME
It is frequently an incomplete lesion
Cauda equina are peripheral nerve injuries (LMN)
Full reinnervation is not possible because
1.Large distance between lesion and point of innervation
2.Axonal regeneration may not occur along the original
distribution of nerve
3.Axonal regeneration may be blocked by scarring
4.The end organ may no longer be functioning once reinnervation
occur
5.The rate of regeneration slows and finally stops after about 1
year
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Traumatic SCI

16. MECHANISM OF INJURY
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17. MECHANISM OF INJURY
Common mechanisms –flexion, compression,
hyperextension, and flexion-rotation.
Forces results in either fracture or dislocation of the
vertebrae.
The highest frequency of injury between C5 and C7in
the cervical region and between T12 and L2 in the
thoracolumbar region
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Traumatic SCI

18. Force Etiology Associated
fracture
Associated
injuries
Flexion •Headon
collision
•Blow to the
back of head
•Most
common
•Wedge # of
antor
vertebral
body
•High
percentage
of injuries
occur from
C4 to C7
and from
T12 to L2
•Tearingof
post
ligaments
•#s of post
elements
•Disruption
of disk
•Ant
dislocation of
vertebral
bodies
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19. Force Etiology Associated
fracture
Associated
injuries
Compression •Vertical or
axial blow
tohead
•Closely
associated
with flexion
injuries
•Concave #
of the end
plate
•Explosion or
burst #
•Tear drop #
•Bone
fragments
may lodge in
the cord
•Rupture of
the disk
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20. Force Etiology Associated
fracture
Associated
injuries
Hyperextension •Strong post
force such
as rear end
collision
•Falls with
chinhitting a
stationary
object
•#sof post
elements
•Avulsion # of
ant aspect o
vertebrae
•Rupture of
ant
longitudinal
ligament
•Rupture of
disk
•Associated
with cervical
lesions
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21. Force Etiology Associated
fracture
Associated
injuries
Flexion –
rotation
Post toant
force
directed at
rotated
vertebral
column
# of post
pedicles,
articular
facets, and
laminae
Rupture of
post and
interspinous
ligament
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22. MECHANISM OF INJURY
Two additional mechanism :
1.Shearing –when horizontal force is applied to the spine relative
to the adjacent segment.
2.Distraction –involves traction force and is least common
mechanism of injury
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Traumatic SCI

23. CLINICAL MANIFESTATIONS
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Traumatic SCI

24. SPINAL SHOCK
Believed to result from very abrupt withdrawal of
connections between higher centers and spinal cord.
Absence of all reflex activity, flaccidity and loss of
sensation and motor function below the level of
lesion.
May last from several days to several weeks
First indicator of the resolving spinal shock is a
positive bulbocavernous reflex
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Traumatic SCI

25. MOTOR AND SENSORY IMPAIREMENTS
Complete or partial loss of muscle function below the
level of lesion.
Impaired or absent sensation below the level of
lesion
Clinical presentation depends on neurological leve,
the completeness of the lesion, and symmetry of the
lesion
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Traumatic SCI

26. AUTONOMIC DYSREFLEXIA
It is acute onset of autonomic activity from noxious
stimuli below the level of lesion.
Occurs in lesions above T6 (above sympathetic
splanchnic outflow)
Following SCI, the impulses from the vasomotor
centers cannot pass the site of lesion to counteract
the hypertension by vasodialatation.
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Traumatic SCI

27. AUTONOMIC DYSREFLEXIA
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Traumatic SCI

28. AUTONOMIC DYSREFLEXIA
Initiating stimuli:
Baldder distension
Rectal distention
Pressure sores
Urinary stones
Bladder infections
Noxious cutaneous stimuli
Kidney malfunction
Urethral or bladder irritation
Environmental temperature changes
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Traumatic SCI

29. AUTONOMIC DYSREFLEXIA
Symptoms :
Hypertension
Bradycardia
Headache (severe and pounding)
Profuse sweating
Increased spasticity
Restlessness
Vasoconstriction below the level of lesion
Vasodialatation above the level of lesion
Constricted pupils
Nasal congestion
Piloerection and blurred vision
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Traumatic SCI

30. AUTONOMIC DYSREFLEXIA
Intervention:
It is a medical emergency
Pt brought to sitting position
Bladder drainage system should be examined
immediately
Check for irritating stimuli such as tight clothing,
restricting catheter, straps or abdominal binder
If the symptoms do not subside, medical and/or
nursing assistance should be sought immediately
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Traumatic SCI

31. POSTURAL HYPOTENSION
Decrease in blood pressure that occurs when
assuming and erect or vertical posture
Mechanism:
Loss of sympathetic vasoconstriction control + reduced muscle
tone peripheral venous and splanchnic bed pooling 
reduced cerebral blood flow and decreased venous return 
lightheadedness, dizziness and fainting
Frequent with cervical and upper thoracic lesion
Related problem –edema of legs, ankles and feet
(symmetric and pitting)
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Traumatic SCI

32. POSTURAL HYPOTENSION
The CVS should be allowed to adapt gradually by a
slow progression to the vertical position.
Vital signs should be monitored
Use of compressive stockings and abdominal binder
may help
Drug therapy –ephedrine to increase blood pressure
and low dose diuretics to relieve persistent edema of
legs
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Traumatic SCI

33. IMPAIRED TEMPERATURE CONTROL
Control of hypothalamus on cutaneous blood flow is
lost
Autonomic dysfunction loss of internal
thermoregulatory responses
Lost ability to shiver
Absence of thermoregulatory sweating below the
level of lesion excessive compensatory
diaphoresis above the level of lesion
Body temperature significantly affected by external
environment
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Traumatic SCI

34. RESPIRATORY IMPAIREMENT
Respiratory function varies considerably,
depending on the level of lesion
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Traumatic SCI

35. RESPIRATORY IMPAIREMENT
The level of respiratory impairementis directly
related to:
1.The lesion level
2.Residual respiratory muscle function
3.Additional trauma sustained at the time of injury
4.Premorbidrespiratory status
Pulmonary complications –high mortality during
early stages of tetraplegia
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Traumatic SCI

36. RESPIRATORY IMPAIREMENT
Higher the lesion, greater the loss of respiratory
function
Paralysis of external intercostals muscles 
decreased chest expansion and lower inspiratory
volume
Higher level of lesion increased involvement of
accessory muscles (sternocleidomastoid, trapezius,
pectoralis minor, serratus anterior)
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Traumatic SCI

37. RESPIRATORY IMPAIREMENT
Loss of abdominals and internal intercostals 
significant decrease in expiratory efficiency
The lowered position of the diaphragm and lack of
abdominal pressure to move the diaphragm up 
decrease the effectiveness of cough and decreased
expiratory reserve volume
Altered breathing pattern lead to permanent postural
changes
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Traumatic SCI

38. SPASTICITY
Results form release of intact reflex arcs from CNS
control and is characterized by:
Hypertonicity
Hyperactive stretch reflex
Clonus
Gradual increase in spasticity in first 6 months
Plateau reached in 1 year
Spasticity increased by multiple internal and external
stimuli
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Traumatic SCI

39. SPASTICITY
Some spasticity may assist in functional activities
Strong spasticity interferes with function
Drugs used for spasticity (muscle relaxants and
spasmolytic agents):
Diazepam (valium)
Baclofen (lioresal)
Dantrolene sodium (dantrium)
Peripheral nerve blocks / intrathecal injections
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Traumatic SCI

40. SPASTICITY
Orthopedic surgical procedures:
Myotomy
Neurectomy
tenotomy
Neurosurgical procedures:
Rhizotomy
myelotomy
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Traumatic SCI

41. BLADDER DYSFUNCTION
UTIs are most frequent medical complication
Stage of spinal shock –flaccid bladder
Treatment focused on effective system of drainage
and prevention of urinary retention and infection
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Traumatic SCI

42. BLADDER DYSFUNCTION
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Traumatic SCI

43. BLADDER TRAINING
Primary goal –pt free of catheter
-control bladder function’
Spastic bladder –using micturition reflexes and
trigger stimulus to establish planned reflex voiding
Flaccid bladder –intermittant catheterization
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Traumatic SCI

44. BOWEL DYSFUNCITON
Level of lesion at/above T11,T12 –spastic bowel
Level of lesion below T12 –flaccid bladder
Bowel training programme for spastic bladder –
regularly scheduled evacuation, usually every other day
Responsible to a combination of laxatives(milk of magnesia), stool
softner and suppositories (Ducolax)
Digital stimulation can be used to initiate a planned reflex bowel
evacuation
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Traumatic SCI

45. BOWEL DYSFUNCITON
Bowel training programme for flaccid bowel
Daily evacuation necessary to keep the rectum clear of feces
and prevent incontinence
Response to medication less effective than with spastic bowel
dysfunction
Nonresponsive ot digital stimulation
Manual removal of stool from the rectum may be required
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46. INDIRECT IMPAIREMENTS
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Traumatic SCI

47. RESPIRATORY COMPLICATION
Most common cause of death
Reduced ventilation and weak cough makes it
difficult to clear secretions
Atelectasis and pneumonia
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Traumatic SCI

48. PRESSURE SORES
Ulceration of the soft tissue caused by unrelieved
pressure or shearing force
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Traumatic SCI

49. PRESSURE SORES
CAUSES:
1.Impaired sensory function
2.Inability to make appropriate postural changes
3.Loss of vasomotor control lowering tissue resistance to
pressure
4.Spasticity with resultant shearing force between surfaces
5.Skin maceration from exposure to moisture (e.g., urine)
6.Trauma such as adhesive tapes
7.Nutritional deficiencies
8.Poor general skin condition
9.Secondary infections
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50. PRESSURE SORES
Pressure sores develop over bony prominences
subjected to excessive pressure
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Traumatic SCI

51. PRESSURE SORES
INTERVENTION:
2 hourly turning regimen
Regular observation of the skin
Gradually pt assumes responsibility for skin care
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Traumatic SCI

52. DVT
Results from the development of thormbus within the
vessel wall
It has potential to form emboli
Contributing factors:
Loss of normal pumping mechanism
Age
Prolonged pressure
Loss of vasomotor tone
Immobility
Sepsis
Hypercoagulability
trauma
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Traumatic SCI

53. DVT
Clinical features:
Local swelling
Ereythema
Pain
Heat
Management :
Prophylactic anticoagulant therapy continued for 2-3 months
following injury
A turning programme designed to prevent pressure over large
vessels
Passive Range of motion exercise
Elastic support stockings
Positioning of the L.L
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Traumatic SCI

54. CONTRACTURES
Contractures develop secondary to prolonged
shortening of structures across and around a joint.
Initially affect muscle tissue
Later involves capsular and pericapsular structures
Causes:
Spasticity
Flaccidity
Faulty positioning
Heterotropic ossification
Edema
Management: early ROM exercises, positioning and
splinting
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Traumatic SCI

55. HETREOTROPIC OSSIFICATION
Osteogenesis in the soft tissue below the level of
lesion
Predisposing factors:
Tissue hypoxia secondary to circulatory stasis
Abnormal calcium metabolism
Local pressure and
Micro trauma related to aggressive range of motion
It is always extra articular and extracapsular.
Develops in tendon, connective tissue, aponeurotic
tissueor peripheral aspect of muscles
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Traumatic SCI

56. HETREOTROPIC OSSIFICATION
Typically develops adjacent
to large joints
Symptoms include –
swelling, decreased ROM,
erythema, and local warmth
near the joint
Initial stage –elevated
serum alkaline phosphatase
Late stages –positive
radiographic findings
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Traumatic SCI

57. HETREOTROPIC OSSIFICATION
Management:
Pharmacological therapy (diphospahtes)
Physical therapy
Surgery (resection of ectopic bone)
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Traumatic SCI

58. PAIN
TRAUMATIC PAIN
Causes:
Fractures
Ligamentous or soft tissue damage
Muscle spasm
Early surgical intervention
Management:
Immobilisation
Analgesics
TENS
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59. PAIN
Nerve root pain:
Causes:
Acute compression/tearing of the nerve roots
Periradicular scar tissue and adhesion formation
Improper reduction
Management:
Pharmacological therapy Analgesics
TENS
Neurectomy
rhizotomy
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Traumatic SCI

60. PAIN
Musculoskeletal pain
Frequently involves shoulder joint
Related to:
Faulty positioning
Inadequate ROM
Role as tonic stabilizer to subsitute for trunk
Management:
Regular ROM exercise
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Traumatic SCI

61. PAIN
Osteoporosis and renal calculi:
Imbalance between bone resorption and bone formation
Secondary to immobility and lack of stress on skeletal system
Management:
Dietary consideration
Prevention of urinary tract infections
Early wt bearing activities
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62. PROGNOSIS
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63. PROGNOSIS
Potential for recovery is influenced by:
1.Degree of pathological changes imposed by the trauma
2.Precaution taken to prevent further damage
3.Prevention of additional damage to neural tissue from
hypoxia and hypotension
After spinal shock complete lesion with early
appearance of reflex activity poor prognosis
Incomplete recovery good prognosis
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64. PROGNOSIS
Improvement begins immediately after spinal shock
Consistent progression of muscle return further
recovery expected.
After a plateau is reached no additional recovery
expected
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65. Traumatic SCI 65
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