Traumatic spinal cord injuries can cause tetraplegia or paraplegia depending on the level of the lesion in the spinal cord. Injuries are often classified based on whether they are complete or incomplete. Common clinical manifestations include motor and sensory impairments, autonomic dysreflexia, respiratory issues, spasticity, and bladder and bowel dysfunction. Indirect impairments from SCI can also occur and include respiratory complications, pressure sores, deep vein thrombosis, and other issues.
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
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
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
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 •Head on
collision
•Blow to the
back of head
•Most
common
•Wedge # of
ant or
vertebral
body
•High
percentage
of injuries
occur from
C4 to C7
and from
T12 to L2
•Tearing of
post
ligaments
•#s of post
elements
•Disruption
of disk
•Ant
dislocation of
vertebral
bodies
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Traumatic SCI
19. Force Etiology Associated
fracture
Associated
injuries
Compression •Vertical or
axial blow
to head
•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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Traumatic SCI
20. Force Etiology Associated
fracture
Associated
injuries
Hyperextension •Strong post
force such
as rear end
collision
•Falls with
chin hitting a
stationary
object
•#s of post
elements
•Avulsion # of
ant aspect o
vertebrae
•Rupture of
ant
longitudinal
ligament
•Rupture of
disk
•Associated
with cervical
lesions
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Traumatic SCI
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
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
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
35. RESPIRATORY IMPAIREMENT
The level of respiratory impairement is directly
related to:
1. The lesion level
2. Residual respiratory muscle function
3. Additional trauma sustained at the time of injury
4. Premorbid respiratory 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
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
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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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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Traumatic SCI
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
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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Traumatic SCI
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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Traumatic SCI
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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Traumatic SCI