Aprilia

i) Trauma langsung
ii) Kompresi oleh fragmen tulang/
hematom
iii) Iskemik karena
kerusakan/penekanan pada arteri
spinalis
 National Spinal Cord Injury
Database
{ USA Stats }

55% usia 16 30 tahun

81.6% pria
South African Statistics (GSH
Acute Spinal Cord Injury Unit
2007)
Anatomi Medulla Spinalis
Medulla Spinalis
 Normal Spinal Cord
Dermatones
Skin innervated by
sensory spinal nerves
Myotome- muscle
group innervated by
motor neurons
 Nervous System and the
Spinal Cord
ANS can be affected
by SCI
Sympathetic chains
on both sides of the
spinal column (T1-
L2)
Parasympathetic
nervous system is
the cranial-sacral
branch (brainstem,
S2-4)
Kolumna
Vertebra
 Spinal Cord Protection

Internal and
external ligaments
Dura
Meninges
CSF in subarachnoid
space allow for
movement within
spinal canal
 Etiology of Traumatic SCI
MVA- most common cause
Other: falls, violence, sport injuries
SCI typically occurs from indirect injury
from vertebral bones compressing cord

SCI frequently occur with head injuries

Cord injury may be caused by direct
trauma from knives, bullets, etc
 Etiology of Traumatic SCI
78% people with SCI are male
Typically young men 16-30
Number of older adults rising (>61
yr)
Greater complications
Life Expectancy 5 years less than
same age without injury
90% go home
 Spinal Cord Injury- SCI
Compression
Interruption of blood supply
Traction
Penetrating Trauma
 Spinal Cord Injury
Primary
Initial mechanism of injury
Secondary
Ongoing progressive damage
Ischemia
Hypoxia
Microhemorrhage
Edema
 Spinal Cord Injury
Hemorrhage and edema occur in the cord
post injury, causing more damage to cord

Extension of the cord injury from cord

edema can occur over the first few days
watch the phrenic nerve!

Initially SCI experience spinal shock

depression of all cord & ANS function below
injury. Lasts from few min to wks
 Spinal and Neurogenic
Shock
Spinal Shock
Decreased reflexes and loss of sensation
below the level of injury
Motor loss- flaccid paralysis below level
injury
Sensory loss- loss touch, pressure,
temperature pain and proprioception
perception below injury
Lasts days to months
 Spinal and Neurogenic
Shock
Neurogenic shock
Due to loss of vasomotor tone
SNS loss results in parasympathetic
dominance with vasomotor failure
Loss of SNS innervation causes
peripheral pooling and decreased cardiac
output
Hypotension and Bradycardia
Orthostatic hypotension and poor
temperature control (poikilothermic)
 How do you know spinal shock is
over?

Clonus is one of the

first signs
Hyperreflexia of foot
Test by flexing leg at
knee & quickly
dorsiflex the foot
Rhythmic oscillations
of foot against hand
clonus
 Classifications of SCI
Mechanism of Injury
Skeletal and Neurologic Level
Completeness (degree) of Injury

Mechanism of Injury
Flexion
Hyperextension
Compression
Flexion /Rotation
 Classifications of SCI
Mechanism of Injury

Flexion (hyperflexion)
Most common
because of natural
protection position.
Generally cause neck
to be unstable
because stretching of
ligaments
 Classifications of SCI
Mechanism of Injury

Hyperextention
Caused by chin hitting
a surface area, such
as dashboard or
bathtub
Usually causes central
cord syndrome
symptoms
 Classifications of SCI
Mechanism of Injury

Compression
Caused by force from
above, as hit on head
Or from below as
landing on butt
Usually affects the
lumbar region
 Classifications of SCI
Mechanism of Injury

Flexion/Roatation
Most unstable
Results in tearing of
ligamentous
structures that
normally stabilize the
spine
Usually results in
serious neurologic
deficits
 Skeletal level
Vertebral level where
the most damage to
the bones
Neurologic level
The lowest segment
of the spinal cord
with normal sensory
and motor function
on both sides of the
body

Levels of Function in
Spinal Cord Injury
 Classification of SCI-
Level of Injury
Spinal cord level

When referring to spinal

cord injury, it is the reflex
arc level (neurologic)not
the vertebral or bone
level.

the thoracic, lumbar &

sacral reflex arcs are
higher than where the
spinal nerves actually
leave through the
opening of vertebral bone
 Classifications of SCI
Completeness (Degree) of
Injury
Complete
Incomplete
Central cord syndrome
Anterior Cord syndrome
Brown-Sequard Syndrome
Posterior Cord Syndrome
Cauda Equina and Conus Medullaris
 Classification of SCI
Completeness (degree) of
Injury
Complete (transection)
After spinal shock:
Motor deficits-
spastic paralysis
below level of injury
Sensory-
loss of all sensation
perception
Autonomic deficits-
vasomotor failure and
spastic bladder
 Classification of SCI
Completeness (degree) of
Injury
Incomplete

Central Cord Syndrome

Injury to the center of

the cord by edema
and hemorrhage
Motor weakness and
sensory loss in all
extremities
Upper extremities
affected more
 Classification of SCI
Completeness (degree) of
Injury
Incomplete
Brown-Squard Syndrome

Hemisection of cord
Ipsilateral paralysis
Ipsilateral superficial
sensation, vibration and
proprioception loss
Contralateral loss of
pain and temperature
perception
 Classification of SCI
Completeness (degree) of
Injury
incomplete
Anterior Cord Syndrome

Injury to anterior cord

Loss of voluntary motor,
pain and temperature
perception below injury
Retains posterior column
function (sensations of
touch, position, vibration,
motion)
 Classification of SCI
Completeness (degree) of
Injury
incomplete
Posterior Cord Syndrome

Least frequent syndrome

Injury to the posterior
(dorsal) columns
Loss of proprioception
Pain, temperature,
sensation and motor
function below the level
of the lesion remain intact
 Classification of SCI
Completeness (degree) of
Injury
incomplete

Conus Medullaris
Injury to the sacral
cord (conus) and
lumbar nerve roots
Cauda Equina
Injury to the
lumbosacral nerve
roots
Result- areflexic
(flaccid)bladder and
bowel, flaccid lower limbs
 Clinical Manifestations of
SCI
Skin: Cardio:
pressure ulcers dysrhythmias
spinal shock
Neuro: loss of SNS control
pain over blood vessels
sensory loss orthostatic
upper/lower motor hypotension,
deficits poikilothermic
autonomic
dysreflexia
 Respiratory- GU
decrease chest upper/lower motor
expansion, cough bladder
reflex & vital Impotence
capacity sexual dysfunction
diaphragm function- Musculoskeletal
phrenic nerve joint contractures
GI bone demineralization
stress ulcers osteoporosis
paralytic ileus muscle spasms
muscle atrophy
bowel- impaction &
incontinence pathologic fractures
para/tetraplegia
 Common
Manifestation/Complications
Upper and Lower Motor
Deficits

Upper motor deficits

result in spastic
paralysis

Lower motor deficits

result in flaccid
paralysis and muscle
atrophy
 Common
Manifestations/Complications
Spinal cord injuries are described by the level of the injury the
cord segment or dermatome level
Such as C6; L4 spinal cord injury

Terms used to describe motor deficits

Prefix:
para- meaning two extremities
tetra- or quadra- all four extremities
Suffix :
-paresis meaning weakness
-plegia meaning paralysis

Quadraparesis means what?

 Common
Manifestations/Complicat
ions
C1-3 usually fatal-
Loss of phrenic
innervation ventilator
dependent
No B/B control
Spastic paralysis
Electric w/c with
chin/mouth control
 Common
Manifestations/Complicat
ions
C6- weak grasp
Has shoulder/biceps to
transfer & push w/c
No bowel/bladder
control.

Considered level of
independence
 Common
Manifestations/Complicat
ions
T1-6- full use of upper
extremity
Transfer
Drive car with hand
controls and do ADLs
No bowel/bladder
control
 Immediate Care
Emergency Care at Scene,
ER & ICU

Transport with cervical

collar
Assess ABCs; O2;
tracheotomy/vent
IV for life line
NG to suction
Foley
 Diagnostic Studies for SCI

X-ray of spinal column

CT/MRI
Blood gases
Therapeutic Interventions
Medications
IV methylprednisolone (Solu-Medrol) within
8 hrs to decrease cord edema
 Therapeutic
Interventions
Medications
To control or to prevent complications of
SCI and immobility:
Vasopressors to maintain perfusion
Histamine H2 blockers to prevent stress
ulcers
Anticoagulants
Stool softeners
Antispasmodics
Therapeutic
Interventio
ns
Stabilization/
Immobilization

Traction-
Gardner-wells
tongs
Halo

Casts
Splints
Collars
Braces
Therapeutic Interventions
Surgery for SCI

Manipulation to
correct dislocation or
to unlock vertebrae
Decompression
laminectomy
Spinal fusion
Wiring or rods to hold
vertebrae together
 Nursing Management
Assessment
HEALTH HISTOY
Description of how and when injury
occurred
Other illnesses or disease processes
Ability to move, breathe, and associated
injury such as a head injury, fractures
 Nursing Management
Assessment
PHYSICAL EXAM

LOC and pupils- may have indirect SCI from

head injury
Respiratory status- phrenic nerve
(diaphragm) and intercostals; lung sounds
Vital signs
Motor
Sensory
Bowel and bladder function
 Nursing Management
Assessment
Motor Assessment Upper
Extremity

Movement, strength
and symmetry

Hand grips

Flex and extend arm

at elbow- with and
without resistance
 Nursing Management
Assessment
Motor Assessment
Lower Extremity

Flex and extend leg

at knee with and
without resistance
Planter and dorsi
flexion of foot
Assess for Clonus
 Nursing Management
Assessment
Sensory assessment

With the sharp and dull

ends of a paperclip have
the individual, with their
eyes closed identify

Use the dermatome as

reference to identify level

C6 thumb; T4 nipple; T10

naval
Nursing Problems/Interventions

1.Impaired mobility
2.Impaired gas exchange
3. Impaired skin integrity
4. Constipation
5. Impaired urinary elimination
6. Risk for autonomic dysreflexia
7. Ineffective coping
 1. Impaired Physical Mobility
Log roll as a single unit; provide
assistance as needed to keep
alignment; teach patient
Care traction, collars, splints, braces,
assistive devices for ADLs
Flaccid paralysis- use high top tennis
shoes or splints to prevent
contractures. Remove at least every 2
hrs for ROM (active ROM best)
 1. Impaired Physical Mobility
Spastic Paralysis
Prevent spasms by avoiding; sudden
movements or jarring of the bed; internal
stimulus (full bladder/skin breakdown; use of
footboard; staying in one position too long;
fatigue
Treat spasms by decreasing causes; hot or
cold packs; passive stretching; antispasmodic
medications
Assess skin break down thrombophlebitis;
remove TED hose at least every shift
 1. Impaired Physical Mobility
Prevent/treat orthostatic hypotension
Abdominal binder, calf compressors, TED hose
when individual gets up
Assess BP, especially when rising

Teach use of transfer board

Assist Physical Therapy with tilt table as
individual gradually gets use to being in an
upright position
 2. Impaired Gas Exchange
Phrenic nerve (C3-5) controls the
diaphragm bilaterally. If nerve is
nonfunctioning then individual is
ventilator dependent.
Thoracic nerves control the
intercostals muscles for breathing
and abdominal muscles aide in
breathing and coughing
 2. Impaired Gas Exchange
Respiratory rate, rhythm,
depth, breath sounds,
respiratory effort, ABGs, O2
saturation

Signs of impending
extension of SCI up cord to
phrenic nerve level (C3-5)
Need for ventilatory
assistance tracheotomy,
ventilator

Quad cough (assistive

cough) as needed
3. Impaired Skin Integrity
Change position frequently
Protection from extremes in temperature
Inspect skin at least 2x/day especially over boney
prominences
Avoid shearing and friction to soft tissue with
transfers
Removal of TED hose every 8 hours
Nutritional status
 4. Constipation

Bowels rely more on bulk than on nerves

Stimulate bowels at the same time each day.
Best after a meal when normal peristalsis
occurs
Individual may progress from Dulcolax
suppository to glycerin then to gloved finger
for digital stimulation
Assess bowel sounds prior to giving food for
the first time paralytic ileus!
 5. Impaired Urinary
Elimination
Flaccid bladder (lower motor neuron lesion)
No reflex from S2,3,4
Automatic empting of bladder
Urine fills the bladder and dribbles out
Need Foley or freq intermittent self catheterization

Spastic bladder (upper motor neuron lesion)

Reflex arc but no connection to or from brain
Reflex fires at will
Bladder training- trigger points to stimulate empting; self
catheterization
 5. Impaired Urinary
Elimination
Use bladder scan to see amount of urine in
bladder
Goal- residual <100ml/20% bladder capacity
Some individuals may need suprapubic
catheter
Assess effectiveness of medication
Urecholine to stimulate bladder
contraction
Urinary antiseptic
 6. Risk for Autonomic
Dysreflexia
SCI above T6
Results in loss of normal compensatory
mechanisms when sympathetic nervous
system is stimulated
Life threatening- if goes unchecked BP can
result in cerebral hemorrhage

Vasodilatation symptoms above SCI

Vasoconstriction symptoms below SCI
The cause of SNS stimulation
 6. Risk for Autonomic
Dysreflexia
Elevate head of bed- causes orthostatic
hypotension
Identify cause/alleviate- if full bladder- cath; if
skin- remove pressure, if full bowel- empty, etc
Remove support hose/abdominal binder
Monitor blood pressure- can get > 300 S
Give PRN medication to lower BP
If above not effective call physician
 7. Ineffective Coping/
Grief and Depression
Assess thoughts on quality of life;
body image; role changes
Physical and psychological support
Most common SCI is 15-30 yeas old
and generally a risk taker this
greatly affects their perception of life
and rehabilitation
 7. Ineffective
Coping/sexuality
Male Female
UMN lesion hormones more than
reflexogenic (S2,3,4) nerves regarding
erections fertility.
LMN lesion C-section because of
psychogenic erections chance for autonomic
(psychological dysreflexia during labor.
stimulation) Lack of
sensation/movement
Ejaculation/fertility affects sexual
may be affected performance
 7. Ineffective
Coping/sexuality
Assess readiness/knowledge/your ability
Use proper terminology
Suggestions:
empty bladder before sex
withhold fluids and antispasmodics
certain positions may increase spasms
explore new erogenous zones
penile implants
Refer to specially trained counselor
 Home Care
Assess psychological, physiological
resources
need for rehabilitation (in-house or
out patient)
need for community resources

Home assessment
 Whats new in SCI
treatment?
Superman breather
YouTube - Superman breather USA

Kevin Everett
hypothermia treatment for SCI
Standing Tall
Travis Roy- 11 Seconds

Stem Cell treatment for SCI

Lipitor for SCI
 Case study- Jim Valdez
1. Why does Jim have flaccid paralysis on
admission to ICU?
2. What symptoms indicate that he is in spinal
shock? What was done about these symptoms?
3. How will we know when he is out of spinal
shock?
4. How does progressive mobilization assist
with orthostatic hypotension? What else can be
done?
5. What are realistic functional goals for Jim?