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Curriculum vitae

Nama : dr. Tjokorda Agung Yavatrisna Vidyaputra, M.Biomed, Sp.OT


Tempat Tanggal Lahir : Surabaya, 16 Januari 1985
Riwayat Pendidikan : SMA Negeri 1 Denpasar (1999-2002)
FK Universitas Wijaya Kusuma Surabaya (2003-2010)
Magister Biomedik Universitas Udayana
PPDS-1 Orthopaedi & Traumatologi Universitas Udayana
(2012-2017)
Riwayat Pekerjaan : RSUD Kabupaten Klungkung
Spinal Cord Injury
dr. Tjokorda Agung Yavatrisna Vidyaputra, M.Biomed, Sp.OT
RSUD Kabupaten Klungkung - Bali
Spinal Cord Injury: The First 72 hours
“The early management of a patient with an acute spinal cord injury is one of the
most difficult tasks in trauma cases.
During the first few days after an acute cord injury, every physician, nurse, or
paramedical person coming in contact with a spinal cord injured patient bears a
major responsibility”
“final outcome of a spinal cord injury depends upon the accuracy, adequacy, and
speed of first aid management, diagnosis, and treatment within the first few hours”
Charles Tator, 1982, 1990
Epidemiology

• Incidence: 10-12,000/ yr
• 80-85% males (usually 16-30 y/o), 15-20% female
• 50% of SCI’s are complete
• 50-60% of SCI’s are cervical
• Immediate mortality for complete cervical SCI ~ 50%
Trauma

Causes of Ischemia
Spinal Chronic Cervical Myelopathi
Cord Lumbar Spinal Stenosis
Injury
Transverse Myelitis

Multiple Sclerosis
Spinal Cord Injury
pathophysiology

Primary injury
• Initial insult to cord

• Local deformation

• Energy transformation
Spinal Cord Injury
pathophysiology

Secondary injury

• Biochemical cascade

• Cellular processes
Most acute therapies aim to limit
secondary injury cascade
Classification

Complete
• absence of sensory & motor function in lowest sacral segment
after resolution of spinal shock

Incomplete
• presence of sensory & motor function in lowest sacral segment
(indicates preserved function below the defined neurological level)
Neurologic Examination

• American Spinal Injury Association (ASIA)


• A = Complete – No Sacral Motor / Sensory
• B = Incomplete – Sacral sensory sparing
• C = Incomplete – Motor Sparing (<3)
• D = Incomplete – Motor Sparing (>3)
• E = Normal Motor & Sensory
ASIA Sensory Exam
• 28 sensory “points” (within dermatomes)
• Test light touch & pin-prick pain

**Importance of sacral pin testing**


• 3 point scale (0,1,2)
• “optional”: proprioception & deep pressure to index and
great toe (“present vs absent”)
• deep anal sensation recorded “present vs absent”
Motor Examination

• 10 “key” muscles (5 upper & 5 lower extremity)

C5-elbow flexion L2-hip flexion


C6-wrist extension L3-knee extension
C7-elbow extension L4-ankle dorsiflexion
C8-finger flexion L5-toe extension
T1-finger abduction S1-ankle plantarflexion

• Sacral exam: voluntary anal contraction (present/absent)


Motor Grading Scale

• 6 point scale (0-5) …..(avoid +/-’s)


• 0 = no active movement
• 1 = muscle contraction
• 2 = active movement without gravity
• 3 = movement thru ROM against gravity
• 4 = movement against some resistance
• 5 = movement against full resistance
Classification
Incomplete SCI syndromes

Central Cord Syndrome


• Motor loss UE>LE
• Hands affected
• Common in elderly w/ pre-
existing spondylosis and
cervical stenosis.
• Substantial recovery can be
expected.
Classification
Incomplete SCI syndromes

Brown Sequard
• Ipsilateral motor,
proprioception loss.
• Contralateral pain,
temperature loss.
• Penetrating injuries.
• Good prognosis for
ambulation.
Classification
Incomplete SCI syndromes

Anterior Cord Syndrome


• Motor loss
• Vibration/position
spared
• Flexion injuries
• Poor prognosis for
recovery
Classification
Incomplete SCI syndromes

Posterior Cord
Syndrome
• Profound sensory loss.
• Pain/temperature less
affected.
• Rare.
Classification
Other SCI syndromes

Conus Medullaris Syndrome


• Loss of bowel or bladder function
• Saddle anaesthesia
• Looks like cauda equina
• Skeletal injuries T11-L2
Clinical finding

Patient at risk

• back or neck pain


• polytrauma
• head injury
• facial injuries
• unconscious or obtunded
Clinical Finding

• Difficult in the unconscious or intoxicated patient.


• Inspection and palpation of the entire spine
• motor , sensory, autonomic function
• pathologic and physiologic reflex
• digital rectal examination for voluntary or reflex
(bulbocavernosus) anal sphincter.
• The conus medullaris (upper motor neurons) and
cauda equina (lower motor neurons) sign must be seek
  Conus Medullaris Syndrome Cauda Equina Syndrome
Presentation Sudden and bilateral Gradual and unilateral

Reflexes Knee jerks preserved but ankle jerks affected Both ankle and knee jerks affected

Radicular pain Less severe More severe


Low back pain More Less

Numbness tends to be more localized to


saddle area; asymmetrical, may be unilateral;
Numbness tends to be more localized to no sensory dissociation; loss of sensation in
Sensory symptoms and signs perianal area; symmetrical and bilateral; specific dermatomes in lower extremities
sensory dissociation occurs with numbness and paresthesia; possible
numbness in pubic area, including glans
penis or clitoris

Typically symmetric, hyperreflexic distal Asymmetric areflexic paraplegia that is more


Motor strength paresis of lower limbs that is less marked; marked; fasciculations rare; atrophy more
fasciculations may be present common

Less frequent; erectile dysfunction that


includes inability to have erection, inability
Impotence Frequent to maintain erection, lack of sensation in
pubic area (including glans penis or clitoris),
and inability to ejaculate

Urinary retention and atonic anal sphincter


cause overflow urinary incontinence and Urinary retention; tends to present late in
Sphincter dysfunction
fecal incontinence; tend to present early in course of disease
course of disease
Imaging Study
• Plain X-rays (AP, Lateral, open mouth view) : Alignment, Bony
fracture, Facet joints
• CT scan :
- asses spinal canal compromise
- show detail of bony fracture
• MRI :
- complement plain X-ray and CT scan
- excellent soft tissue details : ligamentous injury
cord infarction, hemorrhage, and oedema
Principles of treatment

Resuscitation Restore Spinal


Alignment

Prevent further spinal Maximal


Mobile and Stable
cord injury possible
spine
function
recovery

Prevention and treating


Rehabilitation complication
EMERGENCY MANAGEMENT
Primary Survey
• An initial survey of vital signs : ABCDE

Secondary survey
• Identify multiple injury : head injury, thorax, abdominal, and
skeletal trauma
• Assess and determine neurological status
Breathing
• Of patients with CSCI above C5, 87.5 per cent Intubation after cervical spinal cord injury:
to be done selectively or routinely?
required intubation compared with 61 per cent
of patients with CSCI at C5-C8 (P = 0.026).
• Similarly, of patients with complete
quadriplegia, 90 per cent required intubation
compared to 48.5 per cent of patients with
incomplete quadriplegia or paraplegia (P <
0.001).
• There were 3 independent risk factors for the
need of intubation:
• Injury Severity Score > 16
• CSCI higher than C5
• complete quadriplegia.
• The combination of the 2 latter risk factors
resulted in intubation in 21 of 22 patients
(95%).
• The majority of patients with CSCI require
intubation.
• In patients with CSCI above C5 and complete
quadriplegia, intubation should be offered
routinely and early because delays may cause
preventable morbidity. Velmahos GC, Toutouzas K, Chan L, Tillou A, Rhee P,
Murray J, Demetriades D. Am Surg. 2003 Oct;69(10):891-4.
Circulation
• Early appropriate fluid resuscitation is necessary to maintain tissue
perfusion
• Avoid fluid overload!

• Appropriate resuscitation endpoint and optimal mean arterial blood


pressure for maintenance of spinal cord perfusion are not known
• Uncontrolled studies using vasopressin to maintain a MAP of 85 for 7 days
have shown improved outcomes
Spinal Shock
• Clinical condition a loss of somatic motor, sensory and sympathetic function occur immediately
after spinal cord injury
• Clinically :
- no voluntary movement and sensory perception below the level of injury
- areflexia (bowel and bladder reflexes)
- vasodilatation  low blood pressure and bradycardia  “neurogenic shock”
- paralytic ileus
• Generally recovery within 24 hours
Differentiate between Hypovolemic and
neurogenic shock

Shock
Neurogenic Hemorrhagic

Pulse Bradycardia Tachycardia


Skin Warm/dry Cool/clammy
Mental status Normal Confused
Urine output Normal Low
Treatment of a patient in neurogenic shock

• Placing the patient in


the Trendelenburg
position
• Judicious administration
of intravenous fluids.
• Cardiac pressors agent
If the circulation
problem persist
Spinal stabilization :
• Cervical spine fracture : a skull traction + sand bag or strapping or
sand bag only. Hard cervical collar are preferable
• Thoracolumbar spine fracture : immobilized back spine board
• All emergency procedure, always do in proper log-roll technique
Steroids
methylprednisolone sodium succinate

• Large body of animal


studies
• Various
neuroprotective
mechanisms
postulated
Neuroprotection w/ MPSS
Preservation of
Spinal Cord
Blood Flow
Preservation of Preservation of
Calcium Homeostasis Aerobic Metabolism

Inhibition of
Lipid Peroxidation

Attenuation of delayed
Glutamate release
Inhibition of
Calpain-mediated
Cytoskeletal damage
Preservation of
Na, K Homeostasis
National Acute Spinal Cord Injury Studies

NASCIS III
II
• 16
10 hospitals, 499
487 patients
• 3Compared:
treatment arms (all got MPSS bolus)
MPSS 5.4
(30 mg/kg 24
bolus
hrs+ 5.4 mg/kg x 23°)
Naloxone
MPSS 5.4 (5.4
mg/kgmg/kg
48 hrs
bolus + 4.5mg/kg x 23°)
Placebo 2.5 mg/kg Q6 hr for 48 hrs
Tirilazad

 8hrhours,
• 48 protocol neurologic
better than
steroids 24 hr protocol (if treated between 3 and 8 hours)
improvement
•• 2x incidence PE
Infections, of pneumonia,
 but not sepsis in 48 hr group (NS)
significant

Bracken, N Engl J Med, 1990 Bracken, JAMA, 1997


Bracken, N Engl J Med, 1992 Bracken, J Neurosurg, 1998
Neuroprotective Tx

• Steroid Protocol for SCI


( NASCIS 3rd - National Acute Spinal Cord Injury Study ).

methylprednisolone

• 0 to 3 hours: 30 mg/kg loading dose, then 5.4 mg/kg for 23 hr

• 3 to 8 hours: 30 mg/kg loading dose, then 5.4 mg/kg for 48 hr

• > 8 hours : no methylprednisolone


Steroid :
• Reduces tissue oedema  improve blood supply
• Stabilizes cellular membrane by
- reduces accumulation of Ca++ intra cell
- reduces free radicals
- limits lipid peroxidation
- regulate gluthamate release
Steroid
• Administration of methylprednisolone  controversial.
• Nowadays, methylprednisolon is not “ the recommended
treatment” , but become “a recommended treatment “.
• Warning : severe contaminated wound, pregnancy, less than 13 y.o. ,
infection , unregulated diabetes.
Intensive care management
Medical stabilization
• Cardiovascular monitoring (CVP)
• Pulmonary care : chest physiotheraphy
• Urological care : continuous 24-48 h  intermittent
catheter, to maintain automatic bladder reflex
• Gastrointestinal care (NGT/ H2 Agonist)
• Skin care (spinal bed/ log roll)
Surgery
Early (<24 hrs) VS late surgical decompression
• Controversies (AAOS Federation of Spine Association 2009)
• 6 month : no significant difference
• 1 year : early surgery had 2 grade of improvement
• less complication
• early surgery is beneficial

Keith H. Bridwell, Paul A. Anderson, Scott D. Boden, Alexander R. Vaccaro and Jeffrey C. Wang : What’s New in Spine
Surgery. J Bone Joint Surg Am. 2009;91:1822-1834
Early surgical intervetion
An early surgical intervention (<24 hours) :
• Progressive neurological deficit
• Dislocation with partial neurological deficits

Goals :
• Dural sac decompression
• Preventing dural sac tethering prevent further injury
• Spinal stabilization
Arguments againts
early intervention
• Acute systemic trauma, need for live-shaving intervention
• Surgery to ensure alignment and stabilization may be implemented
after the failure primary treatment modalities
• Risk of neurological deterioration after early intervention
• No significant improvement in overall outcome
• Required of intensive care capability, specific equipment, and
experienced personel
Pressure sores.
Complication Infection - urinary, respiratory, skin.

Gastrointestinal perforation or haemorrhage.

Deep venous thrombosis (DVT) and pulmonary embolism.

Shock.

Autonomic dysreflexia.

Joint contractures.

Death.
Complication
Rehabilitation

MULTIDISCIPLINARY TEAM PHYSIOTHERAPY, OCCUPATIONAL


APPROACH THERAPY, ORTHOSESA, AND
SOCIAL AND WELFARE SUPPORT.
Prognosis
Life Expectancy ( years )
Prediction of Ambulatory Ability from
Motor Score
Expected Neurorecovery
Complete Tetraplegia

• Little chance for functional


motor recovery in LE’s

• extent of neurorecovery in
UE’s determines functional
independence
Expected Neurorecovery
Complete Tetraplegia

• 70-85% chance of gaining at least one additional level

• Motor grade 2/5 for a given level @1 week, all gained functional
strength at next level

Ditunno, Arch Phys Med Rehabil, 2000


Expected Neurorecovery
Incomplete Tetraplegia

• >90% gain at least one UE


motor level

• If pinprick spared in same


dermatome, 92% chance of
recovery to  3/5 motor
strength
Ditunno, Arch Phys Med Rehabil, 2000
Poynton, JBJS-Br, 1997
Expected Neurorecovery
Incomplete Tetraplegia

• Majority of
improvement in first
6-9 months.

Waters, J Spinal Cord Med, 1998


Thank You

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