Spinal Injury and Spinal

Cord Injury

Geizar Arsika Ramadhana

• Anatomi Spinal
• Cedera spinal
• Syok neurogenic
• Syok spinal
• Cedera spinal komplit dan inkomplit
• Komplikasi
Anatomi
Protection
Bones – Vertebral Column :
•7 Cervical
•12 thoracic
•5 lumbar
•5 sacral
Spinal Cord Protection
•Internal and external ligaments
•Dura
•Meninges
•CSF in Subarachnoid space
Epidemiologi
•50% kasus cedera spinal adalah tipe komplit
•50 – 60% kasus cedera spinal terjadi pada daerah cervical
•Immediate mortality pada kasus cedera spinal tipe komplit adalah
50%
•Terjadi sebagian besar pada C5, C6, C7, Th 12, L1

Definisi SCI
•Cedera pada kolumna vertebralis dan/ atau korda spinalis

Mekanisme of injury
•Flexion
•Hypertension
•Compression
•Rotation
Cedera Kolumna Vertebralis
•Cedera tulang belakang
1.Fraktur vertebra
2.Subluksasi vertebra
•Cedera non tulang
1.Ligamen : Sprain/ over stretching dan Ruptur/ robekan
2.Otot : Sprain/ over stretching dan Ruptur/ robekan

Cedera Korda Spinalis

Mekanisme cedera
1.Cutting (terpotong oleh segmen patahan tulang yang tajam)
2.Kompresi
3.Streching (akan lebih berat pada pasien dengan tethered cord)
Classifications of SCI
Mechanism of Injury
•Flexion (hyperflexion)
1.Most common because of natural protection position
2.Generally cause neck to be unstable because stretching of ligaments
• Hyperextension
1.Caused by chin hitting a surface area, such as dashboard.
2.Usually causes central cord syndrome symtoms
• Compression
1.Caused b y force from above, as hit on head
2.Or from below as landing on but
3.Usually affects the lumbar region
• Rotation
1.Most unstable
2.Results in tearing of ligamentous structures that normally stabilize
the spine
3.Usually results in serious neurologic deficit
Pasien dengan kecurigaan cedera spinal
•Pasien tidak sadar (termasuk curiga intoksikasi)
•Defisit neurologis
•Nyeri/ nyeri tekan pada posterior midline
•Cedera multiple (multitrauma)
•Umur tua
•Cedera maksilofacial
•KLL dengan kecepatan tinggi
Syok Neurogenik
• Akibat hilangnya tonus vasomotor simpatik
1.Mengakibatkan rangsang dominan oleh parasympatis
2.Kehilangan rangsang simpatik menyebabkan peripheral pooling
(vasodilatasi perifer) dan menurunnya cardiac output
• Hipotensi dan bradikardia
1.Hipotensi orthostatica dan gangguan control suhu (poikilothermic)
• Gangguan fungsi autonomy spinalis setinggi level cedera
1.Akibat cedera cervical atau thoracal atas
• Gejala
1.Flacid paralysys distal dari level cedera
2.Kehilangan fungsi otonomik : hipotensi, bradikardi, vasodilatasi,
kehilangan control saluran kemih dan pencernaan, kehilangan control
termoregulasi
Syok Spinal
• Kehilangan seluruh atau sebagian reflek motoric dan kehilangan
fungsi sensoris dibawah level cedera
• Motor loss – flaccid paralysis dibawah level cedera
• Sensory loss – loss touch, pressure, temperature pain, dan
propriosepsi
• Dapat berlangsung berhari – hari hingga bulan

Perbedaan antara syok spinal dan syok neurologis

• Syok spinal didominasi oleh hilangnya/ menurunnya reflek – reflek
(flaccid paralysis)
• Syok neurogenic didominasi oleh kelainan fungsi otonom biasanya
terjadi hipotensi dan bradikardia karena hilangnya tonus atau
rangsang simpatis
Cedera Spinal komplit VS inkomplit
Klasifikasi Frankel:
•Grade A : motoris (-), sensoris (-)
•Grade B : motoris (-), sensoris (+)
•Grade C : motoris (+) dengan ROM 2 atau 3, sensoris (+)
•Grade D : motoris (+) dengan ROM 4, sensoris (+)
•Grade E : motoris (+) normal, sensoris (+)
Klasifikasi ASIA (American Spinal Injury Association)
•Grade A : motoris (-), sensoris (-) termasuk pada segmen sacral
•Grade B : hanya sensoris (+)
•Grade C : motoris (+) dengan kekuatan otot < 3
•Grade D : Motoris (+) dengan kekuatan otot > 3
•Grade E : motoris dan sensoris normal
Incomplete cord injury
•Sindroma anterior cord
1.Hilang fungsi motoric, suhu, dan nyeri
2.Propriosepsi dan sensoris baik
•Sindroma brown sequard
1.Hilang motorik dan propriosepsi ipsilateral
2.Hilang fungsi nyeri dan suhu kontralateral
•Sindroma central cord
1.Atas > bawah
2.Hilang sensoris bervariasi
3.Sacral sparing
Pemeriksaan Fisik
• Inspeksi dan palpasi
1.Occiput to coccyx
2.Kemerahan dan bengkak pada soft tissue
3.Titik nyeri tekan (pasien sadar)
4.Gap or step off
5.spasme
• Lanmark dermatome
1.Nipple line – T4
2.Xiphyd process – T7
3.Umbilicus – T10
4.Inguinal region – T12, L1
5.Perineum dan perianal region (S2, S3, dan S4)
Pemeriksaan Radiologis pada
Spine
1. Plain films
• AP, Lateral and open mouth view
1. CT Scan
2. MRI
3. Flexion – Extension Plain Films
• Untuk menentukan stabilitas
Management of SCI
• Spinal motion restriction : immobilization device
• ABCs
• Look for other injuries
• High dose methylprednisolone (kontroversi)
Evaluasi Radiologi
Pedoman X-ray Cervical
AABBCDS
•Adequacy, Alignment
•Bone abnormality, base of skull
•Cartilage
•Disc space
•Soft tissue
Adequacy
•Harus menunjukkan seluruh 7 C-Spine
•X-ray yang tidak menunjukkan batas atas dari VTh1
•Kadang dibutuhkan traksi pada lengan
•Bila sulit diperlukan swimmer’s view atau CT
Allignment
HNP (Hernia Nucleus pulposus)
Lumbar Spine Motion Segment
• Three joint complex
• Intervertebral disc + 2 facet joint
• Ligamentous structure, vertebral body
Intervertebral Disc
• Hydrostatic, load bearing structure between
the vertebral bodies
• Nucleus pulposus + annulus fibrosus
• No blood supply
• L4-5, largest avascular structure in the body
Nucleus Pulposus
• Type II collagen strand + hydrophilic
proteoglycan
• Water content 70 ~ 90%
• Confine fluid within the annulus
• Convert load into tensile strain on the annular
fibers and vertebral end-plate
• Chondrocyte manufacture
the matrix component
Annulus Fibrosus

• Outer boundary of the disc

• More than 60 distinct, concentric layer of
overlapping lamellae of type I collagen
• Fibers are oriented 30-degree angle to the disc
space
• Helicoid pattern
• Resist tensile, torsional, and radial stress
• Attached to the cartilaginous and bony end-
plate at the periphery of the vertebra
Vertebral End-Plate
• Cartilaginous and osseous component
• Nutritional support for the nucleus
• Passive diffusion
Facet Joint
• Synovial joint
• Rich innervation with sensory nerve fiber
• Same pathologic process as other large synovial joint
• Load share 18% of the lumbar spine
Vital Functions
• Restricted intervertebral joint motion
• Contribution to stability
• Resistence to axial, rotational, and
bending load
• Preservation of anatomic relationship

Biochemical Composition
• Water : 65 ~ 90% wet wt.
• Collagen : 15 ~ 65% dry wt.
• Proteoglycan : 10 ~ 60% dry wt.
• Other matrix protein : 15 ~ 45% dry wt.
Spondylosis
• Generalized process of the axial skeleton
• Sequence of degenerative change
• Start biochemical and cellular level
• Manifest biomechanical and morphologic level
Initiating Factor in
Degenerative Cascade
• Injury to annulus fibrosus
• Matrix composition alteration of the nucleus
pulposus
• Vascularity and permeability change of end-plate

• Primary causitive agent??

• The process of disc degeneration is multifactoral
Disc Degeneration
• Environmental factor
• Genetic predisposition
• Normal aging process

* Biomechanical stress
 Degeneration of soft tissue and
bone
 progressive morphologic change
 Intervertebral Disc
Cellular and Biochemical Change

• Decrease proteoglycan content

• Loss of negative charged proteoglycan
side chain
• Water loss within the nucleus pulposus
• Decrease hydrostatic property
• Loss of disc height
• Uneven stress distribution on the
annulus
Morphologic Changes
• bulging of the annulus fibrosus
• radial tear
• in-growth of granulation tissue in the annulus
• annular defect, cleft and fissure
• cellular necrosis  loss of distinction between
the nucleus and annulus
• focal extrusion of disc material

Aging Progress
• disc become more fibrous and disorganized
• replaced by amorphous fibrocartilage
• no clear distinction between nucleus and
annulus
• gas formation and vacuum disc sign
Vertebral End-Plate
• Become thinner and hyalinized
• Decrease permeability
• Inhibit nucleus metabolism
• Disc space narrowing
• Osteophyte formation at the end-plate
and annular junction
• Marrow change with increased axial
loading
• Subluxation and instability
Facet Joint

Disc height reduction 

• Facet joint capsule become lax
• Increased load transfer to the
facet joint
• Accelerate degeneration
• Joint subluxation,
hypertrophy,
osteophyte formation

** Primary disc degeneration

 Secondary change in the
posterior facet joint and
soft tissue
Lumbar Disc Disease

Discogenic Back Pain

A. Internal Disc Disruption (IDD)

B. Degenerative Disc Disease (DDD)
C. Segmental Instability

Lumbar Disc Herniation and

Radiculopathy
 Lumbar Disc Herniation
How pain is generated?

• Inflammatory
• Biochemical
• Vascular
• Mechanical compression
Inflamation
• Central role in radiculopathy
• Olmarker(1995, spine)
   Epidural application of autologous nucleus
without any pressure
 Nerve function impairment
 Axonal injury with significant primary
cell damage
• Nucleus is totally avascular
 Perceived as an antigen
 Intense inflammation response
• Application of annulus fibrosus
 No reduction of nerve conduction velocity
Biochemical Effect
• Nuclear herniation
 Incsease phospolipase A2, prostaglandin E2
cytokine, nitric oxide
• Disc herniation and sciatica
 Neurofilament protein and S-100 increase
in CSF
 Axonal and Schwann's cell damage

Mechanical Compression
• Local damage and intraneural ischemia
Vascular Pathophysiology
* Application of nucleus pulposus to nerve root
 increase endoneurial pressure
 decrease blood flow in the dorsal root
ganglia
 compartment syndrome
Clinical Anatomy
• Disc injury
- annular disruption, fissuring, annular
defect

• Contained herniation
Noncontained herniation
Extruded
Sequestrated

• L4-5 and L5-S1 herniation most common

- 90% of disc herniation
- Great axial load, lordotic shear
History
• symptom of disc herniation : acute or gradual
• after trauma or without and inciting event
• most common 3rd and 4th decade

Chief Complain
• Pain, radiating from the back or buttock into the
leg
• Numbness and weakness
• Sharp, lancinating, shooting/radiating down the leg
posteriorly below the knee
• Coughing, Valsalva maneuver  increase intracecal
pressure  increase pain
• Sitting position, driving  out of lordosis 
increase intradiscal pressure  increase pain
Sciatica
- radiating pain down the leg
Radiculopathy
-radiating pain down the leg as a result of nerve
root irritation

Back Pain
• irritation of the posterior primary ramus
- facet capsule, local musculature
• sinuvertebral branch - posterior annulus
• change in disc loading and shape, biomechanics
• loss of viscoelasticity.
• 90% of radiating pain have long-standing prior
episodic low back pain
Quality of pain and associated symptom

• dullache or sharp, stabbing pain?

• eletricity, tingling, numbness, shooting down the
leg?
• any associated weakness?
• dose anything make the pain better or worse?
• forward flexion or hyperextension exacerbate or
relieve pain?
• standing more comfortable than sitting?

** Back pain abated when leg pain developed

 relief of annular tensile stress, nerve root
irritation
** Isolated leg pain  acute disc extrusion
Differential Diagnosis

Vascular claudication
• Vascular assessment and flow study
• Dorsalis pedis palpation
Spinal stenosis
• leg pain, dysesthesia, paresthesia, often not
dermatomal
• pain d/t mechanical compression of spinal canal
and foramen
• lordosis and axial loading
• symptomatic on walking, relief by sitting
Thrombophlebitis
Metabolic and peripheral neuropathy
Physical Examination

Inspection
• Old scar, muscle spasm, cutaneous stigma, spinal
alignment, loss of lordosis
Palpation
• Midline, sciatic notch, iliac crest, SI joint, coccyx
• Paraspinal tenderness, rigidity
• Costovertebral angle, abdomen
• Kidney, stone, retroperitoneal abnormality
Hip pathology
• Patrick test
Skin
• Temperature and atrophic change
Neurologic Examination
 Root Tension Signs

• Straight-leg raising : L5, S1 root

• Contralateral SLR : sequestrated or
extruded disc
• Femoral stretching, reverse SLR : L3, L4
root
Diagnostic Test

Simple x-ray
• Disc space narrowing

MRI(magnetic resonance imaging)

• Disc pathology, neural structure,
musculoligamentous structure
• Soft tissue edema, hematoma,
intrinsic cord abnormality
• Synovial cyst, neurofibroma, perineural cyst
• 30% of asymptomatic individual have abnormal MRI

CT, Myelography
Nonoperative Treatment

• 90% of patient improve with conservative

treatment
• Short-term rest, NSAID, analgesics,
antispamodic medication, exercise
• Physical therapy
• Oral corticosteroid

** Conservative treatment should continue for

6weeks, before other measure are attempted
Exercise
• stretching and strengthening exercise
• debate on mechanism of pain relief
• protective effect of strong abdominal muscle
 load share, partially shield the disc from
excessive load

Physical therapy
• heat, cold, massage, ultrasonography
• helpful but scientifically not proven
Epidural steroid injection

• If leg pain persist beyond 4 weeks

• Maximum 3 injection per year

• Response vary greatly

- Hagen,2002 : short-term effect 40%. no significant
long-term effect
- Wiesel, 1995 : 82% relief for 1 day, 50% for 2 weeks,
16% for 2mo.
- White 1983 : 77% avoid surgery after injection
- Carette, 2002 : neither significant functional
benefit nor reduction in need for
surgery
Indication of Surgery
Ideal candidate
• history, physical examination, radiographic
finding, are consistent with one another
• when discrepancy exist, the clinical picture should
serve as the principal guide.
Absolute surgical indication
• cauda equina syndrome
• acute urinary retension/incontinence,
saddle anesthesia, back/buttock/leg pain, weakness,
difficulty walking
Relative indication
• progressive weakness
• no response to conservative treatment
Best predictive factor
1. persistent leg pain, that fail to respond to a 6-
week trial of nonoperative care
2. well-defined neurologic deficit
3. positive SLR test
4. positive imaging that correlates anatomically to
clinical findings
** 3 of these factor, at least 90% success rate

Other factors
• duration of sciatica, sick leave stress, depression,
level of education, work/disability