1.
TRAUMATIC SPINAL CORD INJURY
Prepared by Dr Kung Khai Shien, Cesar

2.
Corticospinal
tract

3.
Lateral Spinothalamic Tract
-

4.
Anterior Spinothalamic Tract
Destruction will cause:
- Loss of light touch and
pressure contralateral side
below the level of lesion

5.
Dorsal column pathway

6.
INTRODUCTION
•Spinal cord injury (SCI) :
•damage to the spinal cord that results in a loss of function.
•Cord Injuries: Cervical = 60%, Thoracic = 30%, lumbar = 4%, and Sacral = 2%
•Most common at C5,6,7 due to greatest mobility at these levels.
•Caused by:
•Cutting, compression, or stretching of the spinal cord
•Unstable or sharp bony fragments pushing on the cord
•Pressure from bone fragments or swelling that interrupts the blood supply to the cord causing ischemia.

7.
MECHANISMS
Distraction –
Hanging), significant impact on
in hyperextension (eg.
the
head or face.
Compression of the bony spine –
directly compromise the spinal canal
and spinal cord.
Torsion – falls, high energy vehicle
collisions – can tear the spinal cord
tissue.
Penetration – in gun shot or stab injury

8.
TYPES OF SPINAL CORDINJURY
COMPLETE SPINAL CORD INJURIES
•Total motor & sensory loss distal to the injury
INCOMPLETE SPINAL CORD INJURIES
•Some motor or sensory functions is spared distal to the cord injury.
•Voluntary sphincter contraction, toe flexor contraction–present.
•Prognosis-Good

9.
SPINAL CORD INJURY SYNDROMES
•Anterior Cord Syndrome
•Central Cord Syndrome
•Posterior cord syndrome
•Brown-sequard syndrome
•Cauda Equina Syndrome
•Conus medullaris syndrome

10.
ANTERIOR CORD SYNDROME
•Due to ischemia – blood supply from
anterior spinal artery is distrupted
(compressed by bone fragments).
•Damage to cortico-spinal and spinothalamic
tracts
•Posterior columns unaffected.
•Flexion/rotation injury

11.
CENTRAL CORD SYNDROME
•Central gray matter is damaged.
•Bladder dysfunction – present as
urinary retention.
•Hyperextension injury
•Motor: Arm > Leg weakness
•Sensory: Arms>Legs
•Usually sacral sensory sparing

12.
POSTERIOR CORDSYNDROME
•Rare
•Loss of proprioception and vibration
•Good prognosis
•Penetrating back trauma or
hyperextension injury.

13.
BROWN-SEQUARDSYNDROME
•Hemisection of the cord
•Usually in penetrating trauma,
Knife in back or
rotational or fracture/dislocation.
•Ipsilateral paralysis and loss of
vibration and joint position sense,
with contralateral loss of
pain and temperature sensation
.

14.
CAUDA EQUINASYNDROME
•Presents with loss of bowel and baldder function with LMN signs on lower limbs.
•Sensory signs – unpredictable.
•Not a cord syndrome. Technically a LMN lesion.
•Saddle anaesthesia
•Loss of anal tone
•Sexual dysfunction

15.
Conus medullaris syndrome Cauda equina syndrome
Vertebral level L1-L2 L2-sacrum
Spinal level Sacral cord segment and roots Lumbosacral nerve roots
Presentation Sudden and bilateral Gradual and unilateral
Radicular pain Less severe More severe
Low back pain More Less
Motor strength Symmetrical, less marked hyperreflexic
distal paresis of LL, fasciculation
More marked asymmetric areflexic
paraplegia, atrophy more common
Reflexes Ankle jerks affected Both knee and ankle jerks affected
Sensory Localized numbness to perianal area,
symmetrical and bilateral
Saddle anaesthesia,asymmetrical,
unilateral
Sphincter
dysfunction
Early urinary and fecal
incontinence
Tend to present late
UMN or LMN Lesion? UMN & LMN LMN
Impotence Frequent Less frequent
7 06/08/2014
Conus Medullaris vs. Cauda Equina Syndromes

16.
SIGNS ANDSYMPTOMS
AIRWAY:
•Airway reflexes are lost and gastric stasis – can have aspiration.
BREATHING:
•Above C4 – diaphragm is paralysed – apnea.
•T2-T12 – innervates intercostal muscles – fractures above – diaphragmatic
breathing – limited expansion, decreased TV and FRC, impaired cough, inc RV.
•Decreased muscle power – pneumonia is common.
•ARDS and pulmonary emboli also occur

17.
CIRCULATION:
•Damage above T6 – sympathetic innervation of heart lost – loss of reflex,
tachycardia, impaired LV function and risk of severe bradycardia and
asystole following unopposed vagal stimulation.
NEUROLOGICAL:
•Spinal shock – flaccidity and areflexia – duration is variable.
•Following a/c phase of spinal shock – majority of patients with lesion above
T6 – autonomic dysreflexia (mass spinal reflex when area below the lesion
is stimulated)
•Develops severe bradycardia, hypertension, flushing and sweating above the
lesion – triggered by distended bladder or bowel, pressure sores etc

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TEMPERATURE:
•Hypothermia due to peripheral vasodialatation.
BIOCHEMICAL AND ENDOCRINE:
•Increased ADH – water retention
•Glucose intolerance
•NG tube – hypokalemic metabolic alkalosis
•Hypoventilation – respiratory acidosis
•Osteoporosis and hypercalcemia

19.
SKIN – pressure sores
THROMBOELASTOGRAM – DVT and embolism.
MUSCULOSKELETAL – muscle spasms and contractures.
PSYCHOLOGICAL – reactive depression

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DIAGNOSTIC TESTS
•Complete blood count (e.g. Hb, RBC, WBC)
•Arterial blood gas level
PaO2:85-95 mm of Hg
PaCO2:35-45 mm of Hg
•X- RAYS
•COMPUTERIZED TOMOGRAPHY (CT) SCANS
•MAGNETIC RESONANCE IMAGING (MRI)
•MYELOGRAPHY

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General Pattern
• Vertebral bodies
• Intervertebral discs
• Spinal cord/canal
• Marrow Signal
• Individual levels
 Sagittal T2 & axial T2
 Rate the spinal canal and
neural foramen at each
level

22.
40 yo, fell 4 stories, lower
extremity paralysis
T1 hyperintense blood products
compressing on the spinal cord

23.
40 female, MVA, Power bilateral C8 & T1 2/5

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40 female, MVA, Power bilateral C8 & T1 2/5

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40 female, MVA, Power bilateral C8 & T1 2/5

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- Hemodynamic phenomenon: loss of vasomotor tone &
loss of sympathetic nervous system tone
- Hypotension, Bradycardia, Pokilothermia
- Cause: Spinal cord injury above T6, Some drugs with
effect on medulla (opioid, benzodiazepine)
- Atropine, Vasopressor, beware of fluid overload
Neurogenic Shock

27.
- After spinal cord injury, temporary depressed spinal reflexes, loss of
neurologic function including loss of sensation and flaccid paralysis
below the level of injury
- syndrome lasts days to months
Spinal Shock

28.
Neurogenic
shock could
persist
through
Phases 2-3
Hyperreflexia

29.
- Exaggerated autonomic response secondary to stimuli that would only be mildly
noxious under normal circumstances
- Only in lesion T6 & above
- Such hypersensitivity is partially due to subnormal resting levels of catecholamines
- Noxious stimuli is below T6
Autonomic Hyperreflexia

30.
- Noxious stimuli:
The 6 B’s
- Bladder
- Bowel
- Back passage
- Bones
- Boils
- Babies
Autonomic Hyperreflexia

31.
Autonomic Hyperreflexia
90%
paroxysmal
hypertension
85% have triad of
• Headache
• Hyperhidrosis
• Cutaneous
vasodilatation

32.
- Elevate HOB
- Check BP every 5 mins
- Identify & eliminate the offending stimulus
- Antihypertensive if HTN is extreme or doesn’t resolve quickly
a) SL Nifedipine 10mg
b) IV Phentolamine
- Relieves spasm of skeletal and smooth muscle – IV Diazepam 5mg
- Prophylaxis
a) Good bowel/bladder & skin care
b) Alpha blocker in resistant cases
c) Prophylactic treatment(nifedipine) / anaesthetic prior to procedure
Autonomic Hyperreflexia -
Treatment

33.
MANAGEMENT:
The major causes of death in spinal cord injury (SCI) are aspiration and shock.
Initial survey under ATLS protocol: (“ABC’s”). This is followed by a brief neurologic exam.
Any of the following patients should be treated as having an SCI until proven otherwise:
1. all victims of significant trauma
2. trauma patients with loss of consciousness
3. minor trauma victims with complaints referable to the spine (neck or back pain or tenderness) or
spinal cord (numbness or tingling in an extremity, weakness, paralysis)
4. associated findings suggestive of SCI include
a) abdominal breathing
b) priapism (autonomic dysfunction)

34.
MANAGEMENT:
Primary(Pre-hospital) management-
Initial treatment of patients with cord injury focuses on two aspects -preventing further
damage and resuscitation.
Immobilization with a hard cervical collar
Resuscitation is aimed at airway maintenance, adequate oxygen saturation, preventing
bradycardia to prevent any ischemic damage to the already compromised cord

35.
MANAGEMENT:
Secondary (Hospital) Management:
Medical Management
Surgical Management
• Surgical Decompression
• Surgical Stabilization
• Fixation of Vertebra
• Fixation of Spine
• Artificial disc implantation Spinal

36.
MEDICAL MANAGEMENT:
1. Immobilization (Philadelphia or Aspen Collar)
2. Hypotension
- Keep SBP ≥ 90mmHg
- Keep MAP 85-90mmHg for 1st 7 days after SCI to improve spinal cord perfusion
- Combination of factors
- Pressor if necessary ( Dopamine is the choice), avoid phenylephrine
3. Oxygenation
- Indication of Intubation? Level of SCI C5 & above?
- During intubation, use chin lift without neck extension

37.
MEDICAL MANAGEMENT:
4. NG Tube
- Paralytic ileus is common
5.Indwelling Foley Catheter
6.DVT prophylaxis
7. Temperature regulation: vasomotor paralysis may produce poikilothermy
8. Electrolytes imbalance such as Hypokalemia

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MEDICAL MANAGEMENT:
9. Detailed neuro exam

39.
Functional Independence Measure

40.
The modified Barthel Index

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MEDICAL MANAGEMENT:
10. Should we give steroid?
The answer: NO

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SURGICAL MANAGEMENT:
- When surgical decompression is indicated, it is usually combined with a stabilization procedure
- Contraindication to emergency operation:
a) Medically unstable patient
b) Complete spinal cord injury ≥ 24 hours

43.
SURGICAL MANAGEMENT:
Modified recommendations of Schneider
In patients with complete spinal cord lesions, no study has demonstrated improvement in
neurologic
outcome with either open decompression or closed reduction.
surgery is reserved for incomplete lesions—possibly excluding central cord syndrome with
extrinsic compression,
After maximal possible reduction of subluxation, show:
1. progression of neurologic signs
2. complete subarachnoid block by Queckenstedt test or radiographically (on myelography or MRI)
3. compression of spinal cord
4. necessity for decompression of a vital cervical root
5. compound fracture or penetrating trauma of the spine
6. acute anterior spinal cord syndrome
7. non-reducible fracture-dislocations from locked facets causing spinal cord compression

44.
Timing of surgical decompression