spinal cord injury Flashcards

1
Q

define spinal cord injury

A

a complete or partial interruption of the sensory and motor tracts of the spinal cord
leading to loss of ability to feel or move below the level of the lesion

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2
Q

level of injury

A
C1-4 breathing head and neck mvmt 
C4-T1 = HR control UL mvmt 
T1-12 - trunk control 
temp reg 
abdominal muscles 
L1-S1- lower limb movement 
S2-S4/5 - bowel bladder and sexual function
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3
Q

SCI causes
non traumatic
traumatic

A
non traumatic 
vascular 
tumour 
infection 
degenerative cervical myelopathy 
traumatic 
falls RTC
sports 
assault / violence 
rarer - natural disaster 
self harm 
occupational injury
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4
Q

SCI prevalence

by age

A

male 71.5%
falls > half

age <1 medical / iatrogenic causes 
birth - young adult - RTC 
adults - high velocity trauma or violence 
men > women 
>60 years: falls, non traumatic SCI
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5
Q

financial cost of SCI

A
nature of injury 
timeliness of initial Rx
length of stay hospital 
direct costs higher first year 
indirect costs - earning potential may exceed direct costs
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6
Q

diagnostic information

A

classification of LEVEL of injury
degree of completeness

level 
vertebral level 
neurological level 
sensory and motor levels 
zone of partial preservation 
mixed LMN and UMN presentation 

neurological level
lowest segment of the spinal cord with normal motor function and sensory function

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7
Q

clinical assessment of SCI

A

(ISNCSCI)
motor and sensory function
to determine the neurological level of injury

degree of completeness to determine ASIA impairment scale AIS

motor assessment
10 muscle groups
Oxford scale
lowest intact myotome = motor level

sensory assessment - pinprick and light touch 
28 dermatomes 
graded 0 - absent 
1- partial or absent 
2 - normal sensation 
lowest intact dermatome = sensory level 

anorectal examination
assesses S4/5 dermatome and voluntary anal contraction
indentifies presence or absence of sacral sparing
determines if injury is complete or incomplete

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8
Q

classification of injury
complete
incomplete

A

Complete

No anal contraction or sensation (no
“sacral sparing”)
Complete loss of motor and sensory
function below the level of injury*

*Potential Zone of Partial Preservation

Incomplete
MUST have anal sensation or
contraction
Preservation of some motor or sensory fibres (or both) below the level of the injury
Further classified according to the extent of motor or sensory loss below the level of the injury

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9
Q

ASIA impairment scale score

A

A = Complete: No motor or sensory function is preserved in the
sacral segments S4-S5
B = Incomplete: Sensory but not motor function is preserved
below the neurological level and includes S4-S5

C = Incomplete: Motor function is preserved below neurological level, and more than half of key muscles below level have a grade less than 3

D = Incomplete: Motor function is preserved below neurological  level, and at least half of key muscles below level have a grade 3  or more
E = Normal: Motor and sensory function is normal
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10
Q

prognostic value of AIS

A

AIS score A have a 91.7% negative predictive probability for independent ambulation at one year

AIS D have a 97.3% positive predictive probability for independent ambulation at one year (Middendorp 2017)

2.1% of AIS A patients improve to an incomplete injury in 5 years (Kirshblum 2004)

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11
Q

incomplete SCI syndromes

A
Central cord syndrome
Brown-Sequard syndrome
Anterior cord syndrome
Posterior cord syndrome
Conus medullaris
Cauda equina lesions
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12
Q

central cord syndrome

A

Incomplete SCI (usually cervical) causing weakness ULs > trunk > LLs
Hyperextension injuries
Cervical spondylosis or stenosis in older people can predispose
Compression of the cord anteriorly by osteophytes and posteriorly by ligamentum flavum
Associated with fracture dislocation and
compression fractures

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13
Q

outcomes

A

Good prognosis for independent walking with or without aids, though LL spasticity may persist

Good recovery often in hands but lack of proximal stability → limited selective movement

Depending on severity, some degree of motor deficit in trunk may persist → impaired posture and balance

Complications: shoulder pain, hand oedema, spasticity, neurogenic
pain

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14
Q

brown sequard syndrome

A
same side as lesion 
UMN weakness 
loss of position and vibration 
side opposite lesion 
loss of pain and temp 
A lesion that produces relatively greater ipsilateral proprioceptive and  motor loss and contralateral loss of sensitivity to pain and temperature  (Maynard et al 1997)

First described by Galen

Damage occurs to one side of the cord (hemi-section)

Gunshot or stab wounds, lateral vertebral fractures

Majority of people with this injury will walk

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15
Q

anterior spinal cord syndorme

clinical presentation

A

A lesion that produces variable loss of motor function and sensitivity to pain and temperature whilst preserving proprioception (Maynard et al 1997)

Traumatic
Forced flexion / compression injury, e.g. diving or RTC
Non traumatic
Vascular: anterior spinal artery thrombosis, aortic aneurysm, angioma

Severe motor loss due to anterior horn cell damage and damage to the motor tracts at ventral aspect of cord
Loss of temperature & pain sensation (LST)

Preservation of tactile, joint position sense and vibration (posterior column)
Preservation of proprioception → significant difference to rehabilitation

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16
Q

other incomplete

A

cancer - primary or secondary tumours
transverse myelitis
decompression sickness - usually produces an incomplete lesion
cauda equina syndrome

17
Q

trauma management

A
  1. resp mimt
  2. CV
  3. Vertebral stability
  4. neuro-protection
18
Q

vertebral stability

A

SCI may or may not be associated with structural damage and instability of the vertebral column

If no vertebral instability: generally mobilized within a few days if medically stable

If vertebral instability: conservative or surgical management

Surgery: spinal fusion, or halo traction and brace

19
Q

early physio precautions

A

Surgeon / physician clearance required for:

Any rotation of the spine
Rolling
Unilateral arm movement
Long sitting in the initial phases of rehabilitation
Sitting out
Standing
20
Q

spinal shock

A

Acute reaction immediately post-injury Flaccid paralysis
Loss of reflex activity
Associated with hypotension and paralytic ileus
Extent of disruption is variable
Precise definition and duration is debated
Gradually resolves, takes days to months (Ditunno, 2004)
Duration of spinal shock is a potential indicator of outcome

21
Q

CV complications

A

neurogenic shock
orthostatic hypotension
autonomic dysreflexia

22
Q

neurogenic shock

A

Classic triad = Hypotension + Bradycardia + Hypothermia

Incidence 7%-45%
More commonly in injuries above T6 (disruption of sympathetic outflow)
Loss of sympathetic tone → ↓ systemic vascular resistance and dilation of venous vessels → ↓ cardiac preload
(Hypotension can also be contributed by severe haemorrhage at injury site or associated injuries)
BP restored by fluid administration + vasopressor drugs (avoid pulmonary oedema)
Atropine to treat bradycardia

23
Q

orthostatic hypotension

A

Can occur in lesions above T6
Occurs with movement into gravity dependent positions

Signs: feel faint and loss of consciousness
Treatment: Lie down and raise the legs; or tilt the wheelchair backwards

Implications:
Use compression stockings and abdominal binders
Graduated programme against gravity is essential

Moderate evidence for use of FES

24
Q

autonomic dysreflexia

A

Potentially life threatening complication of SCI (mortality 22%)
Dysregulation of the autonomic system in people with SCI above T6
Uncoordinated reflex sympathetic discharge in response to a noxious stimulus below the level of the SCI
Acute episode of systolic BP >25 mm Hg above baseline due to
vasoconstriction
Risk of stroke and cardiac arrhythmia or arrest
Can occur anytime throughout a patient’s lifetime

Triggers: The 6 B’s
Bladder (over-distension, UTI)
Bowel (constipation, impaction)
Boils (skin – sores, pressure, breakdown)
Bones (fractures)
Babies (pregnancy)
Back passage (haemorrhoid, fissure
25
Q

treatment of autonomic dysreflexia

A

Position the patient upright
Remove tight clothing
Systematically check for 6 Bs and remove obvious triggers –
check catheter, skin
Monitor BP
Escalate to medical support – management of 6 Bs, vasodilation
If BP doesn’t drop after 10 mins or SBP > 150 mm Hg, medical team will administer vasodilators (nifedipine, GTN)

26
Q

venous thromboembolisation

A

Deep vein thrombosis (DVT)
Increased vulnerability in first 2 weeks of injury
Common in veins of calf; more serious in veins of the thigh and groin Q: How do you recognise DVT?
Pulmonary embolism (PE) Dislodgement of DVT Life threatening
Q: How do you recognise PE?
DVTs likely to be dislodged during movement (active or passive) – implications for physiotherapy?
Interventions: Calf compressors, anticoagulants

27
Q

pressure sores prevention

A
Positioning
Changes of position
Care of Skin
Posture correction
Correct seating
Pressure relief (cushions and mattresses)
28
Q

clinical predictors of outcome after traumatic SCI

A

Positive predictors (apart from level and completeness):
Sensory and motor zones of partial
preservation in complete SCI
Positive features of the upper motor neuron syndrome
Female*
Younger**

29
Q

prognosis

A

Most neurological recovery occurs within the first 2 months (Waters et al., 1994)

Complete lesions have low probability of extensive neurological recovery (Marino, 2005), might regain one neurological level

Motor recovery following an incomplete lesion is more common (50% of AIS B/C improve over the 1st few months by 1 AIS level)

Predicting ability to walk is difficult and depends on level and completeness (unlikely in AIS A except low paraplegia, 30-45% AIS B walk short distances, most people with AIS C and D are community ambulators)