Spinal

Front 1

Tetraplegic & Paraplegic Levels

Back 1

T1/C8 above and below

Front 2

SCI Epidemiology

Back 2

• Incidence of Traumatic SCI in Australia (>15
y.o.) : 15-17 cases per million per year
• Peaks at 15-24 & 65-74
• 82% male
• 52% paraplegic and 47% quadriplegic.
• Average age of spinal cord injured person is 31.

Front 3

Causes of SCI

Back 3

Cause (04-05) %
Motor Vehicle 25
Motorcyclists, cyclists, pedestrians 24
Low Falls (< 1 m) 10
High Falls (> 1m) 29
diving or surfing 9
Hit / Struck by an object 10
Other Causes 3

Front 4

Aetiology of Non-traumatic SCI

Back 4

• Spinal Stenosis, Intervertebral disc herniation,
RA
• Vascular
• Inflammatory
– infectious (viral, bacterial, fungal, parasitic)
– Non-infectious (transverse myelitis, MS, polio)
• Tumor
• Iatrogenic: Radiation, Contrast arachnoiditis
• Others: Syringomyelia, MND, vitamin B-12,
Friedreich ataxia.

Front 5

Mechanical Injuries

Back 5

Front 6

Compression Fractures

Back 6

axial forces
- can also cause a burst fracture,
and most are pretty stable if they dont affect the ligaments EXCEPT the jefferson fracture

Front 7

Flexion Rotation Injuries

Back 7

rotatory component involved
- shallow and slopy facets joints
- flat cevival
CERVICAL joints can therefore jump ontop of each other, thus locks ontop of each other (need surgical to unlock)

can also affect the ligaments as well as the verterbral aa. thus causing clots or stuff...

Front 8

Flexion Injuries

Back 8

BILATERAL DISLOCATION: one part of the spinal column moves anteriorly the other moves posteriorly thus the cord is dramatically affected
TEARDROP FRACTURE: osteoarthritic spurs also can affect the spinal cord (compressions)

Front 9

Most Spinal Cord Injury occurs at:

Back 9

C4,5,6 (the most flexible part of the spinal column)

Front 10

Standard Neurological Classification of SCI

Back 10

- classify the last level with some preservation still on each side
AIS-A complete injury
AIS-B incomplete injury

Front 11

Syndrome of Spinal Cord Injury

Back 11

Central Cord Syndrome
Brown Sequard Syndrome
Anterior Cord Syndrome

Front 12

Central Cord Syndrome

Back 12

greater weakness in upper limb, rather than lower lims

Front 13

Anterior Cord Syndrome

Back 13

anterior spinal aa. comes form the aorta, thus hypertension here can cause the syndrome (affects motor power)

Front 14

Brown-Sequard Syndrome

Back 14

contralateral loss of pain and temp, and ipisilateral of touch, power...

Front 15

Crossection of spinal cord with main tracts

Back 15

central cord syndrome because the cervical tracts are laminated nearer to the tracts-
thus the upper tracts are more affected

Front 16

Consequences of SCI

Back 16

• Impairment of control of movement
& sensation
• Defective/absent bladder & bowel
function
• Impaired fertility and sexuality
• Defective control of autonomic
function
• Blood pressure (Autonomic
dysreflexia)
• Sweating
• Temperature
• Inadequate respiratory function
• Uncontrolled activity of the isolated
spinal cord
• Spasticity
• Pain
• Musculoskeletal complications
• Psychosocial impact

Front 17

Autonomic Dysreflexia (AD)

Back 17

• Sudden onset of severe hypertension
– At or above T6
– Isolation of Sympathetic Nervous System
(SNS) from vasomotor centres of brain
• Potentially life threatening condition
– requires immediate attention.
– Can lead to:
- Hypertensive encephalopathy
- Intracerebral haemorrhage
- Seizures
- Cardiac Arrhythmias

Front 18

Pathophysiology of AD

Back 18

SYMPATHETIC OUTFLOW: can recieve input for strong spina reflexes below and causes SNS thjus vasoconstrictors
BRAIN: will try to decreases, the BP, slow HR, and vasodilate only where there is still brain control (since it has no idea of what is going on below the injury)

Front 19

Triggers of AD

Back 19

• Genitourinary - Over distension, UTI, stones, DSD, epididymoorchitis
• Bowel – impaction, hemorrhoids, gastric ulcers, appendicitis, gallstones
• Sexual stimulation, labour, menstruation, vaginitis
• Skin - Ingrown toe nails, pressure areas, burns, insect
bites, tight clothing, shoes, or appliances
• MSK: Heterotopic bone, #s
• Procedures - Urodynamics, Cystoscopy
• Others: DVT, PEs, Temperature fluctuations

Front 20

Presentation of AD

Back 20

- pounding headache
- SoB
- Sweating
- Goose Bumps
- Slow pulse
- Flushing or blotching of the skin
- Slow pulse
- Nasal Congestion
- restlessness or anxiety

Front 21

Tx of AD

Back 21

• Sit patient as upright as possible
• Call for help & monitor blood pressure
• Remove or loosen all tight clothing (TEDS & abdominal binder)
• Check drainage system for kinks/clots/sediment
• Empty leg bag
• Attempt to identify cause
• Refer to AD Treatment Card/Algorithm and RSCIP
Fact sheet

1. BLADDER Tx; catheter..
2. After excluding bladder distention, manually evacuate full rectum with LOTS of lignocaine and watch BP fall
3. If not look for other causes

Front 22

Pharmacological Treatment of AD

Back 22

Medication may be needed if the cause of AD is not
easily remediable / is over 170 mm Hg
• Glyceryl Trinitrate as:
– sublingual spray or
– 1/2 Anginine tablet (repeated every 5-10 min) or
– 5mg/24 hr patch.
Warning: Do not use GTN spray/tablets if PDE5I or other nitrate containing meds have been used)
• Captopril 12.5mg sublingual
• Adequate analgesia when appropriate
• Patient may require admission to Hospital if AD does not resolve

Front 23

Susceptibility to Autonomic Dysreflexia

Back 23

• Susceptibility to Autonomic Dysreflexia is
increased for 48 hours after an episode has
concluded, during that time:
– BP should be monitored
– Invasive procedures/instrumentation should be
minimised
• Patient should have:
– Education on proper bladder, bowel and skin
management techniques
– Plan for when AD does occur
– AD Medical Emergency Card, Medicalert bracelet
– Up to date prescription of GTN

THUS pain relief is important even though they cant feel it

Front 24

Micturition Pathways

Back 24

Front 25

Bladder Goals

Back 25

• Maintain social continence
• Protect upper urinary tracts from sustained high (ie. >40cm H20) pressures
• Prevent complications
• Choose technique compatible with person’s functional capacity and lifestyle

Front 26

UMN vs LMN Bladder

Back 26

LMN bladder, no hyperreflxic but still can be not soo strecthy, so it wont relax as muxh as normal but u wont have the problems with the spincter in the UMN bladder
- more likely to get inconteince in LMN bladder

Front 27

Genitourinary
Complications

Back 27

• Increased intravesical pressures, reduced
compliance, detrusor hyper-reflexia,
incomplete emptying
• Hydronephrosis, upper tract deterioration
& renal failure
• Urinary tract infections, epididymoorchitis
• Bladder & Renal calculi
• Fistulae / stricture of the urethra (CISC)
• Increased risk of bladder cancer with
long-term IDC/SPC
• Do not forget prostate CA

Front 28

Upper vs Lower Motor Neurone Bowel

Back 28

Front 29

Gastrointestinal Complications

Back 29

• Complications increase with time post injury
– Constipation/incontinence
– Abdominal pain & distention (43%)
– Haemorrhoids (74%)
– AD related GIT (43%)
– Difficulty with bowel evacuation (20%)
– Severe oesophagitis
– Gallstone disease (7x)
– Megacolon/ recurrent sigmoid volvulus (poo in the intestines backed up)
• ? Colorectal CA

Front 30

Sexual Function Effects

Back 30

• Changes in arousal response
- decreased sensation
- decreased lubrication
- decreased clitoral engorgement
- erectile dysfunction
• Changes in orgasm
- decreased or absent sensation
- few males achieve true ejaculation (4-5% in complete cords)
- brief erection with rapid dribbling emission

Front 31

Interventions for erectile dysfunction

Back 31

• Education of patient and partner re:preparation, physical techniques and discuss psychosocial aspects
• Oral - Sildenafil (Viagra), Vardenafil (Levitra), Tadalafil (Cialis)
• Nasal, sublingual, intraurethral, transdermal
• Intracavernosal Injection of vaso-active substances (e.g. Prostaglandin E1, Papaverine HCl)
• Vacuum tumescence device
• Newer medications: apomorphine
• Sacral stimulation (Brindley)
• Penile prosthesis (silicone rods or inflatable)

Front 32

Why do UMN become hyperreflexic?

Back 32

the brain has inhibitory input into the spinal cord thats why when u release its control u become hyper reflexic...

Front 33

Male Feritility

Back 33

• Impaired due to
– erectile dysfunction
– reduced ability to ejaculate
– impaired semen quality
• Most will require significant medical intervention to
achieve pregnancy

- normal sperm counts but LOW percent sperm motility

Front 34

Interventions for improving Fertility

Back 34

• Vibroejaculation
• Electroejaculation
• Direct Semen Retrieval
• Assisted Reproduction:
– in-home insemination
– intra-uterine insemination
– in-vitro fertilsation (IVF)
– gamete intrafallopian transfer (GIFT)
– Intracytoplasmic sperm injection (ICSI)

Front 35

Integumentary- organ system that protects the body from various kinds of damage, such as loss of water or abrasion from outside. The system comprises the skin and its appendages

Back 35

• 50-80% of persons with SCI develop a pressure ulcer
• Prevalence ~9% at 1yr vs 23-33% at 15-20yrs post-discharge
• 2nd most frequent cause for rehospitalisation in USA & occupy 30% of non acute SCI hospital beds in NSW.
• Significant morbidity and mortality.
• Consider personal costs.

Front 36

Neurological Complications

Back 36

• Pain & spasticity
• Late onset weakness or sensory loss (~20%)
• Progressive cystic myelopathy (post-traumatic
syringomyelia)
• Compressive neuropathy
– 2/3 in upper limbs
– >50% carpal tunnel
– 25% bilateral neuropathy

Front 37

Clinical Relevance of Spasticity

Back 37

• Disabling if interferes with positioning or ADLs (eg. transferring, dressing, bathing, toileting, sitting balance, pushing wheelchair, gait, driving, etc)
• Exacerbated by noxious stimuli below lesion
(eg infection, fracture, etc)
• May be implicated in falls
• May cause contractures, pain or skin breakdown

Front 38

Musculoskeletal Commilcations

Back 38

• Heterotopic ossification
• Upper limb overuse syndromes
– rotator cuff tears, tendonitis, subacromial bursitis, capsulitis
– shoulder pain
– impact on function
• Osteoporosis & increased risk of lower limb fractures (6%)
• Kyphoscoliosis
• Neck & back pain

Front 39

Cardiovascular

Back 39

• Acute phases – inc risk of arrhythmias
• Prone to postural hypotension, pedal oedema
• Later phases - Hypertension 2x as common
• Increased rate (22% vs 6%) & earlier onset of diabetes mellitus
• 2nd leading cause of death (50% deaths >30 yrs post SCI)

Front 40

Pulmonary

Back 40

• Restrictive disease
– muscle paralysis
– kyphoscoliosis, spasticity
• Obstructive disease
– hyperactive airway disease
• Recurrent respiratory tract infections
• Respiratory failure
• DVTs & PEs
• OSA (40%)
– only 25% are obese

Front 41

Psychosocial Risk Factors for SCI

Back 41

- fewer years of education
- more likely to be unemployed
- more likely to be single

OUTCOME: younger people are more tolerant and less likely to become depressed

Front 42

Community Reintegration

Back 42

75% return home
However, often face barriers (physical, attitudinal, expertise, systemic) For e.g. attendant care, assistive devices, equipment and financial support, accessible transportation, employment opportunities, and
primary health care services
Employment rate 40% (70% in the general population)
Reduction in involvement in active living
Impact on relationships (Postinjury marriages survive better than preinjury marriages)

Front 43

Life Expectancy

Back 43

Front 44

Causes of death after SCI

Back 44

Front 45

Prevention of SCI

Back 45

• Primary – stopping it from happening
– Seat belts, child safety seats, Safer roads & cars
– Random breath testing, legislation
– Helmut use, diving education, workplace safety
– Falls prevention measures and education
• Secondary – reducing severity, managing risk factors
– Improved retrieval, specialised care, early decompression
• Tertiary – mitigating the effects
– Rehabilitation programs
– Education and self management re: health maintenance (regular check ups, nutrition, exercise, pressure area care

Front 46

ASIA
-a, b, c, d,e

Back 46

A indicates a "complete" spinal cord injury where no motor or sensory function is preserved in the sacral segments S4-S5.
B indicates an "incomplete" spinal cord injury where sensory but not motor function is preserved below the neurological level and includes the sacral segments S4-S5. This is typically a transient phase and if the person recovers any motor function below the neurological level, that person essentially becomes a motor incomplete, i.e. ASIA C or D.
C indicates an "incomplete" spinal cord injury where motor function is preserved below the neurological level and more than half of key muscles below the neurological level have a muscle grade of less than 3, which indicates active movement with full range of motion against gravity.
D indicates an "incomplete" spinal cord injury where motor function is preserved below the neurological level and at least half of the key muscles below the neurological level have a muscle grade of 3 or more.
E indicates "normal" where motor and sensory scores are normal. Note that it is possible to have spinal cord injury and neurological deficits with completely normal motor and sensory scores.[4]