Spinal cord injuries - PowerPoint Presentation

Slide1

Spinal cord injuriesSlide2

Overview:

Anatomy of the spinal cord

Case presentation

Spinal cord injuries

Classification

Complete and incomplete syndromes

Respiratory complications of spinal cord injuries

ICU management of spinal cord injuries

Pharmacological managementSlide3

Gross anatomy

Begins at the foramen magnum of the skull, where it is continuous with the medulla oblongata

Cervical enlargement gives rise to the brachial plexus

Lumbar enlargement gives rise to the lumbosacral plexus

Tapers inferiorly to the conus medullaris – from here the filum terminale attaches to the coccyx

Lower end of the spinal cord lies at the lower border of L1

Vertebral column is much longer than the spinal column, so the cord segments do not correspond numerically to the vertebral bodiesSlide4

Columns of the spinal cord

Spinal column stabilised by three major ligaments;

Anterior longitudinal ligament

Posterior longitudinal ligament

Ligamentum flavum

Anterior column: Anterior 2/3 vertebral bodies and the anterior ligament

Middle column: Posterior 1/3 vertebral bodies and the posterior ligament

Posterior column: Ligamentum flavum and everything else

Injury involving > one column is considered unstableSlide5
Slide6

Spinal cord structure

Inner core of grey matter, surrounded by an outer covering of white matter

Grey matter is arranged in an ‘H- shape’, with anterior and posterior horns, joined by a thin grey commissure which contains the central canal

The T1-L3 segments also contain a lateral grey hornSlide7
Slide8

Grey matter of the spinal cord

The anterior horn is divided into medial, central and lateral columns

Medial group is present in most segments



innervating the skeletal muscles of the neck and trunk

Central group is the smallest and is present in some cervical and lumbosacral segments

Lateral group is present in the cervical and lumbosacral segments



innervates the skeletal muscles of the limbs

Posterior horn has four different groups of nerve cells

Substantia gelatinosa group

Nucleus propius

Nucleus

dorsalis

Visceral

afferent nucleus

Lateral grey horns contain pre-ganglionic sympathetic fibresSlide9

Tracts of the spinal cord

Ascending (sensory):

Dorsal (posterior) columns: deep touch, proprioception, vibration

Lateral spinothalamic: pain and temperature

Anterior spinothalamic: light touch

Descending (motor):

Lateral corticospinal: voluntary motor

Anterior corticospinal: voluntary skilled motor

Rubrospinal: control of movement

Vestibulospinal: posture and balance

Tectospinal: reflex postural movements in response to visual stimuliSlide10
Slide11

Spinal cord injuries

Causes:

Majority caused by MVAs; falls; iatrogenic

Mostly young males, but the other demographic includes older people with concurrent degenerative spinal canal narrowing

Frequently associated with other conditions:

Shock syndromes

Other injuriesSlide12

A likely story…Slide13

Say hello to Jim.

85 year old male who slipped backwards and hit head on towbar behind car

Presented to Tenterfield Hospital, then T/F to Armidale, where CT showed unstable C4/5 #

Transferred to JHH for NSx R/V

Conscious and spontaneously breathing

Hard collar in situ, but poorly fitting

GCS 13: E3V4M6, PEARL

B/G: metastatic prostate ca, HTN, T2DMSlide14

Jim’s imaging

Unstable C4/5 fractureSlide15

Further examination…

N

ormal cranial

nerve examination

Decreased strength (2/5) and absent reflexes bilaterally in upper limbs

Decreased pain and temperature sensation bilateral hands

N

ormal

strength (

5/5), reflexes and sensation in bilateral

lower

limbs

Developed urinary retentionSlide16

American Spinal Injury Association Neurological impairment scale

Slide17

Classifications

Quadriplegia

Injury to the cervical spine, leading to impairment in the arms, trunk, pelvis and legs

Paraplegia

Injury to the

thoracic,

lumbar or sacral segments, leading to impairment in the trunk, legs and pelvic organs

Complete

No motor or sensory function below the affect level

Incomplete

Some preserved motor or sensory function below the affected levelSlide18

Complete injury

No voluntary anal contraction

0/5 distal motor score

0/2 sensory score

Bulbocavernous reflex presentSlide19

Incomplete spinal cord injuries

Anterior cord syndrome

Central cord syndrome

Brown-Sequard syndrome

Posterior cord syndromeSlide20

Anterior spinal cord syndrome

Injury to the anterior spinal cord caused by either direct compression of the spinal cord, or damage to the anterior spinal artery

Usually from a flexion/compression injury

Bilateral loss of pain, temperature and light touch below the lesion due to disruption of the anterior and lateral spinothalamic tracts

M

otor dysfunction due to the disruption of the anterior corticospinal tracts, and damage to the anterior grey horn neurons

Worst prognosis of incomplete SCI

10-20% chance motor recovery

AnteriorSlide21

Central spinal cord syndrome

Most common incomplete spinal cord injury

Often in the elderly with extension injury mechanisms, due to anterior osteophytes and posterior infolded ligaments

Motor dysfunction due to disruption of the lateral corticospinal tracts and damage to the anterior grey horn neurons

Bladder and bowel involvement

Bilateral loss of pain, temperature and light touch due to disruption of the spinothalamic tracts

Sacral sparing

Good prognosis, but unlikely to regain full function

AnteriorSlide22

Brown-Sequard syndrome

Caused by complete cord hemitransection

Ipsilateral motor dysfunction, with LMN weakness at the level of the injury, and UMN signs below the injury

Ipsilateral proprioception and vibration loss due to posterior column damage

Contralateral pain and temperature loss 2-3 segments below the lesion due to disruption of the spinothalamic tracts

Good prognosisSlide23

Posterior cord syndrome

Rare syndrome

Most commonly caused by vascular compromise, with occlusion to the posterior spinal artery

Sensory dysfunction with ipsilateral loss of proprioception and vibration, and preservation of pain and temperature

AnteriorSlide24

Cauda equina syndrome

Caused by damage to the cauda equina, a collection of S1-L5 nerves

Technically a peripheral nerve lesion, so will cause lower motor neuron signs

Presentation:

Saddle anaesthesia, bilateral lower limb sensorimotor loss and pain, bowel and bladder symptoms (especially urinary retention)

Absent or reduced lower limb reflexes, decreased rectal tone

MRI best to evaluate nerve compression

Needs urgent surgical decompression within 48 hoursSlide25

Jim’s progress notes…

Admitted under NSx

Few episodes of vomiting on ward, during which he likely aspirated

RRT on ward for respiratory arrest – intubated and T/F to ICU

Some more stuff happened….

Improved and ready to trial extubation….

Unfortunately, he failed

extubation due to hypoxia

Why?Slide26

Respiratory complications with SCI

Spinal cord level

Muscle involvement

Effect on respiration

Clinical consequence

C1-3

Complete paralysis of all respiratory muscles

Vital capacity only 5-10% of normal; absent cough

Apnoea and immediate death

C3-6

Varied impairment of

diaphragmatic contraction

Vital capacity

20% of normal; weak and ineffective cough

Ventilation necessary in acute stages; majority will be weaned from mechanical ventilation

C6-8

Diaphragm and accessory cervical inspiratory muscles intact. Intercostals

and abdominal muscles intact

Expiration

entirely passive. Secretion retention. No respiratory failure unless coexisting lung/chest injury/illness

T2-4

Vital capacity 30-50% normal,

and weak coughSlide27

SCI effects on breathing

Loss of intercostal function:

Failure of AP expansion of the ribcage

Chest wall sucked in during diaphragmatic contraction

Loss of lower thoracic segment innervation:

Diaphragm starts in a flatter position, which decreases contraction pressure

Loss of abdominal muscle tone:

As the diaphragm flattens, abdominal contents are pushed outwards and the lower ribcage is pulled inwards, causing paradoxical see-saw breathing

Diaphragm is pulled down by the weight of the abdomen

Inefficient, rapid, shallow breathing results, with more dead space ventilation

Abdominal muscle weakness results in decreased ability to cough and clear secretionsSlide28

ICU management of SCI patientsSlide29

Respiratory management

Airway management

Physiotherapy

Posture

Mucolytics

Abdominal binding

Monitor for infection

Bronchoscopy Slide30

Longer term respiratory care

Tracheostomy

More comfortable; minimise laryngeal damage; less dead space compared to ETT; associated with fewer respiratory infections

Weaning from ventilation

Portex sprints are as effective or better than PS weaning, with both superior to SIMV weaningSlide31

Cardiovascular complications after SCI

Neurogenic shock

Occurs with lesions above T6 due to loss of sympathetic tone and unopposed parasympathetic tone

Vasodilation and hypotension; bradycardia

Thromboembolism

Due to immobility and venous stasis

Sympathetic hyperreflexia

Unopposed sympathetic tone below the level of injury, triggered by sensory stimuliSlide32

Gastrointestinal complications after SCI

Delayed gastric emptying and ileus

Common and may last 2-3 weeks

Aperients, early feeding, NGT, prokinetic agents

Gastric stress ulceration

PPI prophylaxis

ConstipationSlide33

Metabolic system considerations

Temperature regulation

Hypothermic due to vasodilation

Hyperthermic due to inability to sweat below level of injury

Hyperglycaemia

Common due to stress response

Worsens ischaemic neurological injurySlide34

Pharmacological treatment of SCI

Steroids

Previously, high dose methylprednisone was standard of care for SCI

Since shown to significantly increase mortality in patients, compared to placebo

NOGO-A antibody

NOGO-A is an inhibitory molecule that prevents neuronal plasticity and axonal regeneration

Current clinical trial to determine effects of an intrathecal infusion of NOGO-A antibodySlide35

References

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Management strategies for acute spinal cord injury: current options and future perspectives.

Current Opinion Critical Care. (2012). 18:651-660

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