Spinal cord injuries

The brain communicated with the body via the cranial and spinal verves.

Cranial nerves

I Olfactory - smell

II Optic - sight

III Oculomotor - rectus extrinsic eye muscles, ciliary muscles

IV Trochlear - superior oblique extrinsic eye muscle

V Trigeminal - From 3 areas on the side of face and mastication

VI Abducens - lateral rectus eye muscles

VII Facial - taste, tongue, outer ear, nasal and oral glands, facial muscles

VIII Auditory - vestibulocochlear, hearing and sensitivity to head movement

IX Glossopharyngeal - taste receptors, pharynx, middle ear, carotid body, parotid gland

X Vagus - mouth, thoracic and abdominal viscera

XI Spinal accessory - trapezius and sternomastoid

XII Hypoglossal - tongue muscles

All of these nerve are in pairs and can communicate with the brain without the spinal cord

Spinal cord

Extends from the base of the medulla oblongata to about L1 – L2

Lies in vertebral canal of the vertebral column

Surrounded by meninges and CSF

Motor fibres leave the front, sensory enter via the back, anterior and posterior horns

White matter outside, grey matter inside, central canal contains CSF

White matter contains anterior, posterior and lateral columns

The large nerves below the termination of the cord are termed the cauda equina

Spinal nerves

There are 31 pairs of spinal nerves, named for their associated vertebrae

Cervical I nerve is above the first cervical vertebrae.

There are 8 cervical, 12 thoracic, 5 lumbar, 5 sacral and 1 coccygeal nerves

Dermatomes are areas of skin surface supplied by sensory nerves using specific spinal nerves

Sympathetic spinal nerves leave via spinal nerves T1 down to L2

Parasympathetic nerves leave the CNS via some cranial nerves and S2, S3 and S4

C3, C4, C5, form phrenic nerves supplying the diaphragm

Damage above C3 + C4, often causes death - respiratory paralysis

C5, C6, C7, C8, T1, T2 nerves supply the upper limbs, radial nerve

Aetiology

Patients are often young

Strong acceleration or deceleration forces, e.g. RTA, falls from a height, diving accidents, penetration

Rugby scrum collapse

Whiplash injuries

Injuries caused by roof cave in

Injury severe enough to cause unconsciousness

Pathophysiology

Once damaged the nerve cells of the spinal cord cannot regenerate, this means any injury results in a consequent loss of neurological function

Spinal instability may be caused by fracture, dislocation or subluxation or associated ligament damage

Spinal cord contusion may occur

Damage to the cord may be primary or secondary

Cervical lesions may lead to hypoventilation and CO₂ retention, this makes the patient sleepy

Classifications of SCI

Determined by level and degree of cord involvement

Tetaplegia (also called quadriplegia), from cervical lesions, effects arms, legs, trunk and pelvic organs

Paraplegia, from thoracic, lumbar or sacral lesions, it affects trunk, pelvic organs, legs, depending on level

Complete SCI - total loss of motor and sensory function below level of lesion

Incomplete SCI - some residual motor and sensory function below level of lesion

Anterior cord syndrome

Usually caused by flexion-rotation forces resulting in anterior dislocation or compression fractures of vertebral body, both leading to anterior cord contusion

Flexion means to bend

Spinothalamic tract compromise - reduced pain and temperature sensation

Corticospinal tract compromise - weakness

Central cord syndrome

Mostly seen in older patients with cervical spondylosos (degeneration of vertebral bodies or disks)

May be caused by relatively minor hyperextension

Flaccid weakness of arms due to compression of central tracts

Preservation of leg motor supply

Brown-Sequard syndrome

Hemisection cord compromise

Most common cause is penetrating injury or lateral fractures of vertebrae

On the side of the injury there is reduced or absent power below the level of the lesion but preserved temperature and pain sensation

On the other side to the injury there is normal motor power but inhibited pain and temperature sensation

I.e. ipsilateral weakness and contralateral impaired pain and temperature sensation

Posterior cord syndrome

Usually caused by hyperextension injuries and fractures to posterior elements of vertebrae

Pain, temperature and motor function may be preserved but there will be loss of proprioception leading to ataxia

Immediate clinical features

Pain from the spine

Paresthesia, (numbness, tingling, `pins and needles`)

Weakness or heaviness in limbs

Loss of sensation

Paralysis, muscles may be flaccid

Difficulty breathing

Reduced movement of intercostals muscles (inercostal motor nerves arise from around C5 to C6, giving rise to rapid shallow diaphragmatic breathing

Low systolic BP (typically below 75 mm Hg) – in the absence of other causes of shock

Pulse may be slow

Skin may be warm and dry rather than cold and clammy

Possible abnormal alignment of the spine

Priapism may occur

Initial assessment

Describe the area of anaesthesia

Assess strength of motor function

Monitor changes in neurological function over time

Suspect in any injury which has traumatised the face, neck, head or abdomen

Initial management

ABC

Maintain the airway without neck extension

Gentle jaw thrust if possible

Nasopharyngeal or oropharyngeal airway or intubate

As a last resort apply gentle head traction, maintain the midline and tilt the head slightly back

Always maintain head, neck, body alignment

Immobilise the spinal column

Use spinal boards

Use cervical collars, blocks and tape

Logroll with 5 people

Person with the head is always in charge

Spinal shock

Caused by sudden loss of sympathetic outflow from the cord

Leads to vasodilation and pooling of venous blood reducing venous return

Below level of lesion there is; flaccid paralysis, loss of tendon reflexes, absence of somatic and visceral sensation, loss of bladder and bowel function, motor loss

May be complicated by paralytic ileus

May last for hours, days or weeks and resolves as spinal reflexes recover

Immediate treatment of SCI

Surgical decompression of the cord

Internal fixation of unstable bony injury

Traction

Prevent secondary cord injury

Correct hypotension and hypoxia

Correct spinal shock

Improve local circulation

Methylprednisolone

Prevention

In themselves, fractures of vertebrae are not any more serious than any other fracture; they will heal at the same rate

However fractures weaken the integrity of the spinal column leading to instability and dislocation, this may damage nerve roots or the cord

Any movement of an unstable facture may therefore pinch a nerve root or damage the cord

All potential spinal injuries must be treated as definite injuries until proved otherwise

Patients must not be mishandled at the scent of an accident

Always maintain a high index of suspicion

If you treat a patient without a spinal injury as if they had one it will do no harm

Tell conscious patients to lie still

Health education

Never dive into water unless it is totally transparent, deep and clear of obstacles

Use head restraints, seat belts, air bags in cars

Use risk adjustment psychology to promote dangers

Avoid being struck by lightning

Public awareness of first aid measures

Autonomic dysreflexia

A potentially serious complication in injuries above T6

Caused acutely by uninhibited sympathetic reflexes following noxious stimuli

May be triggered by a distended bladder or bowel or other somatic stimulus, e.g. a pressure sore, ingrowing toenails, sex, tight straps

Most cases caused by bladder distension or infection

Afferent impulses travelling up the cord at blocked at the level of the lesion

This stimulates sympathetic ganglion below the level of the lesion leading to `gooseflesh` and pallor, below level of lesion

Gross sympathetic stimulation causes profound vasoconstriction below lesion level

Increase in BP is detected by aortic and carotid baroreceptors which lower HR and vasodilate where the can, i.e. above the level of the lesion

However tachycardia is a possibility

Headache and nasal congestion (due to vasodilation)

Complications include retinal haemorrhage, SAH, intracerebral haemorrhage, coma, death

Remove cause, e.g. Change urinary catheter, decompress bowel, consider nifedipine as a vasodilatory antihypertensive

Muscle spasms

Spinal reflexes below the level of lesion may be preserved

Spinal reflex activity may result in muscle hypertonia and spasticity

External stimuli may precipitate muscle spasms

Thermoregulation

Regulation of vasotone below the level of the lesion is lost

Ability to sweat and shiver are also lost

Higher level lesions generate greater problems in thermoregulation

Patients become relatively poikilothermic

Nursing problems

Caused by paralysis and inhibition of the autonomic NS

Respiratory problems

Infection

Hypoventilation

Gastrointestinal problems

S2 – S4 regulate defecation reflex and anal tone

Atonic bowel may lead to constipation

Cardiovascular

Postural hypotension and vasovagal response

DVT, especially in the weeks following injury

Oedema due to decreased peripheral vascular resistance

Musculoskeletal changes

Loss of bone density

Metabolic changes

Urinary tract problems

Bladder voiding is S2 – S4

UTIs

Urinary incontinence

Incomplete bladder emptying

Sexual difficulties

Most sexual function is S2 – S4

Women can still have babies

Psychosocial challenges

Communication problems

Skin problems

Pressure sores

Sensory motor loss leading to further damage