Chapte

r7
 
- Injuries ­ 
Spine

   

     
   
• Biomechanics

○ Anatomy of the spinal cord

○ Injury

• Damage to the spinal vertebral column

○ Bones

○ Damage to specific vertebrae

○ Damage to muscles, ligaments and tendons

• Assessing the problem

○ Analysis of the patient with a spinal injury

 When the patient is unconscious

 When the patient is conscious

• Clinical analysis of sensory and motor disturbance

○ In ‘First Aid’

○ Early treatment and investigations

○ X-rays

 Plain radiographs

 Computerised Tomography (CT)

• Soft tissue injuries

• Prevention

○ Primary - avoiding the injury

○ Secondary - avoiding further damage to spine or spinal cord after the initial
injury

• Statistics1
Biomechanics

Anatomy of the spinal cord

Within the human spinal canal the spinal cord extends from the base of the brain to the conus
medallaris usually at the level of the L1/L2 vertebrae when the nerve roots become the cauda
equina. The spinal cord is a soft, pliable mass of nerve fibres and cells supported by glial tissue
and enmeshed in small blood vessels. The cord contains myelinated ‘long’ tracts and
interconnecting fibres described as the ‘white matter’ surrounding the central ‘grey matter’
comprising mostly unmyelinated nerve fibres with supporting glial tissue and a very intense
small blood vessel network. Blood flow to the spinal cord is mainly provided to the anterior tow-
thirds of the cord by the anterior spinal artery which arises from two branches of each vertebral
artery over the medulla and runs superficially in the anterior sulcus to eventually synapse
around the lower end of the spinal cord with the descending branches of the posterior spinal
arteries which arise from the posterior inferior cerebellar arteries. Posterior spinal arteries
provide blood flow to the posterior third of the spinal cord.
These small spinal arteries require additional assistance from the major supplementary arterial
supply usually at two levels of the spinal cord (T1 and T11), from the corresponding intercostal
arteries.
Nerve fibres in the posterior columns of white matter are essentially travelling cephalward and
are uncrossed until higher in the central nervous system carrying sensory modalities for
proprioception, vibration, some touch and appreciation of moderate degrees of temperature
variation. Tracts in the anterior column of white matter are mainly travelling caudalward to
synapse either directly with anterior horn cells or with other interneuronal pathways. In the
lateral column there is a mix of fibres going ‘upwards and downwards’. The lateral column
contains the lateral cortico-spinal pathway (pyramidal pathway) for control of motor power and
anteriorly is the main tract for pain (spino-thalamic) which are mostly crossed fibres. In the
cervical spinal cord the nerves in this tract have a laminated arrangement with the most distant
fibres travelling towards the distal end of the body (sacral) and the cervical travelling more
central within the tract. Anteriorly to the pain pathway is the main pathway for temperature and
further anteriorly again is the pathway for touch. Touch appears to be transmitted in the anterior
and posterior columns. The cortico-spinal pathway also has a layered orientation with those
motor fibres destined to synapse with anterior horn cells in the lower spinal cord (lumbo-sacral)
travelling in the more superficial layers of the tract in the cervical region. There remains a
complex arborisation of synapsing fibres within the spinal cord and many interneuronal
pathways are necessary to achieve balanced efferent and afferent activities within the human
spinal cord. The spinal cord tends to occupy only 50% of the ligamentum denticulatum and in
the intervertebral foramina.
The dura mater is also attached firmly to the base of the skull and at the second fused segment
of the sacrum in the adult (filum terminale).
There is therefore a lateral attachment of the spinal cord to both sides of the spinal canal. The
spinal cord within the dura is a mobile organ which tends to be held more tightly in the flexed
position of the spine and in a more relaxed position when the spine is extended.
The spinal canal is formed by 26 vertebra, 24 usually being separate from each other but
attached with intervening discs, ligaments and muscles. The coccyx is attached to the lower
end of the sacrum and usually comprises 4 small fused vertebrae of a vestigial ‘tail’. The
sacrum usually consists of 5 vertebra also fused together. The stable spinal column is
maintained with a cervical lordotic curve, a thoracic kyphotic curve and a lumbar lordotic curve.
There are fixed kyphotic curves in the fused sacrum and coccyx.
The spinal vertebral column (Fig. 1) can be subdivided into the Denis 3 column classification,
with an anterior column, which includes the anterior longitudinal spinal ligament, the anterior
annulus of the disc and the anterior third of the vertebral body; the middle column under this
classification includes the posterior spinal longitudinal ligament, the posterior annulus of the
disc and the posterior two thirds of the vertebral body; the posterior column involves the
posterior bony arch with the spines, laminae and pedicles, and attached ligaments including
supraspinous, interpinous, ligamentum flavum and capsules of the posterior facet joints.
The muscles immediately surrounding the spinal column and attached to the vertebrae are of
great importance in maintaining stability of the spinal column. In addition to those muscles
which are closely applied to the vertebrae, there is the additional ‘wider circle’ of muscles which
includes the larger spinal muscles, for example, trapezius, latissimus dorsi and the abdominal
muscles.
Each disc has a firm annulus fibrosus surrounding the nucleus pulposus, which is softer, pliable
material and each disc is firmly attached to the adjacent surfaces of the vertebra above and
below. The posterior spinal longitudinal ligament is loosely attached to the discs. The annulus
fibrosus has a nerve supply from the sinu vertebral nerve of Luschka.

Injury
Damage to the spinal cord can either occur from direct injury to the spinal cord tissue, including
nerves, cells and supporting tissue (glia) within the spinal membranes or through injury to the
blood vessels essential for cord function. Damage can occur to the anterior spinal artery,
posterior spinal arteries and the circumferential arteries which give off radiate branches running
into the deeper central regions of the spinal cord. There is also a complex network of very small
vessels, particularly within the grey matter which can be injured. There is now evidence to
suggest further progressive damage will occur to nerves in the spinal cord within hours of the
initial injury due to changes which occur in microvascular tissue within both grey and white
matter. The exact nature of these progressive pathological changes has yet to be fully identified.
A lack of efficient blood flow to the partly damaged nerve tissue can lead to additional ischaemia
and further damage to nerves which may have otherwise survived the initial direct injury.
Damage to the spinal cord is described as ‘complete’ if laceration or severe bruising has
occurred at the level of the lesion. In adults this injury is frequently associated with disturbance
of the bony canal following fracture or fracture dislocation. In children there is often no obvious
radiological evidence of significant damage to the vertebral column. Less serious injuries are
described as ‘incomplete’ spinal cord injuries, eg. in concussion where the pathological changes
are reversible with scattered small areas of haemorrhage in grey and white matter without
disruption of the cord structure.
Contusion, or bruising, which can be described as being (I) ‘mild’ where haemorrhages are
larger in number and size than in concussion and with some permanent damage to nerve fibres
and cells; (II) ‘moderate’ with increased damage and severe bruising resulting in complete loss
of cord function.
The various areas of the spinal cord can be damaged resulting in specific clinical syndromes;
eg. the Brown-Sequard syndrome where damage is confined mostly to one half of the spinal
cord; the anterior column syndrome where the antero-lateral columns are affected often by
damage to the anterior spinal artery; the central cord syndrome where the grey matter is the
essentially affected area resulting in central cystic changes an profound loss of anterior
columns without significant loss in other areas and this injury produces severe disability with
loss of proprioception even though there is usually significant voluntary movement below the
level of the lesion.

Damage to the spinal vertebral column

Bones

Fractures in the vertebral bodies are described as wedge fractures, from flexion and
compression injuries; extension fractures are associated with ‘shearing’ translational injuries;
compression fractures is a burst injury to the vertebral body with retropulsion; a slice injury
which can occur as a flexion and rotation causing damage to the vertebral body and
interspinous and supraspinous ligament between the vertebrae.
Spondylolysis (Fig. 2) occurs with a defect in the pars interarticularis of the vertebral body. If the
defect is bilateral possible shift may occur in the anterior and middle column segments of the
spine following separation from the posterior spinal column segment. This is described as
spondylolisthesis (Fig. 3) and identified as grade 1, i.e. 25% of the shift forward of one vertebra
in relationship to another, up to greater than 50% of the vertebral displacement (grade 4).
Ligaments and joint capsules are usually damaged including the interspinous ligaments, facet
joint capsules, posterior longitudinal and anterior longitudinal ligament to allow subluxation of
facet joints with the anterior vertebral subluxation. These injuries can be found in fast bowlers,
baseball pitchers, gymnasts and weight lifters.
Damage can occur to the intervertebral discs (Fig. 4) resulting in mild bulging of the annulus,
increasing to bulging with tearing of the fibrous annular tissue if more severe. Rupturing of the
disc results when the nucleus pulposus herniates through a break in the annular wall frequently
impinging on nearby spinal cord, cauda equina or emerging nerve roots.

Damage to specific vertebrae

The C1 and C2 vertebrae (atlas and axis) damage. Fracture of the C1 ring secondary to axial
compression can result in a Jefferson type fracture. Rupture of the transverse ligament of the
atlas produces instability. Consider potential instability if the atlanto-axial space is greater than
3mms in flexion in the adult and 4mms in a child. Fractures of the odontoid frequently produce
pain which radiates posteriorly into the occipital area. The odontoid fractures are divided into
type 1 where there is a small segment of the odontoid fractured; type 2 where the base of the
odontoid is fractured; and type 3 where the fracture extends from the base of the odontoid into
the body of the C2 vertebra.
A ‘hangman’s fracture’ (traumatic spondylolisthesis) occurs through the pedicles of C2 following
hyperextension of the head and neck.

Damage to muscles, ligaments and tendons

Mild damage to muscles involves over stretch or direct bruising with more severe injury when
muscle fibres are torn or disrupted at the insertion of the tendon. The ruptured fibres in the
muscle belly will retract and ultimately heal with less elastic scar tissue.
The post traumatic inflammatory process can localise at the insertion of muscles, tendons and
ligaments near bone and is described as enthesopathic inflammatory process which can lead to
calcification. The sites commonly involved are the insertion of the outer layer of the annulus
fibrosus into the vertebral body, sometimes causing bony bridges between adjacent vertebrae
(syndesmophytes). Injury to musculo-skeletal tissue may highlight previously undiagnosed
spondylarthropathies including ankylosing spondylitis, spondylitis associated with psoriasis,
enteropathic syndromes, Reiter’s disease and arthritis associated with positive ‘rheumatoid
factor’.

Assessing the problem

Analysis of the patient with a spinal injury

When the patient is unconscious

If there is an associated head injury and the patient is unconscious, consider also spinal injury
particularly involving cervical spine. Observe whether breathing is diaphragmatic. When
intercostal muscles are weakened or paralysed from cervical spinal cord injury there will be a
‘paradoxical’ type respiration with in-drawing of the weakened intercostal muscles and
prominent movement of the diaphragm. (Phrenic nerve supply is usually from (C3, C4, C5
levels).

Mild and Lower Cervical Spine1 (Fig. 5)

Compression fractures
Include wedging of anterior vertebral margin, secondary to flexion injury. Treatment: SOMI
brace immobilisation. If associated with posterior instability - require fusion (greater than 50% of
anterior vertebral height and associated posterior ligament injury).

1 Farey I and Huynh C. The Spine in Sherry E and Bokor D. Manual of Sports Medicine, 1997, GMM, London.
Unilateral facet fracture/dislocation

Flexion rotation injury. Less than 33% subluxation on lateral x-ray. Neurological deficit usually
root lesion or Brown-Sequard syndrome.

Bilateral facet fracture/dislocation

Flexion distraction injury with greater than 50% subluxation on lateral x-ray. Spinal cord injury is
commonly associated with this injury. Treatment: Require reduction, posterior stabilisation and
fusion. Pre-operative evaluation with CT scan is required. MRI is required to exclude disc
protrusion behind superior vertebral body in all cases of bi-facetal injury to prevent compression
of spinal cord by disc material following reduction of dislocation as profound neurological deficit
may result.

Burst fracture

Axial compression injury with fracture displaced into spinal canal. High incidence of spinal cord
injury. Non-operative treatment may produce kyphosis and late neurological deficit generally
require anterior vertebrectomy and fusion.

Clay shoveller’s fracture

Avulsion injury of spinous process (C7, C6 or T1). Stable requires soft collar immobilisation for
comfort. Flexion extension radiographs required to exclude instability.

Neurological deficit without fracture

Occurs in patients with congenital narrowing of spinal canal and central disc protrusion, hyper
extension injury or following spontaneous reduction of dislocation. MRI mandatory for
evaluation.

Children’s spine injuries

Are rare and when they do occur are at the C1-2 level. It is often a soft tissue injury with
subluxation. Vertebral growth plates may be damaged with later spinal deformity. Spinal cord
injury can occur with a normal x-ray (SCIWORA).

Thoraco-Lumbar Spine

The thoracic spine is least susceptible to injury. The rib cage coupled with relative sagittal
orientation of the facet joint protects the thoracic spine against injury. However, the thoraco-
lumbar junction is the fulcrum between the mobile lumbar spine and relatively immobile thoracic
spine and is very susceptible to injury.
The spinal cord usually ends at the L1/2 interspace. Structural damage in the thoracic spine
 tends to be associated with neurological deficit. Only 3% of patients with lumbar spine
dislocations have neurological deficit. These tend to be at root level and are less debilitating.
However, clinical instability of lumbar fractures is common. The lumbar spine supports high
physiological loads. Late deformity, pain and occasionally neurological deficit may develop
following lumbar fractures. The three column concept of the spine allows stability to be
assessed. Instability is present when 2 or 3 columns are disrupted. The treatment is outlined in
Tables 1 and 2.

Table 1
General treatment thoraco-lumbar spine fractures and dislocations
In general for stable fractures (well aligned, less than 30° kyphosis and no

neurological deficit) is rest, followed by bracing.

Unstable injuries or those with neurological deficit usually requires surgery to
   
stabilise the fracture/dislocation to preserve or improve neurological function

and to prevent late pain, instability and neurological deficit.

  Treatment of specific injuries is outlined in Figure 2.  

  Table 2  

Specific Thoracic and Lumbar Spine Injuries

Injury Mechanism/Type Treatment Comment

Compression Flexion Bed rest/orthosis Neurological deficit 

(wedge) (Less than 50% uncommon. 

loss of vertebral Stabilisation and fusion 

height) if associated posterior 
   
instability
Chance fracture Flexion, distraction Bed rest, Neurological

bony and hyperextension, deficit uncommon.

ligamentous orthosis or Duodenal or

involvement stabilisation and pancreatic injury

fusion common
 Shear fracture and Flexion/rotation Spinal stabilisation Neurological

slice dislocations and fusion deficit common

Burst Axial compression Controversial

Deficit

surgical

decompression and

fusion

No neurological

Deficit

bed rest, orthosis

unless kyphosis

greater than 300

and canal intrusion

greater than 50%.

  When the patient is conscious  

Ask the patient whether there is any pain and where this pain is located. Whether the patient
can move upper or lower limbs and whether there is any loss feeling. When pain is present from
injury to the spinal column or adjacent muscles ligaments or capsules, inevitability there is
inhibition when movements precipitate or aggravate pain. The resultant restricted movement is
therefore not necessarily the result of involvement of the spinal cord.

In all patients with suspected spinal injury:

Consider the following important clinical signs:-

• Spinal Shock

All patients with significant spinal cord injury will have a period of spinal shock which may last
as long as two days and occasionally for several weeks. This phenomenon produces loss of
neuronal and reflex activity at and below the lesion, and is a pathophysiological phenomenon
producing difficulties for the clinician who is attempting to identify the degree of underlying
pathology within the apparently injured spinal cord. Complete spinal cord injury cannot be
diagnosed until spinal shock has passed. Spinal shock has resolved when the bulbo-
cavernosus reflex returns (anal sphincter contracts after squeezing the glans penis or by
tugging on the urinary catheter.

• Deformity

Fracture and fracture dislocations often do not produce obvious deformity. Fractures of the
vertebrae can follow flexion, rotation and compression injuries. Soft tissue damage such as
bruising or laceration to the face and skull help to identify specific forces which produced the
spinal injury. In children, frequently there is little evidence of external injury or bony
displacement, although profound loss of motor power and sensory function has occurred from
the spinal injury.

The site of the spinal cord lesion will eventually be identified as an ‘upper motor neurone’ lesion
producing spastic tetraplegia or paraplegia or a ‘lower motor neurone’ lesion involving the
central nerve cells, emerging nerve roots or cauda equina with persisting flaccid paraplegia.
Some patients remain with a ‘flaccid’ upper motor neurone type lesion where there is significant
damage to length of spinal cord, such as in a gun shot wound or where there is obstruction to a
main artery supplying the spinal cord, eg. ruptured aortic aneurysm.

Clinical analysis of sensory and motor disturbance (Figs. 6, 7, and 8)

If spinal cord damage is considered likely then the clinical examination must include an
assessment of the dermatomes (Last’s R.J. Anatomy, Regional and Applied) and in the
conscious patient assess movements in both upper and lower limbs. For example, the spinal
centres for elbow movements are C5/C6/C7 and C8 levels with C5/C6 supplying the flexor
movement of that joint C7/C8 essentially the extensor movement. In the lower limbs the hip
movements are controlled by L2/L3/L4 and L5 spinal cord centres with the more distal knee
joint controlled mainly by L3/L4/L5 and S1. The figs will demonstrate these levels and their
relationship to joint movement. Reflexes when present identify the viability of corresponding
levels in the spinal cord. To find normal resting muscle tone and normal reflex activity are
reassuring signs and even with apparent loss of motor power, a degree of guarded reassurance
can be given to the patient.

In ‘First Aid’

1. Always consider the possibility of spinal cord injury in both the conscious and unconscious
patient.
2. Avoid further damage to the spinal column and spinal cord with extrication and
transportation of the patient from the scene
3. At the scene of the injury check the airway as the first priority.
4. If the accident victim is not in further immediate danger avoid unnecessary movement of
the patient.
5. Apply the ABC rules of first aid ie:-
Maintain -
- airway (A)
- breathing (B)
- circulation (C)

Keep the injured cervical spine in the ‘mid position’ particularly avoiding flexion and rotation. If a
cervical injury is suspected apply a cervical collar. Lateral tilt and rotation of the head and neck
must be avoided. If necessary use a makeshift pillow under the side of the head. If a collar is
not available, use a jacked or jumper which can be rolled and the long sleeves of the garment
tied in front to form a supportive collar. A rolled up towel or newspaper can also be a useful
temporary substitute.
The patient must be observed at all times. If a lone attendant has to leave the patient to seek
help, then the patient should be left in the lateral coma position with the underside leg bent and
back supported to reduce the danger or inhalation should vomiting occur. In the conscious
patient roll the patient gently into the supine position provided there is no increase in the
patient’s symptoms or aggravation of pain with this movement. In the unconscious patient roll
the patient to the supine position and transfer to an appropriate frame or stretcher with constant
observation of the airway. The ‘first aider’ must be prepared to move the patient to the lateral
coma position immediately if vomiting occurs.
Transportation of the spinal patient to a specialised unit for further assessment and treatment
should be arranged as soon as possible and a skilled attendant accompany the injured person
during transfer. A patient with a higher level cervical spinal cord lesion requires oxygen by mask
or intranasal catheter and in all patients, if possible the stomach aspirated by an intragastric
tube before transfer to reduce the danger of inhalation of gastric contents.

Early treatment and investigations

Early treatment of the spinal injured patient will frequently include intravenous infusion avoiding
fluid overload and the development of pulmonary oedema. Assessing cardio-vascular efficiency
is important since the hypotension following spinal cord injury is the result of the profound
paralysis below the level of the lesion, loss of the ‘peripheral pump’ and the bradycardia as a
result of loss of sympathetic activity to the heart. In addition there may be the added
complication of surgical shock from multiple injuries.
In the patient with a spinal cord injury, an infusion of less than 3 litres of an appropriate
intravenous fluid should be given over the first twenty four hours and the patient carefully
assessed. Radiological investigations will be necessary to clarify the lesion involving the spinal
column. Radiological investigations will be necessary to clarify the lesion involving the spinal
column. Identifying directly the damage to the spinal cord will necessitate the use of CT and
MRI scars.
Damage to the spinal cord is classified under the headings of:-
1. Concussion where there is a transitory loss of function without permanent sequelae.
2. Contusion with bruising - mild, moderate or severe
3. Laceration which is equivalent to severe bruising and will have a poor prognosis.

There are now an increasing number of spinal injuries where there is partial damage to the
spinal cord. Within recent years the proportion of the incomplete spinal cord lesions now
approaches almost 50% of patients admitted to specialised spinal units and these patients will
have useful recovery. There will always be a degree of associated soft tissue injury and
ligaments, muscles, discs and joint capsules will all require an appropriate period of time to
adequately heal and for the scar tissue to develop a degree of elasticity and allow return of ‘pain
free’ range of movement.
The patient will be assessed by the spinal surgeon and frequently internal fixation, with or
without traction, will be required for cervical fracture/dislocations.
The patient with suspected spinal cord injury should be nursed in the Spinal Unit with
specialised nursing staff and with the assistance of mechanised beds and special mattresses to
avoid trophic skin ulceration which develops rapidly if patient are left immobile. Regular turning
of lifting of the patient requires the skilled nursing team. Physiotherapy services will also be
required constantly, more frequently for patients with higher lesions where there is the danger of
sputum retention and pulmonary collapse. The paralysed neurogenic bladder requires drainage
with an indwelling urethral catheter or suprapubic drainage during the period of spinal shock
and the usually replaced with intermittent catheterisation or use of reflex stimulation to promote
intermittent emptying of the bladder. Urodynamic studies will assist in identifying which type of
neurogenic bladder is present after the period of spinal shock and investigations with
intravenous pyelograms and cystograms will assess the dangers of reflux and the development
of hydronephrosis from chronic over distention of the bladder.
The paralysed neurogenic bowel will require specialised nursing procedures to ensure
adequate emptying and later with the introduction of appropriate medications and enemas or
suppositories.
The continuing monitoring of respiratory function is important since even a detailed clinical
examination may overlook the development of progressive pulmonary congestion and
consolidation. Diminishing vital capacity measurements will alert the clinician to the
development of these serious problems and necessitate intensifying chest physiotherapy and
posturing of the patient. Tracheostomy may be necessary, particularly if the measured vital
capacity remains below 600 mls.
Repeated neurological assessment is essential in the patient with spinal injuries where spinal
cord damage is susceptible and should be repeated daily during the first ten days. Any sudden
loss of motor power or sensation at or above the level of the lesion will alert the spinal surgeon
to the possibility of continuing displacement or instability of the injured spinal column. Further
compression may occur on the injured spinal cord with extradural haematoma which will require
urgent evacuation.
Always consider the additional complications of associated injuries. In a review of a series of
330 patients admitted to 2 major Spinal Units in Sydney, 36 patients had associated significant
abdominal injuries. Laparotomy was necessary in 50% of these patients with the indication for
exploration being:-

1. Position peritoneal lavage for blood

2. Free gas on plain x-ray
3. Persistence of unexplained abdominal tenderness (12 patients)

Always consider the possibility of associated intra-abdominal and intra-thoracic injuries,

particularly in thoracic-lumbar spinal lesions. Consider splenic rupture, liver laceration
diaphragmatic rupture, traumatic pancreatitis, intestinal injury, renal injury, haemothorax,
pneumothorax and haemopericardium. Retroperitoneal haemorrhage associated with fractures
and fracture dislocations of the lumbar spine frequently produce prolonged paralytic ileus
persisting for up to eighteen days. While the loss of neural pathways below the level of the
spinal cord injury results in diminished generalised rigidity and rebound tenderness, intact vagal
afference and spared sympathetic afference still allow localisation of pain and tenderness with a
modified guarding response in patients with significant spinal cord injury.

X-rays

Plain radiographs
are an appropriate initial investigation to identify vertebral alignment, fractures and the
possibility of ligamentous injury. Adequate views of the cervical spine must include the C1
vertebra down to the T1 vertebra. Spinal canal narrowing and congenital fusions/abnormalities
or old injuries may be identified. Careful flexion and extension views in the conscious patient will
assist in determining whether there is instability present by identifying shift in the vertebral
alignment and/or abnormal increase in the interspinous space. A unilateral cervical facet
dislocation may only be confirmed by oblique views - a single lateral view may not be sufficient.

Computerised Tomography (CT)

This investigation provides a useful additional assessment of the fracture or fracture dislocation
including the size and position of bony fragments and their encroachment on the spinal canal.
The spinal canal contents are only vaguely visualised and CT Myelography may be necessary
to adequately identify the presence of significant disc prolapse causing further compression on
the spinal cord.

The magnetic resonance imaging can identify disc protrusion with a clearer assessment of
spinal cord or nerve root compression.

Bone scans are not usually recommended in the ‘acute lesion’ but may be of assistance in
assessing progress or the possibility that an apparent injury to bone is old rather than new.

Myelography may be of assistance particularly in the lumbar spinal injury where the damaged
intervertebral disc may bulge significantly in the upright position rather than in the supine
position.
Treatment of the patient with spinal injuries

Consider:
• Soft tissue injuries which include damage to ligaments, muscles, capsules of joints and discs
as well as nerve root neuropraxia are present.
• Fracture and fracture dislocations and subluxations of the vertebrae of the spinal column -
which will require more detailed assessment and complicated treatment.

Soft tissue injuries

Treatment of the ‘soft tissue’ injury will require initially an appropriate period of rest with gradual
introduction of controlled pain free range of movements at the effected level.

The patient with suspected damage to the vertebral column and/or spinal cord will be assessed
by the spinal surgeon and frequently internal fixation, with or without traction, will be indicated.

Torn ligaments and muscles will require at least ten days for healing and a further ten days
where the scar tissue formed will ‘mature’ with return of come degree of elasticity. The
application of cold assists in the reduction of the initial oedema and associated pain from tissue
tension - improvement in blood flow should then be encouraged after eight hours with
applications of heat, gentle massage and vibration. Improving blood flow assists the healing
process and the subsequent period of tissue maturation.

Persistence of pain despite controlled mobilisation necessitated detailed review of the

underlying pathology and if necessary repeating the appropriate x-ray investigations.

Nerve root irritation can occur with narrowing of the intervertebral exit foramen or lateral disc
protrusion. Traction injury to the brachial plexus (stinger/burner) from falling in water skiing or in
contact sports such as football cause severe nerve root pain. Nerve root pain is identified by a
specific distribution of pain often subsequent loos of sensation in the appropriate dermatome
distribution and weakness in the corresponding myotome segments. Injury to peripheral nerves
nay lead to nerve ‘sheath’ repair.

Intervertebral disc lesions are most commonly seen in the lumbar spine, particularly at the L4/5
and L5/S1 levels. Occasionally cervical disc lesions are associated with cervical spinal cord (eg
injury from diving into shallow water). Thoracic disc lesions are rare and when they occur
produce unusual clinical syndromes (eg loss of posterior column with a severe functional
impairment due to loos of proprioception). The injured thoracic frequently calcifies.

A central disc protrusion or rupture may produce bilateral signs. The lateral disc protrusion
causes unilateral symptoms and signs. Apart from direct injury to the nerve roots, compressions
may also produce ischaemia in the spinal cord and cauda equina due to obstruction of the
normal blood flow. The anterior spinal artery lies superficially in the anterior spinal sulcus and is
particularly at risk when there is congenital narrowing of the spinal canal or cervical spondylosis
with osteophyte formation allowing direct pressure on the vulnerable anterior spinal artery.
Compressive injuries to the vertebral column can occur in weight lifting and in contact sport, eg
‘spear tackling’ in football. Spear Tackler’s Spine occurs when the head/neck is used to tackle
opponents. Axial loading occurs. There is a high risk of quadriplegia. XR5 show congenital
narrowing of the canal, reversal of cervical lordosis and torticollis (such athletes should not play
contact sport). Fractures of the pars interarticularis occur in cricket (eg fast bowlers) usually at
the L5 level as well as in gymnastics, running, golf and tennis. Ligament and muscle strain as
well as recurrent tearing of pre-existing scar tissue from earlier injuries can be associated with
the identified bony injuries.

Transient Quadriplegia is an acute transient neurological event of the cervical cord with
motor/sensory charges in both arms and legs. Lhermitte’s symptoms maybe present. Maybe
congenitally narrow canal, disc otaophyte compression of the cord.

Indications for urgent surgery to remove a damaged disc include canda Equina (Surgical
Emergency) (I) the development of progressive major neurological deficit, (ii) presence of a foot
drop and (iii) disturbance of bladder control. Where there is a diffuse distribution of limb pain
and less specific loss of sensation or motor power in the lower limbs then a non-operative
approach should be seriously considered.

A short period of immobilisation in order to control pain more appropriate than controlled
mobility in pain free range to encourage repair and improve muscle efficiency. Use analgesic
medication sparingly in order to asses the level and distribution of pain and provide a guide to
the patient’s response to treatment. Anti-inflammatory medication should be avoided
immediately following injury.

Hydrotherapy with gravity controlled or eliminated allows total body activity and will assist in
improving movements of the spinal column while not exposing the paraspinal soft tissue to
undue stress and strain during the healing period. Persisting radicular pain will necessitate
further clinical assessment and radiological studies to identify whether discectomy, with or
without fusion is necessary.

Rehabilitation programs to prepare the athlete for return to sport

Consider a period of two to three weeks as appropriate for adequate healing of torn paraspinal
ligaments, muscles and joint capsules before returning to the field of play. Damage to bones of
the vertebral column will necessitate a period of at least three months absence from sport
particularly when there is a degree of uncertainty to unexpected impact and degree of repetitive
effort. Patients with damage to the vertebra with or without involvement of the spinal cord
should not return to play competitive contact sport such as football even if there is only a single
level cervical fusion involved. The initial damage to produce bony disruption will inevitably
cause ligament and capsule damage and expose the patient to undue risk in the future. Where
there has been damage only to ligaments, muscle or disc and an appropriate period of
preparation without any recurrence of transient symptoms or signs has passed and on
radiological evidence of instability or canal stenosis is present, then the player should be
considered suitable to return to contact sport within three to six months of the initial injury.
Where there have been no neurological signs and only soft tissue injury to the spine then return
to playing contact sport can be considered at an earlier stage when the player continues to be
symptom free.

The other conditions which may be identified in the patient complaining of persistent symptoms
after spinal injury include: vertebral apophysitis; where mechanical pain is worse with activity
and relieved by rest and confirmed by radiological evidence; Scheuermann’s disease affecting
the spine at multiple levels in the thoracic spine can contribute to a thoracic kyphosis and a
compensatory lumbar lordosis; symptoms precipitated by rowing and butterfly swimming.
Schmorl’s nodes are associated with intravertebral disc herniation.

Treatment emphasises paraspinal muscle strengthening exercises with particular attention to

posture. Surgery is infrequently indicated. Congenital abnormality may be found with single or
multiple levels of fusion within the vertebrae of the spine (eg. Klippel-Feil anomaly which
involves multiple levels of the cervical spine, should not play contact sport as incidence of spinal
canal narrowing and risk of quadriplegia).

Players who have had treatment for spinal injuries and returning to their sport should be
encouraged to report any recurrence of symptoms relating to the previous injury or the
development of further symptoms relating to the previous injury or the development of further
symptoms not necessarily related to the spine. Sports men and women should report injury.

Prevention

Primary - avoiding the injury

• Prepare for the sport for which you have chosen to participate. Enjoy the play and being
involved. Be comfortable in the position for which you are chosen. In contact sport prepare with
specific exercising to protect vulnerable regions, for example the head and neck in
scrummaging and tackles in the various codes of football.
• Neck exercises will help to strengthen the paraspinal cervical muscles and assist with the
transmission of impact from the head to the shoulders without unduly exposing the small
cervical vertebra particularly in flexion and rotation.
• Prepare for play with an adequate period of warm up which includes repetitive movements
gradually developing into full range for each major joint in limbs and spine. Avoid overstretching
particularly in the cold weather where active muscle relaxation may be limited. Remember (a)
muscle not only actively contracts but actively relaxes, (b) muscles work as members of a group
of muscles, either as a ‘protagonist’ or ‘antagonist’ and (c) input is as important as output to
achieve efficient and balanced coordinated limb and trunk function.
• Play to the rules and report injury.
• Avoiding returning to the field of play while there is still pain suggesting continuing healing
and repair.
• Use protective equipment as necessary, for example (a) the approved full face helmet in
motor cycling and professional motor car racing to assist in the transmission of force from
impact which can occur to the head, to the shoulders often avoiding damage to the cervical
spine and spinal cord and (b) be appropriately restrained in a motor vehicle whether
participating in a competitive sporting event or travelling to or from your sporting event.

Secondary - avoiding further damage to spine or spinal cord after the initial injury

• Accurate diagnosis of the injured person at the site of the accident.

• Careful extrication and transportation from the scene of injury.
• Improved intensive care with control of fluid balance, support of respiration and avoidance of
inhalation of gastric contents.
• Differentiate between surgical shock with hypotension and tachycardia and the hypotension
in spinal cord injury where there is usually bradycardia in the patients with high level lesions
above T6.
• Identify associated complications of long bone fractures, intra-abdominal pathology,
particularly haemorrhage or intra-thoracic damage with pneumothorax and haemorthorax.
• Be prepared to review the patient’s (player’s) clinical condition.

Statistics1 (Table 3)

This study was initiated to see if the reduction of spinal cord injuries in motor vehicle accidents
has been paralleled by a corresponding reduction in sports related spinal cord injuries. The
Committee also sought to identify sports which resulted in admissions to spinal injuries units
and the associated frequencies of these admissions.

A retrospective review of log book records of acute admissions to the spinal units of Royal North
Shore Hospital and Prince Henry Hospital was performed. The count included those admissions
with and without neurological deficits. Excluded were admissions related to physical assault,
accidental falls, falls from buildings, trees or any other structure unless clearly related to a
sporting activity. Motor vehicle accidents, motor cycle and pedestrian accidents were also
excluded.

1 Incidence of spinal injuries/spinal cord injuries from: Sporting Injuries Committee (Ref: Wilson SF, Atkin PA, Engel

S, Lawson J, Rotem J, Rutkowski S).

 Table 3. Sports related spinal injuries
High Frequency (>10 Medium Frequency (>2 Low Frequency (<3 cases)

cases) and <10)

Diving 147 Trailbike/Pro- Water slide 2
Rugby Football 127 motorbike 9 Scuba Diving 2
Equestrian 52 Swimming 6 Motor Boat 2
Water Skiing 18 Para/hand Gliding 5 Rodeo 2
Bicycle 17 Soccer 5 Soft/Base Ball 2
Surfing 14 Fishing 5 Glider Plane 2
Snow Skiing 11 Gymnastics 5 Trampoline 2
Rock Climbing/ Wrestling 2
Abseiling 4 Cricket 1
   
Parachuting 4 Basketball 1
Bodyboard 4 Bushwalking 1
Touch Football 3 Australian Rules 1
Netball 1
Flying Fox 1, Swing 1
Judo 1
Golf 1, Hockey 1
Snowboard 1, Dune

Buggy 1
Slippery dip 1