Spinal Injuries And Sport

Chapte r7   - Injuries ­  Spine      

   

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Anatomy of the spinal cord

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Injury

Damage to the spinal vertebral column ○

Bones

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Damage to specific vertebrae

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Damage to muscles, ligaments and tendons

Assessing the problem ○

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Biomechanics

Analysis of the patient with a spinal injury 

When the patient is unconscious

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When the patient is conscious

Clinical analysis of sensory and motor disturbance ○

In ‘First Aid’

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Early treatment and investigations

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X-rays 

Plain radiographs

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Computerised Tomography (CT)

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Soft tissue injuries

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Prevention ○

Primary - avoiding the injury

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

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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 towthirds 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 thoracolumbar 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 

(Less than 50%

uncommon. 

loss of vertebral

Stabilisation and fusion 

height)

if associated posterior 

(wedge)

 

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 Burst Axial compression Controversial

deficit common

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 bulbocavernosus 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

cases) Diving 147 Rugby Football 127 Equestrian 52 Water Skiing 18 Bicycle 17 Surfing 14 Snow Skiing 11

and <10) Trailbike/Promotorbike 9 Swimming 6 Para/hand Gliding 5 Soccer 5 Fishing 5 Gymnastics 5 Rock Climbing/ Abseiling 4 Parachuting 4 Bodyboard 4 Touch Football 3

 

Low Frequency (<3 cases) Water slide 2 Scuba Diving 2 Motor Boat 2 Rodeo 2 Soft/Base Ball 2 Glider Plane 2 Trampoline 2 Wrestling 2 Cricket 1 Basketball 1 Bushwalking 1 Australian Rules 1 Netball 1 Flying Fox 1, Swing 1 Judo 1 Golf 1, Hockey 1 Snowboard 1, Dune Buggy 1 Slippery dip 1