Cervical Spine Injury

• The majority of C-spine injuries arise as a result of trauma; road traffic collisions (50 - 70%) and falls (6 - 10%) account for the majority
• C-spine injuries occur in 1.5 - 3% of all major polytrauma, although the incidence is lower in paediatric trauma (0.5%)
• The presence of any of the following factors places a patient at >5% chance of C-spine fracture:


Road traffic collision >35mph

Death at scene of road traffic collision

Fall >3m

C-spine pain, spasm, deformity or altered neurology

Significant closed head injury

Pelvic fracture or multiple extremity fractures



• 50% of C-spine injuries are potentially unstable
• There is a bimodal age distribution (15-33yrs and >65yrs) and a male preponderance

• Down's syndrome
• Degenerative disease
• Rheumatoid arthritis
• Ankylosing spondylitis
• Infectious or neoplastic processes
• Post-laminectomy kyphosis

• Airway considerations
• Immobilisation aims to prevent secondary injury via the classic trinity (semi-rigid collar, blocks and tape) or MILS

• Inspiration is governed by the diaphragm and phrenic nerve (C3 - 5), intercostal muscles/nerves (T1 - T11) and accessory muscles
• Expiration, although predominantly passive, is aided by the abdominal muscles (T6 - T12) particularly for forced expiration and coughing


• Respiratory complications are the commonest cause of post-spinal cord injury morbidity and mortality
• The risk of respiratory failure is associated with the level and completeness of injury
• C1 - 4: 40%
• C5 - 8: 23%
• Thoracic spine: 9.9%

• Spinal cord injury leads to immediate, massive sympathetic stimulation followed by reflex parasympathetic activity for 3 - 4 mins
• Loss of sympathetic outflow below the level of transection results in 'neurogenic shock':
• Loss of vasomotor tone and therefore vasodilation
• Severe hypotension due to loss of SVR as above
• ± bradycardia if level above T1 - 4 (loss of cardioaccelerator fibres) as a result of unopposed vagal tone


• Management should focus on identifying and treating other causes of shock e.g. major haemorrhage
• Fluid resuscitation and use of vasoactive drugs should be used
• Target MAP is controversial, but 90mmHg may be sought as SCPP = MAP - CSFP


• Autonomic dysreflexia is a late manifestation, occurring weeks-to-months post-injury
• Typically in those with injury above T10
• Paroxysmal hypertension and bradycardia to stimulus below the level of the injury

• 10% will have a second, non-contiguous vertebral column fracture
• Patients should have their whole spine imaged if concern about fracture in one area
• There is little evidence to support interventions aimed at improving spinal cord injury such as methylprednisolone or hypothermia

• Reduce risk of further cord injury through:
• Adequate glycaemic control
• Hydration
• Temperature control
• Electrolyte balance

• Plain radiography; lateral C-spine | A-P C-spine | PEG view
• Less commonly used due to poor sensitiviity and the use of cross-sectional imaging
• CT scan to check for bony injury
• MRI whole spine (gold standard)

• Clinical examination can exclude C-spine injury if there are no external signs of injury, no tenderness and a pain-free range of active movements
• However, the following preconditions are mandatory:
• Fully awake, alert and orientated
• Not under the influence of drugs or alcohol
• No head injury
• No neck pain
• No abnormal neurology
• No significant distracting injury

• Consider tracheostomy for patient comfort and cessation of sedation
• Lung protective ventilation (6 - 8ml/kg tidal volume)
• Chest physiotherapy to aid secretion clearance

• Maintain spinal cord perfusion pressure
• Use of vasopressors to target appropriate MAP, although target remains controversial

• Documentation of neurology on ASIA charts to aid prognostication
• Maintain spinal alignment and log rolling
• Referral to spinal surgical team for consideration of surgical fixation
• Pressure care to avoid pressure sores
• Full secondary survey

• Urinary catheter to monitor UO and prevent bladder overdistension, which can precipitate reflex bradycardia

• Stress ulcer prophylaxis
• Glycaemic control
• Bowel care with laxatives/enemas; ileus is common
• Early enteral nutrition

• VTE prophyaxlis with chemical and mechanical means

• Careful temperature control due to loss of cutaneous blood flow to self-regulate temperature
• Sodium management (SIADH common)
• Management of calcium; may have hypercalcaemia from osteoporotic reabsorption