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Spinal injury

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Cervical fractures
Lateral cervical spine X-ray
Steroids in spinal injury

Updated November 2009 by Charles Gomersall

Predisposing factors Pathophysiology Clinical features
Investigations Management Complications


  • mean age 33 yrs
  • 75% males

Predisposing factors

  • degenerative disease of spine
  • spinal canal stenosis
  • ankylosing spondylitis
  • Down's syndrome
  • Klippel-Feil syndrome
  • Arnold-Chiari malformation
  • metastatic CA
  • osteomyelitis
  • rheumatoid arthritis


25% of spinal cord injuries occur after primary injury

Primary injury

Results from focal injuries (eg avulsion, contusion, laceration and intraparenchymal haemorrhage) and diffuse lesions (eg concussive and diffuse axonal injury). Further mechanical disruption can result from external compression or angulation and ischaemic damage from occlusion of arterial supply

Secondary injury

Results from:

  • Cellular hypoxia
  • Oligaemia
    • Immediately after an acute spinal cord injury major reduction in blood flow occurs at the level of the lesion. Becomes progressively worse over the first few hours if left untreated. Pathophysiology underlying this ischaemia is unclear but involves both systemic and local effects. Putative local mechanisms include vasospasm, endothelial swelling or damage, haemorrhage causing obstruction of small blood vessels, loss of autoregulation and impaired venous drainage.
    • Systemic hypotension can cause further decreases in spinal cord blood flow but induced hypertension may not necesssarily reverse the ischaemia. It may instead cause marked hyperaemia in adjacent parts of the spinal cord
    • Pattern of decreased perfusion within the spinal cord differs. Central grey matter, along with adjacent white matter is more severely affected than peripheral white matter.
      • White matter perfusion typically decreases within 5 minutes of injury and begins to return to normal within 15 mins. Thereafter remains near normal during first 24 hours
      • Central grey matter perfusion remains low for at least first 24 hours
  • Oedema due to an injury-induced neurochemical cascade

Exacerbated by hypotension

Site of injury

Most likely to occur at sites of maximum mobility

  • Adults C6
  • Children <8 yrs old C2

Clinical features

  • "level" of cord lesion is conventionally the most caudal location with normal motor and sensory function
  • spinal shock may mimic a complete cord lesion with total loss of motor and sensory function distal to injury. However if lesion is incomplete some function will return
  • 99% of patients with a complete lesion over 24 h will not show functional recovery
  • patients with partial lesion may regain substantial or even normal neurological function even though the initial neurological deficit may be severe
  • presence of bulbocavernous reflex (contraction of anal sphincter on pinching penile shaft) or anal-cutaneous reflex (contraction of anus in response to stroking of perianal skin) indicates sacral sparing and a more favourable prognosis

Central spinal cord syndrome

  • most frequently seen after spinal injury with acute hyperextension of neck in older patients who have varying degrees of congenital or acquired cervival spine stenosis due to spondylosis
  • motor deficit more marked in upper than lower limbs and most profound in intrinsic muscles of hands
  • extent of sensory deficit varies as does degree of bowel and bladder dysfunction
  • although spontaneous improvement in neurological function is the rule residual neurological deficit is common. Appears to be related to severity of initial injury

Anatomy of cervical cord

Effect of central cord lesion


  • ipsilateral weakness and dorsal column loss
  • contralateral pain and temperature deficit
  • usually due to penetrating injury

Brown-Sequard lesion

Spinal shock

  • direct force applied to the spinal cord results in a physiological block to conduction
  • areflexia, loss of sensation and flaccid paralysis below lesion
  • flaccid bladder with retention of urine, lax anal sphincter
  • CV complications include bradycardia and hypotension
  • diagnosis of exclusion

Anterior cord syndrome

Complete loss of motor below the lesion and loss of light touch sensation but preservation posterior column function.

Posterior cord syndrome

Rare condition. Results in loss of position sense

Cauda equina lesions

  • due to lumbar fracture
  • loss of bowel and bladder functions, with paresis of LMN type.
  • sensory loss may be patchy plus radicular pain exacerbated by straight leg raising.

Root loss

eg in C5/6 unilateral facet joint dislocation.



  • spinal cord injury without radiographic abnormality not uncommon in adults and frequent in children, Occurs in both thoracic and cervical spine
  • if you see one fracture look for another approximately 15% of patients have more than one fracture

Clearing the cervical spine

  • Indications for screening radiology. History of trauma and:
    • not fully conscious
    • drowsy or intoxicated
    • focal neurological deficit
    • midline cervical tenderness
    • other painful injury that may mask neck pain, particularly fractures
    • additional indications (not evidence based):
      • extremes of age
      • mechanism of injury highly suggestive of cervical spine injury
      • significant facial trauma
  • Cervical spine injury is rare in patients with penetrating injury to the brain, in the absence of a history suggestive of direct trauma to the spine
  • Screening radiology of choice is CT of cervial spine from occiput to T1 with sagittal and coronal reconstruction
    • sensitivity approximately 98% and considerably higher than plain radiography
    • may miss soft tissue injury and spinal cord injury in the absence of bony injury
  • Flexion and extension fluoroscopy no longer recommended to detect ligamentous injury
    • views are usually inadequate
    • pick-up rate very low
    • theoretical risk of exacerbating injury
  • Although CT may miss soft tissue and spinal cord injury and MRI is a sensitive method of picking up these injuries the risk/benefit ratio of obtaining MRI in patients with normal CT cervical spine and gross motor function of limbs is unclear
    • incidence of clinically significant injury much <1%
    • risk of transfer to MRI
    • ability of MRI to detect soft tissue injury may fall after 72 hours
  • Advantages of complete exclusion of cervical spine injury needs to be balanced against risk of prolonged use of cervical collar:
    • pressure sores
    • raised ICP
    • nosocomial pneumonia
EAST guidelines (2009 update)
  • remove cervical collars as soon as feasible after trauma
  • in patients with penetrating trauma to the brain, immobilization in a cervical collar is not necessary unless the trajectory suggests direct injury to the cervical spine
  • trauma patients who meet the following conditions do not need cervical spine imaging and can have their cervical collar removed:
    • awake, alert
    • no neurological deficit
    • no distracting injury
    • no neck pain or tenderness
    • full range of movement of the cervical spine
  • all other patients in whom cervical spine injury is suspected must have radiological evaluation:
    • primary screening radiology is CT from occiput to T1 with saggital and coronal reconstruction
    • plain X-rays add no additional information and should not be obtained
    • if CT cervical spine demonstrates injury obtain spine consult
    • if there is neurological deficit attributable to cervical spine injury obtain spine consult and MRI
    • for obtunded patient with negative CT and gross motor function of limbs:
      • flexion/extension films should not be performed
      • risk/benefit of obtaining MRI not clear. Options are to continue cervical collar immobilization until a clinical examination can be performed, remove collar on basis of CT and gross motor function alone or obtain MRI
      • if MRI is negative cervical collar can be safely removed


  • Anterior column = anterior 2/3 of the vertebral body, disc, and annulus, and the anterior longitudinal ligament)
  • Middle column = posterior 1/3 of the vertebral body, disc, annulus, and the posterior longitudinal ligament
  • Posterior column = pedicles, laminae, facets, capsule, and the interspinous and supraspinous ligament
  • injury is said to be stable if only one of the columns is involved.
  • damage to two or more columns or risking neurological injury (ie damage to the middle column) - unstable.

Classification of cervical spine fractures



Aim is to prevent extension of primary injury, to reduce secondary injury and to treat complications

  • Airway
    • Jaw thrust, chin lift and ventilation with bag and mask can cause displacement of unstable fractures but clinical significance of this is unknown
    • Safest method of intubation controversial and depends in part on skills of operator. 
    • If direct laryngoscopy is deemed necessary assistant should hold head to maintain in-line stabilization with minimal traction (vertebral distraction occurs experimentally and may cause further cord injury). Cricoid pressure causes subluxation of an unstable cervical spine but there is no evidence that this is harmful
    • Avoid cricothyroidotomy or tracheostomy if possible as their site compromises future anterior decompression
    • LMA and Combitube unproven in spinal injuries
  • Breathing
    • beware patient with C3,C4 or C5 lesion who initially has adequate respiratory effort who may progress to ventilatory failure
  • Circulation
    • Shock common but spinal shock is a diagnosis of exclusion
    • CVP/PAWP monitoring usually unnecessary
  • Immobilisation
    • Cervical spine should be immobilised in neutral position (ie position obtained when looking straight ahead)
    • Children <8 yrs may require back elevation with padding to achieve this position.
    • Optimal timing of decompression and surgical stabilization of fractures is controversial
      • Removal of damaging bone, disc and ligament fragments to decompress the swollen cord should limit secondary damage and improve outcome. However early surgery is controversial except when canal integrity is severely compromised. In animals early decompression in the first 6-8 h after injury enhances recovery. In humans early decompression has been defined differently as decompression in the first 72 h after injury. Not surprisingly decompression between 24 and 72 hours yields unsatisfactory results. Trials are needed to assess the effectiveness of surgery within 8 hours of injury.
  • Methylprednisolone
    • use in spinal cord injury controversial
    • acute non-penetrating spinal cord injury
      • <3 hours after injury: 30 mg/kg IV over 1hour followed by 5.4 mg/kg/h for 23 h
      • 3-8 hours: 30 mg/kg IV bolus followed by 5.4 mg/kg/h for 48 h
      • >8 hours: no steroid
    • acute penetrating spinal cord injury: steroid not indicated

  • Penetrating injuries associated with partial lesion: penetrating object should be removed in OT where spinal cord can be visualized


Respiratory dysfunction

  • degree depends on level of lesion. Lesions above C8 result in limited expiratory function. Lesions above C3 result in total loss of ventilatory function. Lesions at C3-5 result in similar levels of inspiratory dysfunction but higher lesions have a greater respiratory complication rate
  • leading cause of death, mainly due to pneumonia
  • as spinal shock resolves and the paralysis of the intercostal muscles becomes spastic the chest wall becomes rigid and no longer collapses with inspiration, resulting in an improvement in ventilatory (predominantly inspiratory) function.

  • In the initial phase decreased tidal volumes can be compensated for by an increase in respiratory rate. However the relatively high proportion of minute ventilation that is dead space ventilation means that this respiratory pattern is inefficient. In addition progressive atelectasis results in increasing shunting and oxygenation failure. The decision to intubate and ventilate the patient requires clinical judgement. On the one hand 1/3 of patients with a cervical spine injury will require intubation, many in the first 24 h. On the other hand intubation is associated with many adverse effects, particularly nosocomial pneumonia
  • Avoid suxamethonium if patient requires intubation between 3 days and 6 months as it may precipitate hyperkalaemia
  • Wean patient in upright position
    • In the upright position the paralysed abdominal muscles allow the abdominal contents to descend. This results in the diaphragm being in an inefficient starting position for contraction
    • In the supine position the abdominal contents push the diaphragm into a more efficient position for contraction

Haemodynamic instability

  • Spinal shock
    • NB Does not occur in low thoracic and lumbar spine lesions and is always a diagnosis of exclusion
    • Usually persist for weeks to months
    • As hypotension is due to a combination of peripheral vasodilatation and bradycardia the appropriate treatment is fluid resuscitation followed by an agent that has vasoconstrictor and chronotropic effects such as epinephrine. The appropriate target blood pressure, in terms of spinal perfusion, is not clear but at the very least mean arterial pressure should be raised to a level that is associated with adequate urine output and resolution of any other signs of inadequate tissue perfusion
  • Arrhythmias
    • Bradycardia most common
    • Supraventricular and ventricular tachycardias may occur
    • Most common in first 14 days after injury
    • More common and severe in more severely injured patients
  • ~50% with lesion above T7 demonstrate episodes of hypertension, bradycardia, hypertonicity and cutaneous changes (either pallor or vasodilatation) triggered by cutaneous, proprioceptive or visceral irritation (often an overdistended bladder or rectum). Due to a loss of inhibition from above. Sudden increase in BP stimulates a vagal response which can produce bradycardia, heart block and vasodilatation above level of injury. 
    • Management: good bladder and bowel care and alpha blockade when episode occurs

Visceral dysfunction

  • bladder dysfunction: urinary catheter necessary in acute phase but after 2-3 weeks intermittent catheterisation preferable
  • gastric stasis and ileus
  • constipation. Gentle faecal disimpaction may be necessary in early stages

Venous thromboembolism

  • high risk
    • twice the risk of trauma patients without a spinal fracture
    • spinal cord injury increases risk threefold
  • risk of bleeding with anticoagulation and mechanical devices are not sufficient prophylaxis on their own
  • studies have shown that risk of DVT in first 72 hours is quite low so a reasonable compromise seems to be to use a mechanical device alone in first 72 h and then subsequently to add low molecular weight heparin


  • pressure sores. Greatly increase cost and morbidity
  • poikilothermia in patients with lesion above T1
  • hyponatraemia common in first week


Because of the possibility of spinal shock it is difficult to assess prognosis prior to 72 hours. At 72h patients can be assessed using the ASIA impairment scale. Patients are classified into classes A to E depending on their motor and sensory function.

Bulbocavernosus reflex one of first reflexes to recover




Complete; no sensory or motor function preserved in S4-S5


Incomplete; sensory but not motor function preserved below neurological level and extending through S4-S5


Incomplete; motor function preserved below neurological level. Most key muscles have < grade 3 power


Incomplete: motor function preserved below neurological level. Most key muscles have > grade 3 power


Normal motor and sensory function

  • complete cord lesion at 72 h: 10-15% improve. Only 3% improve to attain class D

  • class B at 72 h: 54% will improve to a lesser degree of weakness

  • class C and D at 72 h: 86% will achieve useful motor function below the level of the lesion

Further reading

P. A. Ball. Critical care of spinal cord injury. Spine 26 (24 Suppl):S27-S30, 2001.

M. G. Fehlings. Editorial: recommendations regarding the use of methylprednisolone in acute spinal cord injury. Spine 26 (24 Suppl):S56-S57, 2001

M. G. Fehlings, L. H. Sekhon, and C. Tator. The role and timing of decompression in acute spinal cord injury: what do we know? What should we do? Spine 26 (24 Suppl):S101-S110, 2001.

© Charles Gomersall and Ross Calcroft September 1999, Charles Gomersall December 2002, March 2003, June 2003

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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