The vertebral column forms the key protective component of the spinal cord. Its integrity is made up of the bone and ligamentous connections. It is common to visualise the column as 3 separate column complexes:
Anterior - anterior half of the vertebral bodies and anterior longitudinal ligament
Middle - posterior half of the vertebral bodies and posterior longitudinal ligament
Posterior - ligamentum flavum, interspinous and supraspinous ligaments.
Disruption of 2 out of 3 of these complexes results in an unstable spinal injury. The posterior complex has the largest impact on stabilising the vertebral column. The facet joints throughout the vertebral column and the ribs in the thoracic region provide additional stability.
The spinal canal contains a number of contents as well as the spinal cord (epidural vessels, fat) and the size of this space varies along the length of the column. As such, vertebral disruption is more likely to result in cord injury at sites where this space is minimal (mid thoracic region) compared to where there is more space (high cervical).
The anatomy of the cord itself is important to know to understand the impact of incomplete spinal injuries. The cord can be sees as composing of ascending and descending tracts.
Ascending tracts transmit sensory information to the brain:
Posterior column - vibration, fine touch, proprioception
Spinothalamic - pain, temperature, coarse touch.
The spinothalamic tracts have an anterior and lateral division. They decussate shortly after arrival in the spinal cord, around a similar level). The posterior column fibres don’t decussate at the cord level and so provide sensory information for the ipsilateral side.
Descending tracts transmit information from the brain to the body, perhaps the most important of which are motor signals.
Lateral corticospinal tracts - limb control
Medial corticospinal tracts - truncal innervation
The lateral corticospinal tracts decussate at the pyramid and then run down the side of the cord on which they will provide motor control. The medial tracts have a less well defined decussation, with a more bilateral influence on the trunk.
The arterial supply can be relevant in injury. Running along the length of the spinal cord is one anterior spinal artery, running in the midline, and two posterior spinal artery. The anterior artery supplies the anterior ⅔ of the cord, with the posterior ⅓ (primarily the posterior columns) being supplied by the posterior arteries. This can manifest itself clinically as an anterior cord syndrome when this supply is disrupted. These arise from the vertebral and posterior inferior cerebellar arteries superiorly, and there is additional input from multilevel radicular arteries, with the artery of Adamkiewicz being the biggest.
Injury to the vertebral column is at the highest risk at the locations where there is a transition in the structure of the column. These sites are: craniocervical, cervicothoracic, thoracolumbar, and lumbosacral. As noted above, disruption of 2 or more of the ‘column complexes’ of the vertebral column will result in bony instability.
The primary injury can involve direct cord compression and traction, and from haemorrhage. This is most commonly from the subluxation of bony structures, with direct mechanical effects on the cord, but can also occur from excessive flexion movement e.g hyperextension. Vertebral fractures can also result in bone fragments being displaced into the canal, causing direct cord injury. This is particularly the case with burst fractures, which may also injure the anterior spinal artery supply as well as direct cord damage. Cord injury is more commonly related to a fracture in the thoracic and lumbar regions, whilst the degree of flexibility of the cervical spine can result in traumatic cord injury without vertebral fractures occurring.
The subsequent response to the primary injury can lead to a secondary injury, and this is often the focus of protective measures. The tissue trauma and associated haemorrhage trigger an inflammatory response which leads to local oedema, vasomotor impairment, free radical generation, and electrolyte changes. This can spread caudally and cranially from the site of the injury and lead to cord ischaemia from the impairment of blood flow, and may manifest of a worsening of the neurological level following the initial injury. This can be especially important at critical sites e.g. C4. The systemic effects of the spinal cord injury e.g. neurogenic shock, may also contribute to these local changes, and these form a lot of the focus of subsequent management.
Consequences of Spinal Trauma
This is heavily dependent on: •The level of the injury •The completeness of the cord injury
The exact anatomical level of a fracture may not necessarily correlate with the traditionally described dermatomes or myotomes. Similarly, the dermatome and myotome level do not necessarily marry up. There are some specific spinal cord syndromes that may result from trauma, although some may be more commonly seen in other pathologies: •Central cord syndrome •Brown-Sequard syndrome •Anterior cord syndrome
Cardiovascular consequences often relate to the impact of the injury on the autonomic nervous system (ANS). As you’ll probably know, the sympathetic ANS arises from the thoracolumbar spinal cord. As such, spinal injuries at lumbar level and above may have an impact on this ANS function. At all levels this will include some vasomotor activity, but the cardioaccelerator fibres arise from the high thoracic level, so injury above this level can result in impact on regulation of heart rate too. The fact that parasympathetic ANS function comes primarily from the vagus nerve (the craniosacral ANS), means that the patient can then experience unopposed vagal neural tone.
Neurogenic Shock This refers to the cardiovascular compromise arising from such a spinal injury. It tends to occur when the neurological injury level is above T6. This is due to the ANS changes described above, resulting in vasodilation, venous pooling, and impaired heart rate responsiveness (often bradycardia in high injuries).
In these patients, preservation of stroke volume (CO = HR x SV) is essential, and thus ensuring adequate ‘filling’ the essential first step in resuscitation. Hypovolaemia is poorly tolerated. Similarly, induction of anaesthesia and instigation of positive pressure ventilation can have profound detrimental effects on CVS stability. A target mean arterial pressure of 80-85 mmHg is recommended, as this is felt to optimise perfusion of the damaged spinal cord, and thus minimise secondary ischaemic injury. If volume replacement is insufficient to achieve this, then instigation of vasopressors may be needed. Alpha adrenoceptor agonist are generally preferred (noradrenaline, phenylephrine) although there can be some resulting bradycardia. Simple anticholinergic agents (glycopyrrolate, atropine) are usually enough to manage this bradycardia, but other chronotropic agents may be needed (e.g. adrenaline instead of NA).
Autonomic Dysreflexia This is a good review of the condition: https://www.youtube.com/watch?v=g-ppZyO_Kqs This is a consequence of the disruption of the ANS pathways that can occur in patients with a spinal cord injury above the level of T7. A painful trigger below this level results in a reflex activation of sympathetic pathways, without susceptibility to descending inhibitory signals. This results in vasoconstriction and a rise in blood pressure, sometimes to severely high levels. Parts of the body with an intact ANS attempt to compensate with vasodilation and bradycardia. Symptoms can include headache, anxiety and symptoms above the level of injury of flushing and sweating. Signs of sympathetic activity may be present below the injury level. The triggers can include: bladder distension, consolidation, somatic nociception. Management involved removing the trigger and, if needed, short acting medications to lower the BP.
Spinal cord injury can have a significant impact on respiratory function, again largely depending on the level of the injury. Most importantly to note is that the phrenic nerve (providing the innervation of the diaphragm) originates from the spinal cord at the level of C3-5. Bearing this in mind, there can be considered to be 3 outcomes of spinal cord injury: 1.Injury above C3 2.Injury around C3-5 level 3.Injury below C5 Significant spinal cord injury above C3 will result in complete respiratory failure, apnoea and rapid death unless artificial ventilation is instigated, as the phrenic nerve will fail. The patient will remain dependent on a ventilator, although there is some role for an artificial diaphragmatic simulator. Spinal cord injuries at the level of C3-5 will have varying degrees of diaphragmatic impairment. Ventilatory support is very likely to be needed acutely, but that can be a good degree of recovery of independent ventilatory function, depending on other comorbidity.
Patients with injuries about T12 will often have some impairment of their cough effort. Regular physiotherapy input to aid with sputum clearance is important
Spinal shock is a term applied to describe the initial clinical picture following spinal cord injury (it has no relationship to the CVS term shock). There is loss of the reflex arc, with a resulting flaccid areflexia. There is then a stepwise change with the return of reflexes (usually day 1-3) and a subsequent development of hyperreflexia and spasticity. There may also be autonomic hyperreflexia (see above).
Some important spinal syndromes are also well described.
Anterior spinal artery syndrome
Loss of the anterior arterial supply results in loss of the anterior ⅔ of the cord and the relevant spinal tracts.
The clinical syndrome is therefore sparing of the posterior columns (proprioception, fine touch, vibration) but loss of the rest (motor, pain).
Posterior cord syndrome
Loss of the posterior artery supply results in the failure of the posterior column and subsequent function (proprioception, fine touch, vibration)
This is rare
A result of a lateral cord injury, with loss of tracts that run on that side
The result is a loss of ipsilateral loss of motor power and posterior column sensation (proprioception, fine touch, vibration), but contralateral spinothalamic tract loss (pain, temp).
Central cord syndrome
Damage to the central gray matter of the cord, usually from bleeding, infarction or oedema.
Most commonly occurs in the cervical cord, where it affects the more medial tracts (generally providing upper limbs) more.
The clinical picture here is mixed upper and lower motor signs and spinothalamic tract sensory loss in the upper limbs, with upper motor neuron signs in the lower limbs, potentially with sacral sparing.
4. Gastrointestinal Disruption of the neurological supply to the GI tract can also lead to some impaired functioning:
Increased PUD risk
Anal tone dysfunction
Management of these problems forms a key part of the chronic management of spinal cord injuries. Other interventions e.g. tracheostomy, may further impact on this.
This will usually be part of a trauma team using an appropriate structured approach to assessing and managing the patient. Whilst this will often be simultaneously undertaken, considering the ABCDE features is a useful structure. Meticulous documentation, especially of neurological findings, is essential as the initial information can be vital later on in the patient’s journey.
Airway/Breathing There may be an urgent need for IMV in patients with high spinal injuries. Features of concern include:
Poor respiratory effort
Depressed conscious level
Impaired gas exchange (including other injuries)
If instigation of IMV is required, important factors to consider include:
Manual inline stabilisation (MILS)
Best possible neurological assessment prior to induction (guided by urgency)
Be alert to potential difficult airway management
Unopposed vagal tone in high spinal injuries can result in bradycardia with airway manipulation, which may warrant atropine premedication. Similarly, the loss of normal sympathetic tone may have a notable negative impact on the CVS stability during induction of anaesthesia.
Circulation Assess for signs of CVS instability. Patients may display signs of neurogenic shock. Haemorrhage should always be strongly considered as a cause of CVS compromise initially in a polytrauma patient. As noted above, suitable volume resuscitation is essential even in cases of neurogenic shock.
Disability A careful neurological examination must be undertaken. This may be limited by instability but key information about neurological compromise should try to be obtained. This involves a top-to-toe assessment of neurological function assessing for:
DRE - perianal sensation and tone
Abnormal features e.g. priapism
Exposure The patient must be kept warm. A careful examination for other injuries must be undertaken when stability has been achieved. When particularly considering spinal trauma, this should include a log roll to exam the patient’s back. Features to assess for include:
American Spinal Injury Association Classification (ASIA) This is a standardised way of assessing the neurological status of someone who has sustained a spinal injury. It is of graded severity from A (complete) to E (normal). The neurological level is defined as the most caudal sensory level with intact sensation and antigravity (MRC 3 or higher) motor strength (assuming there is no rostral deficit).
No motor or sensory function is preserved in the sacral segments
Sensory but no motor function is preserved below the neurological level (including the sacral segments)
Motor function is preserved below the neurological level. More than half the key muscles have a motor power of less than 3
Motor function is preserved below the neurological level. At least half of key muscles have a motor power of 3 or more.
Motor and sensory function are normal
This will be in addition to the management of any other injuries that have occurred with the presenting trauma. The goals of management are centred around preserving cord function and minimising the development of subsequent complications. Much of this will be commenced simultaneously with the initial assessment. Key factors include:
Optimisation of physiology
The concept of spinal immobilisation is to reduce the risk of further spinal cord injury. In the case of loss of vertebral column stability, the spinal cord can be injured by bony movement. The key is to maintain normal spinal alignment at all times, of which patient movement is the clear risk periods. Components of this include:
Cervical collar and blocks
The theory of immobilisation is challenged by the idea that the forces imparted at the time of bony injury are far in excess of any forces that are subsequently imparted on movement. In addition, awake patients are described as naturally assuming the most comfortable position to protect the injury, with muscle spasm aiding this.
The cervical spine protection is classically described as having 3 key components:
Cervical Collar The role of the cervical collar in cervical spine protection is (theoretically) to prevent the movement of any unstable vertebral fracture resulting in cervical spinal cord injury. It is described as achieving this alongside the immobilising effect of head blocks and straps, but there is a fair degree of controversy around this. The controversy stems from the coexisting risk of harm from them, and significant absence of evidence of benefit. Harms include: increased difficulty of airway management, discomfort (which may actually increase the risk of neck movement), pressure sores, increased aspiration risk, and increases intracranial pressure.
Log Rolling Log rolling is the process for rolling the patient to keep all aspects of the vertebral column aligned. It should be undertaken until the spine is cleared. The spinal board is a device used for extracting and transporting patients. It can be useful for aiding easy transport, but the hard nature of it puts patients at risk of pressure injury. As such, on arrival to A&E patients should be quickly taken off them.
As noted, a major focus of the management is to avoid a secondary injury. Much of the focus here is around maintaining normal physiological values, especially as the effects of the spinal injury can impact on many of these. Normal physiological parameters essentially involves:
Maintenance of oxygenation
Normal respiratory status is important as hypoxia and CO2 related blood flow changes may impart a secondary cord injury. This is especially important in the early assessment of high spinal injuries, when ventilation can be severely affected. Patients are best ventilated in the flat supine position if they have a high spinal cord injury. This is because the abdominal contents are an important contributor to diaphragm movement, and they help push the diaphragm more caudally. This allows a better starting position for the diaphragm to move from and thus to improve ventilation. Higher tidal volumes and the use of ‘sigh breaths’ may be considered to reduce atelectasis.
There is a theoretical benefit to driving an appropriately high perfusion pressure to ensure that the injured cord is receiving an appropriate blood flow. Weak historical evidence has led to the suggestion of a MAP of >85mmHg for 5-7 days, but the risks of vasopressor use do need to be taken into account for this, along with other clinical factors e.g patient’s age.
There is some evidence of benefit from the administration of steroids in reducing the injury level (when high dose methylprednisolone used). However, the adverse infective complications (including mortality impact) have provided limitations, and their use is not currently recommended.
Surgical intervention will generally be of the aim to decompress the spinal cord, and stabilise the vertebral column. Urgent specialist surgical review is essential, especially in cases of deteriorating neurology.
Meticulous attention to the important components of good critical care, as these patients are at significant risk of complications.
Pressure ulcer prevention
The use of an Edgerton turning bed can help with position changes to relieve pressure without the need for rolling.
An effective bowel management regime is essential to reduce the risk of complications of a neurogenic bowel. Specific regimes are often implemented and components may include:
Instigation of enteral feeding once any ileus resolves
Regular laxative regime
Long term catheters may be needed.
Epidemiology & Outcome
The incidence of spinal cord injury is fairly low, at around 13/1,000,000 annually in the UK. Approximately 14% of vertebral column injuries result in damage to the cord. Of these, around 50% are incomplete. Patients are often young, male and otherwise well, as is a common feature of major traumatic injuries. Road traffic injuries form a significant part of this, with a smaller number from sports injuries. There is also a fairly large number of older patients with injuries arising from a ground level fall on the background of existing degenerative spinal disease. Penetrating injury is a rare cause of traumatic injury, although may be related to gun and knife attack in locations where these are more prevalent.
Risk factors for a poor outcome include:
Higher level of injury
These factors contribute significantly to the prognosis, which can thus be highly variable. Outside of the acute phase, this is often related to chronic complications.
The long term consequences of spinal cord trauma can be significant and long-term/permanent. This includes significant psychological and social challenges. Ongoing specialist care for severe injuries is needed.