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Related theory

The spinal canal is a rigid, contained cavity. Therefore, any expanding disease process will eventually cause spinal cord and/or nerve root compression. This results in impaired function or loss of function, causing reduced movement or sensation. The spinal cord does not have to be severed in order for a loss of functioning to occur (Lindsay et al. [61]).

Following damage to the spinal cord, ‘spinal shock’ may occur. This is the temporary suspension of spinal cord activity or loss of reflexes caused by oedema at and below the level of the injury. A complex series of physiological and biochemical reactions occur due to resulting oedema and vascular damage. Circulation of blood and oxygen is disrupted, and ischaemic tissue necrosis follows with immediate cessation of conductivity within the spinal cord neurones. Following 2–6 weeks there will be a return of reflex activity, often resulting in spasticity (Bonner and Smith [12]).

The causes of SCC and SCI are characterized as ‘traumatic’ or ‘non‐traumatic’.

Traumatic spinal cord injury

It is estimated that 1000–1200 people sustain traumatic SCI in the UK each year (RNOH [109]). Traumatic injuries are caused by an impact that fractures, dislocates or compresses one or more of the vertebrae. Common causes of trauma include falls, road traffic collisions, sporting injuries, gunshots and stabbing.

Non‐traumatic spinal cord injury

Non‐traumatic spinal cord injuries form a heterogeneous group of diseases, with the leading causes being tumours and degenerative diseases of the spinal column. Due to the heterogeneity of causes, it is difficult to know the numbers of non‐traumatic SCI cases within the UK. They can be split into the following types:

Vascular: involves damage to the blood vessels or supply. This can include haemorrhage, hypotension or embolism (SIA [117]).
Inflammatory and infections: involves conditions such as tuberculosis, abscess, transverse myelitis and autoimmune disorders (SIA [117]).
Degenerative conditions: involves degeneration of the vertebrae surrounding the spinal cord leading to compression. Includes osteoarthritis, osteoporosis and degenerative disc disease (SIA [117]).
Neoplastic: either from a primary spinal tumour or from metastatic disease. Around 5% of all cancers can lead to SCC (SIA [117]).
- Primary tumours: classified into two broad categories: intradural intramedullary tumours and intradural extramedullary tumours. Intramedullary tumours are composed predominantly of gliomas (astrocytomas and ependymomas). Extramedullary tumours are either peripheral nerve sheath tumours or meningiomas) (Louis et al. [62]).
- Metastatic spinal cord compression (MSCC): an oncological emergency caused by direct pressure and/or induction of vertebral collapse or instability by metastatic spread, leading to a risk of (or actual) neurological disability (GAIN [38]).

Classification

SCC and SCI are classified in general terms as being neurologically ‘complete’ or ‘incomplete’ based upon the sacral sparing definition. Sacral sparing refers to the presence of sensory and motor function in the most caudal sacral segments (i.e. preservation of light touch and/or pin prick at S4–S5 dermatome and voluntary anal sphincter contraction) (Kirshblum et al. [58]).

Complete spinal cord injury: when the cord ‘loses all descending neuronal control below the level of the lesion’ (Lundy‐Ekman [67], p.373). There is the absence of sacral sparing.
Incomplete spinal cord injury: when ‘the function of some ascending and/or descending fibres is preserved within the spinal cord’ (Lundy‐Ekman [67], p.373). There is the presence of sacral sparing.

On initial presentation, imaging will confirm both the presence of SCI and whether the spine is ‘stable’ or ‘unstable’:

Stable spine: this is where spinal alignment is intact, with no further risk of progression of neurological symptoms as the spine is still able to maintain and distribute weight appropriately.
Unstable spine: this is where the spinal fractures or lesions pose a risk of potential irreversible neurological symptoms due to movement of the fracture site.

Clinical presentation

The clinical presentations of SCI and SCC are dependent on the location within the spinal cord or cauda equina and the degree and duration of compression. In SCC, early diagnosis is crucial in order to at best prevent and otherwise minimize irreversible neurological damage.

Common symptoms of SCI include:

back pain and/or radicular pain
nerve root symptoms resulting in pain or loss of sensation within a dermatome
respiratory compromise
limb weakness
sensory loss
bladder and/or bowel dysfunction
sexual dysfunction.

The level and extent of the injury will determine the functional impairment. Lesions within the thoracic and lumbar region may lead to paraplegia, and cervical or upper thoracic lesions may lead to quadriplegia/tetraplegia (Table 7.9) (Kirshblum et al. [58]).

Table 7.9 Levels of spinal injury with resulting function loss

Site of spine	Level	Affected area of body
Cervical	C4 (tetraplegia)
Cervical	C6 (tetraplegia)
Thoracic	T6 (paraplegia)
Lumbar	L1 (paraplegia)

It is important to consider respiratory function in patients with lesions of T12 and above due to the involvement of respiratory muscles. Patients with significant respiratory muscle involvement will require assistance with coughing and considerations of positioning to prevent respiratory compromise. Refer to the physiotherapist to assist with respiratory management (Bonner and Smith [12]).

If patients are assessed to have reduced bowel function, they will require a bowel management regime to prevent complications such as constipation, faecal incontinence and autonomic dysreflexia (see the ‘Complications’ section below).