Loss of sensation in a dermatome therefore acts as an indication of the level of SCI. The dermatomes of the trunk do overlap and are not as clearly defined as the dermatomes on the extremities (Marieb, 1992; Gondim, 2013).

The term myotome refers to a group of muscles that are innervated by the motor fibres of a single nerve root and is referred to as the motor equivalent of a dermatome. Myotome testing, using isometric muscle contraction, can assist with determination of the level of SCI.

Blood supply to the spinal cord is provided by the anterior spinal artery and two posterior spinal arteries. The anterior spinal artery supplies blood to two-thirds of the anterior aspects of the spinal cord. The posterior spinal arteries supply blood to most of the posterior aspects of the spinal cord. In addition to these arteries, segmental arteries that arise from various blood vessels in the cervical, thoracic and lumbar areas of the spine assist with blood supply to the spinal cord. The segmental arteries form anterior medullary and posterior medullary arteries. The great anterior medullary artery supplies blood to the lumbar enlargement of the spinal cord (Newton, 2008).

Generally, the most vulnerable areas for SCI through trauma are:

These will be discussed below.

The primary mechanism of injury refers to the initial mechanical trauma to the spinal cord. In cases of violence, the spinal cord may be severed (missile penetration), but more commonly neurological compromise following SCI is the result of ischaemic injury to the cord. Injury to the grey matter occurs within one hour after injury and is irreversible; injury to the white matter becomes irreversible 72 hours after injury (Dumont et al., 2001).

This may occur anywhere in the cervical spine. Most commonly, dislocation occurs between C1 and C2 and C5 and C7 as a result of the lack of a solid vertebral body at C1 (which makes that section of the spine more vulnerable), anatomical curvature of the cervical spine and relative mobility of the lower cervical spine, which attaches to the stiff thoracic spine (Middleditch and Oliver, 2005). Dislocations can also occur in the lower thoracic segments, T11 and T12, but are normally rare in the thoracic region due to stabilisation from the rib cage.

The degree of dislocation does not necessarily parallel the degree of damage to the spinal cord. The degree of injury is influenced by other factors, which include pre-existing degenerative changes in the vertebral spine, blood vessel damage, swelling and disruption of the anterior longitudinal ligament (Sekhon and Fehlings, 2001). Spinal dislocation can also damage nerve roots, intervertebral discs and blood vessels (Baydur et al., 2001).

Although uncommon, haematoma formation results from bleeding from the traumatic incident but can occur in patients with a coagulation defect following anticoagulation therapy (Binder et al., 2004). It may be acute or chronic, spontaneous, posttraumatic, iatrogenic, or associated with specific medications and disease states (Binder et al., 2004; Cha et al., 2011). Spinal epidural haematoma is mostly localised to the cervical or thoracic spine (Cha et al., 2011). If a patient with spinal epidural haematoma presents with abnormal neurological signs, prompt spinal decompression is performed surgically through evacuation of the haematoma (Cha et al., 2011).

This is a rare cause of acute spinal cord compression. It can occur with minor trauma and normally presents with what can be termed dramatic symptoms. Paraplegia is preceded by severe back pain in cases of acute spinal subdural haematoma and emergency surgery is often required; however, there are reports of cases in which spontaneous resolution has occurred (Oh et al., 2009).

This type of injury can result from blows to the head which then result in energy transmission along the brainstem and spinal cord, causing haemorrhages in the grey matter of the upper cervical region.

Severe injury may lead to laceration of the spinal cord. The most common causes of laceration of the spinal cord (partial or complete) include stab wounds, gunshot wounds and fracture dislocations. Surgical error may also lead to partial laceration of the cord. The continuity of the spinal cord is disturbed and there will be oedema and haemorrhage of meninges and cord followed by scarring of nervous tissue (Dumont et al., 2001).

This can occur as a complication of a fracture dislocation or whiplash injury. It produces a spindle-shaped haemorrhage within the substance of the spinal cord located in the grey matter (Pullarkat et al., 2000). It is usually followed by loss of function below the level of the lesion. As oedema subsides and the clot is slowly absorbed, there is a return of function in the posterior and lateral white columns (Rodesch et al., 2004). The patient usually has a flaccid paralysis in muscles supplied by the anterior horn cells at the level of the lesion. There is gradual development of spastic paralysis, with loss of pain and temperature sensation over segments affected by the clot. Pain and temperature sensation are preserved below the level of the haematomyelia and posterior column function is normal. Haematomyelia is managed surgically either through aggressive (urgent clot evacuation) or less aggressive approaches (plateau of neurologic deficit prior to clot removal), depending on the preference of the attending surgeon. Regardless of the management approach used, the underlying cause for the haematomyelia should be adequately addressed (Oskouian, 2012).

Neurogenic shock results from central nervous system injury such as cervical or high thoracic SCI. It causes hypotension and inadequate tissue perfusion due to sudden loss of sympathetic vasomotor function, which leads to severe disruption of the balance between vasodilator and vasoconstrictor functions of the arterioles and venules, hence decreased systemic and vascular resistance and pooling of blood in the peripheries (Denton and McKinlay, 2009). Bradycardia develops and the patient is unable to increase cardiac output by changes in heart rate (Denton and McKinlay, 2009). This shock state leads to ischaemia, which may contribute to secondary injury of the spinal cord (Dumont et al., 2001).

Partial or complete elimination of supraspinal sympathetic control of cardiovascular functions (e.g. coronary blood flow, cardiac contractility and heart rate) occur with moderate to severe SCI. Autonomic dysreflexia is a potentially life-threatening condition that may occur in patients with SCI above level T6 (Furlan, 2013; Stephenson, 2013), whereby an inciting stimulus (not necessarily noxious) below the level of the lesion causes an uninhibited sympathetic reflex and unbalanced physiological response. This sympathetic over-activity causes vasoconstriction and severe hypertension and is also known as hyperreflexia.

An inciting stimulus (originating most commonly from the bladder and bowel) is generated below the level of the lesion and impulses are sent via the spinal cord to the brain. These impulses are prevented from reaching the brain by the cord injury (Stephenson, 2013). However, the sympathetic nervous system is stimulated by the receptors located at the sympathetic ganglion at T5–T6 and a massive sympathetic response is generated, causing widespread vasoconstriction and peripheral arterial hypertension (Stephenson, 2013). The brain detects this sudden increased blood pressure (BP) through the baroreceptors located in the carotid artery and aortic arch; subsequently the parasympathetic nervous system is stimulated via the vagal nerve. Again the SCI (at T6 or above) prevents the inhibitory effect of the parasympathetic descending impulses below the lesion, which normally would cause peripheral vasodilation (Stephenson, 2013); however, there is a parasympathetic response above the level of the lesion that results in the patient presenting with flushed features. Through the vagal nerve, parasympathetic cardiac responses remain intact as the only supraspinal control of the heart. This leads to the development of heart rate irregularities and cardiac arrhythmias. The brain attempts to lower the peripheral arterial hypertension through slowing the heart rate using stimulation of the vagal nerve; however, this compensatory bradycardia is often unsuccessful and the patient’s hypertensive state continues (Stephenson, 2013). The reflex hypertension only resolves once the inciting stimulus is removed (Furlan, 2013; Stephenson, 2013).

The causes of SCI are similar between adults and children, with motor vehicle accidents and falls being the most common (Mortavazi et al., 2011; Clarke, 2012). Sports injuries are also a common cause of SCI in older children (Mortavazi et al., 2011). Non-accidental injuries and penetrating injuries (such as gunshot and stab wounds) have also been reported in small numbers (Mortavazi et al., 2011), along with other rare causes such as high cervical injuries related to skeletal dysplasias (e.g. achondroplasia), juvenile rheumatoid arthritis and Down’s syndrome or Trisomy 21 (Zidek and Srinivasan, 2003).

Distraction forces that stretch the spinal cord, such as flexion, extension, rotation or dislocation, may cause SCI in children. The mechanism of injury, however, is profoundly different between adults and children. Whereas the mechanism of SCI in adults is most commonly that of vertebral fracture, the most common mechanisms for SCI in children younger than 10 years are vertebral dislocations without fracture and SCI without radiological abnormality (SCIWORA). Children younger than eight years are significantly more likely to sustain SCIWORA than older children and adolescents (Pang and Wilberger, 1982; Clarke, 2012). Spinal cord injury without radiological abnormality presents clinically as an SCI, but plain x-ray shows normal alignment and no vertebral fracture; although magnetic resonance imaging (MRI) may show ligament rupture. It is believed that SCIWORA is caused by vertebral displacement followed by re-alignment with stretching, tearing or contusion of the spinal cord and is extremely rare in the adult population (Pang and Wilberger, 1982; Clarke, 2012).

The clinical effects of SCI depend on the extent and location of the damage to the spinal cord. The extent of the damage to the spinal cord may result in either a complete or incomplete lesion. The location of the SCI may result in either paraplegia or tetraplegia.

This type of lesion is characterised by loss of both the motor and sensory abilities of the patient below the neurological level, including the sacral segments S4 and S5 (Kirshblum et al., 2004).

There is preservation of either sensory and/or motor function below the neurological level with an incomplete lesion of the spinal cord. It is now globally agreed that the presence of any sensation in the lower sacral segments of S4–S5 means that the lesion is incomplete. This preservation is a good predictor of improved outcome, especially if there is pinprick sensation 72 hours to one week after injury (Kirshblum et al., 2004).

This syndrome occurs due to injury to the anterior two-thirds of the spinal cord. It often results from compression of the anterior spinal artery caused by flexion injuries, direct damage by bone fragments or disc compression. The resultant neurological deficits are usually due to damage of the corticospinal and spinothalamic tracts. The neurological manifestation includes muscle weakness, incomplete sensory loss, loss of sensitivity to pain and temperature below the level of the lesion with preservation of posterior column function (McKinley et al., 2007; Scivoletto and Di Donna, 2009).

This is the most common of the incomplete traumatic cervical cord syndromes. It is typically seen in older patients with cervical spondylosis and in certain ethnic groups who present with a tight cervical canal (Harrop et al., 2006). In these patients, hyperextension from minor trauma will result in spinal cord compression. This injury can cause ischaemia within the grey matter in the central portion of the cord, but the peripheral area of the cord remains relatively unaffected. The result is that the patient presents with significant loss of function in their upper limbs but relatively preserved function in their lower limbs. Young adults may develop central cord syndrome due to severe spinal column injury from high-energy trauma such as motor vehicle accidents, falls and diving accidents (Harrop et al., 2006). Low-energy traumatic injury that leads to acute central cervical disc herniation may also cause central cord compression (Harrop et al., 2006). The pathogenesis of central cord syndrome suggests the involvement of the lateral white matter columns and corticospinal tracts, which have a great influence on hand function. Patients present with flaccid paralysis of the upper limbs and relatively strong but spastic leg function. This is due to the fact that the cervical tracts are located more centrally within the cord. Sacral sensation and bowel and bladder function are usually partially spared (Harrop et al., 2006; McKinley et al., 2007).

Posterior cord syndrome is a very rare incomplete lesion of the spinal cord. This syndrome is seen in hyperextension injuries and causes contusion of the posterior spinal cord columns. The trauma to the posterior tracts results in loss of proprioception, deep touch and vibration sense. The patient presents with good motor function, pain and temperature sensation, but at times with profound loss of proprioception, which can make walking very difficult and results in an ataxic-type gait (McKinley et al., 2007).

Brown Sequard syndrome refers to injury in one hemi-section of the spinal cord. It usually occurs in stab or gunshot wound trauma. Contralaterally (opposite the side of the injury), there is a loss of sensitivity to pain, temperature and crude touch below the lesion from interruption of the spinothalamic tracts. The spinothalamic tracts cross or intersect at the level of the spinal cord; hence the hemi-section of the cord preserves pain, temperature and crude touch sensation on the side of the injury.

Ipsilaterally (the same side as the injury), interruption of the corticospinal tracts results in paralysis of voluntary movements below the level of the lesion, spasticity, positive Babinski sign and hyperreflexia. Interruption of the posterior columns results in loss of vibration, form perception, two-point discrimination and proprioception (McKinley et al., 2007; Scivoletto and Di Donna, 2009). Patients who present with more upper limb weakness than lower limb weakness are likely to be able to ambulate before discharge from the hospital (McKinley et al., 2007).

The spinal cord ends at the level of L1–L2 vertebrae. Compression of the conus medullaris usually results from a compression fracture of L1, which causes contusion and haemorrhage with damage to sacral segments of the cord. Injuries above the conus are predominantly upper motor neuron lesions, although anterior horn cells of lower motor neurons can be damaged at the site of the injury. Damage to the conus can involve both upper and lower motor neurons (McKinley et al., 2007; Lavy et al., 2009).

Simultaneous compression of several lumbar and sacral nerve roots in the lower lumbar region (L4–S1) lead to the development of cauda equina syndrome. Injuries involving the cauda equina are lower motor neuron injuries and will therefore result in flaccid paralysis. The patient also typically presents with neuromuscular and urogenital symptoms such as low back pain, sciatica (usually bilateral), saddle sensory disturbances, bladder and bowel dysfunction and sensory loss in the lower limbs that may differ in severity from one patient to the next (McKinley et al., 2007; Lavy et al., 2009).

The ASIA includes bilateral assessment of 28 dermatomes using pinprick and light touch sensation and manual muscle testing of 10 key muscles. Total motor and sensory scores are calculated based on these results and are used in combination with anal sphincter sensory and motor function to determine ASIA classification (Eng and Chan, 2013). It is important to note that, in SCI rehabilitation, short-term and long-term goals are established based upon the patient’s neurological level and degree of preserved function below the level of injury.

Respiratory complications encountered by patients in the acute stage after SCI include the overproduction of pulmonary secretions, bronchospasm, atelectasis, ventilator-associated pneumonia, pulmonary oedema or respiratory failure.

Patients with cervical SCI often suffer from bronchospasm, even in the absence of a history of asthma, due to autonomic nervous system dysfunction seen in the acute phase after injury. Resting airway tone is increased due to the interruption of sympathetic nervous system supply to the lungs in the presence of intact parasympathetic nervous system activity, as mentioned previously. Bronchospasm contributes to secretion retention and respiratory distress. Therefore the patient will be in need of bronchodilator therapy before physiotherapy treatment is initiated during the acute phase (Berlly and Shem, 2007; Vásquez et al., 2013).

Atelectasis may occur due to poor lung expansion as a result of weak or paralysed inspiratory muscles, retained bronchial secretions, weak cough effort, cephalad movement of abdominal content and decreased production of surfactant in lung segments that have lost volume. These changes can also lead to the development of pneumonia and respiratory failure (Berlly and Shem, 2007).

Respiratory failure has a direct influence on the patient’s mortality and therefore patients with cervical or thoracic SCI (especially above T6) should be closely monitored for signs of respiratory distress, which is a precursor to respiratory failure, in the acute phase after injury.

Similar to other patients who are intubated and mechanically ventilated, patients with SCI are at risk of developing ventilator-associated pneumonia (VAP) due to the presence of the endotracheal tube (ETT) and impaired mucociliary function and cough ability (Mietto et al., 2013). Ventilator-associated pneumonia is associated with increased mortality, hospital length of stay and health care cost (Mietto et al., 2013). Patients with SCI and weaning and extubation failure face a high risk for the development of VAP (Call et al., 2011).

In the later stages following SCI, patients develop changes in respiratory pattern, chest wall and lung compliance, lung capacity and lung volumes, and may also develop aspiration pneumonia or pulmonary thromboembolism.

Within one month following SCI, reductions in lung compliance is observed. The exact cause of reduced lung compliance in this early stage after injury is unknown. It is suggested that reductions in lung volumes due to respiratory muscle weakness and changes in the mechanical properties of the lung from alterations in surfactant production in areas of atelectasis may be contributing factors to the reduction in lung compliance (Brown et al., 2006; Harvey, 2008).

A reduction in chest wall compliance is observed in patients with tetraplegia due to the rigidity of the chest wall from muscle spasticity. Articular changes occur over time at the costosternal and costovertebral joints due to poor inspiratory muscle performance, which restricts the stretching of the chest wall to the level of total lung capacity (TLC) (Brown et al., 2006; Harvey, 2008).

Patients with complete cervical lesions below C2 experience decreases in VC of 20–50% of predicted values due to changes in lung compliance and impairments in inspiratory and expiratory muscle function (Brown et al., 2006; Berlly and Shem, 2007). This drastic reduction in VC leads to inefficient ventilation and poor cough ability. Gaseous exchange is affected by reductions in VC, TLC and VT as hypoventilation leads to carbon dioxide retention and hypoxaemia (Harvey, 2008). Reductions in mean values for FEV₁ and FVC to 40–50% of predicted values have also been reported (Brown et al., 2006). Over time, there seems to be an improvement in VC, FEV₁ and FVC values by approximately 10–15% as a result of improved diaphragmatic efficiency (Brown et al., 2006).

Changes in body positioning influence lung volume and lung capacity in patients with tetraplegia. When a person without SCI moves from a seated to supine position, VC reduces by approximately 7% and inspiratory capacity (IC) increases by approximately 55%. These changes in lung capacity are attributed to fluid shifts in and out of the thorax, resulting in a larger intrathoracic volume in the supine position (Baydur et al., 2001). In tetraplegia, movement into the supine position leads to increases in VC and IC, not only because of increased intrathoracic volume but also due to the effect of gravity on the abdominal contents (Baydur et al., 2001). This explains why patients with tetraplegia report less breathlessness and greater ability to cough without an abdominal binder in a supine position compared to seated position.

Patients with SCI have a three times higher risk for the development of pulmonary embolism and deep venous thrombosis than the general population from 72 hours following injury onwards (Miranda and Hassouna, 2000; Berlly and Shem, 2007). Pulmonary embolism develops in approximately 5% of patients with SCI and deep venous thrombosis in 15% of these patients (McKinney, 2013). Deep venous thrombosis develops as early as 72 hours following injury and the risk remains high until two weeks after SCI (McKinney, 2013).

Possible explanations offered for this increased incidence of thrombosis include metabolic changes in blood vessels due to the interruption of neurologic impulses and resultant paralysis, decreased venous distensibility and increased resistance to venous blood flow, sluggish vasomotor tone and, lastly, vascular adaptations to inactivity and muscle atrophy (Miranda and Hassouna, 2000; McKinney, 2013). Prophylactic therapy in the form of low molecular weight heparin and the use of intermittent pneumatic compression devices as precautionary methods are recommended for a minimum of eight weeks following SCI (Berlly and Shem, 2007). Regular screening of the patient for sudden onset of shortness of breath, difficulty breathing and hypoxia or limb pain, limb swelling, limb tenderness, limb discolouration and increased skin temperature is of vital importance.

Respiratory function improves spontaneously in patients with low level tetraplegia or paraplegia within the first year after injury, and only a small percentage of patients require further ventilatory support. This improvement is ascribed to small improvements in general motor function. Very little improvement is noted after the first year, and in some cases loss of function is even observed (Zimmer et al., 2007). Breathlessness is a symptom that many patients with chronic SCI report and seems to be more prominent in patients with tetraplegia than in those with paraplegia. Environmental factors, such as exposure to hot air, or lifestyle choices, e.g. exposure to direct or second-hand smoke and increased body mass index, may increase the sensation of breathlessness in tetraplegic patients (Stepp et al., 2008; Schilero et al., 2009). Increased body mass index leads to decreased TLC, FRC and RV. Patients with thoracic SCI between T1 and T6 have permanently altered lung mechanics, but have a greater chance of recovering from future lung infections than those with tetraplegia. In those with thoracic lesions below T6, lung mechanics are less altered and their ability to recover from future lung infections is greater.

Not all SCIs result in respiratory function abnormalities. Patients with central cord syndrome present with minimal to no respiratory system involvement if they are mobilised early during their admission. Posterior cord syndrome does not affect the respiratory system much and hence chest complications are rare. The effects of Brown Sequard syndrome on the chest are minimal, and if the patient does not develop other complications they are unlikely to develop respiratory complications. If a patient with compression of the conus medullaris and cauda equina is mobile, there should not be any complications concerning the respiratory system. Early mobilisation, in patients with stable SCI, or prophylatic chest physiotherapy should help prevent any respiratory system complications.

On admission to the emergency department, the patient with suspected acute SCI undergoes assessment through use of primary and secondary survey procedures; thereafter, definitive care is provided.