Traumatic Spinal Cord Injury

Question 1

Spinal Cord Injury definition

Answer 1

• Spinal cord injury = damage to the spinal cord that temporarily or permanently causes changes in its function.
• SCI can be either traumatic or non-traumatic.

Question 2

Traumatic SCI definition

Answer 2

Traumatic SCI is due to external physical impact, e.g. car accident,
sports-related injury, violence) resulting in acute damage

Question 3

Non-traumatic SCI

Answer 3

Non-traumatic SCI occurs when an acute or chronic disease process, such as tumour, infection or degenerative disc disease generates the primary injury.

Question 4

Biological overview of consequences to SCI

Answer 4

• When injured in trauma, cells are damaged and can trigger a complex secondary injury cascade which cyclically results in the death of neurons and glial cells, ischaemia and inflammation.
• This cascade is followed by changes in organization and structural architecture of the SC, including formation of glial scars and cystic cavities.
• There may also be poor endogenous remyelination and axonal regrowth, which means that the SC has poor intrinsic potential for recovery; SCI is likely to cause permanent neurological deficits.

Question 5

Impact on society and patients

Answer 5

• In addition to the challenges of the injury sustains there will be impacts that are social, vocational and physical consequences for patients and their families
• A loss of independence and increased lifelong mortality rates are hallmarks of SCI
• Direct costs for patient care with SCI are estimated to be US$1.1-4.6 million per patient over their lifetime
• The role of prevention cannot be underestimated!

Question 6

Epidemiology

Answer 6

Traumatic SCI occurs more commonly in males (79.8%) than in females (20.2%).

The age profile of such patients have bimodal distribution, with one peak at 15- 29 years and a second smaller but growing peak at >50 years.

Traffic accidents are the primary cause of all traumatic SCIs in North America (38% between 2010 and 2014), with falls being second (31%) and sports injuries third (10-17%).

Younger individuals are more prone to high energy impacts, while older patients are more low-energy impacts, such as falls.

In the general population, traumatic SCI occurs most often in the cervical spine (~60%), then thoracic (32%) and lumbosacral (9%).

Question 7

Mortality

Answer 7

• Despite modern medical care, patients with traumatic SCI have a significantly reduced lifespan.
• The risk of mortality increases with more-severe injuries, higher injury levels (that is, cervical SCIs are associated with higher mortality than lumbar SCIs), increasing patient age, the presence of multisystem trauma and higher-energy injury mechanisms.
• For example, the life expectancy after SCI for an individual 40 years of age is lowered to 23 years after cervical level 5 (C5)-C8 injury, 20 years after C1–C4 injury and 8.5 years if they are ventilator dependent.

Question 8

Pathology of Traumatic SCI: acute phase

Answer 8

a | The initial mechanical trauma to the spinal cord
initiates a secondary injury cascade that is characterized in the acute phase (that is, 0–48 hours after injury) by oedema,
haemorrhage, ischaemia, inflammatory cell infiltration,
the release of cytotoxic products and cell death. This secondary injury leads to necrosis and/or apoptosis
of neurons and glial cells, such as oligodendrocytes, which can lead to demyelination and the loss of neural circuits.

Question 9

Pathology of Traumatic SCI: subacute phase

Answer 9

b | In the subacute phase (2–4 days after injury), further ischaemia occurs owing to ongoing oedema, vessel thrombosis and vasospasm. Persistent inflammatory cell infiltration causes further cell death, and cystic microcavities form, as cells and the extracellular architecture of the cord are damaged. In addition, astrocytes proliferate and deposit extracellular matrix molecules into the perilesional area.

Question 10

Pathology of Traumatic SCI: intermediate and chronic phases

Answer 10

c | In the intermediate and chronic phases (2 weeks to 6 months), axons continue to degenerate and the astroglial scar matures to become a potent inhibitor of regeneration. Cystic cavities coalesce to further restrict axonal regrowth and cell migration.

Question 11

Adult CNS myelin

Answer 11

Even if regenerative efforts are able to overcome spinal cord lesions, properties of the adult mammalian CNS can still limit nerve regrowth.
For example, molecules present in myelin are potent inhibitors of axon regeneration, and several molecules released by degenerating oligodendrocytes can contribute to the failure of regeneration.
There are endogenous mechanisms for at least partial regeneration of injured spinal cord, which may contribute to ongoing recovery for years after injury, but there are many barriers to significant success.

Question 12

Clinical features of SCI

Answer 12

• Fractures of the spinal column are often described by their vertebral level, but the neurological injury is described by the SC level at which the nerve roots emerge.
• The clinical manifestations of SCI depend on the level of neurological injury and the amount of preserved spinal cord tissue.
• SCI can result in the partial or complete loss of sensorimotor function below the level of the injury, e.g. above C5 may disrupt innervation to the diaphragm, above T11 may affect intercostal chest muscles and above L1 may affect abdominal muscles

Question 13

Sympathetic and parasympathetic outflow

Answer 13

Injuries in the cervical and high thoracic cord can disrupt the sympathetic outflow (blue line) to the heart and the peripheral vascular system, while preserving baroreceptor inputs (red line) and parasympathetic output (green line). As a result, parasympathetic innervation to the heart
dominates in patients with cervical and upper thoracic injuries, which causes bradycardia and decreased cardiac
output.
Patients often experience hypotensive symptoms, particularly with exertion or upright positioning.
The parasympathetic–sympathetic imbalance can also allow unchecked reflex spinal sympathetic stimulation
as a consequence of noxious triggers (such as bladder distension or pressure sores), which leads to sudden peripheral vasoconstriction and acute hypertension.
As a response, parasympathetic outflow above the injury level increases, leading to vasodilation, headaches, sweating and sinus congestion. This dangerous acute syndrome is known as autonomic dysreflexia.
S2–S4, sacral levels 2–4.

Question 14

Spinal shock

Answer 14

• Spinal shock: Post SCI, a temporary state of flaccid paralysis may occur, including loss of motor, sensory, autonomic and reflex function at or below the level of injury.

Question 15

Neurogenic shock

Answer 15

• Neurogenic shock: due to loss of sympathetic outflow - usually most often found with injury above T6, and has hypotension, bradycardia, wide pulse pressure (difference between systolic and diastolic) and warm pink extremities. This affects up to 20% of patients with cervical level injuries. Bradycardia is found in nearly all patients with severe SCI during the acute phase.

Question 16

Diagnosis

Answer 16

After any traumatic injury, first responders rapidly assess patients in the field and attempt resuscitation en route to the hospital.
During this period, the advanced trauma life support protocols dictate initial care, which includes airway, breathing and circulation support, along with the immobilization of the potentially injured and unstable spinal column using a rigid cervical collar and backboard.
Although individual hospital approaches vary, most patients with trauma will undergo a gross neurological examination (which includes a voluntary motor and sensory examination of each limb and a rectal examination) and spinal imaging (using, for example, X- ray or CT imaging) if a SCI is suspected.
Concerns on clinical examination or early radiographic imaging are followed by advanced imaging and detailed neurological examinations.

Question 17

Imaging and electrophysiology

Answer 17

X-ray, CT and MRI are the most commonly used radiological tools when investigating damage to the spine and SCI.
CT has largely supplanted X-ray for the diagnosis of bone injuries in patients with trauma.
Although extremely sensitive for diagnosing a fracture or dislocation of the spine, CT is less effective at evaluating the integrity of soft tissue structures, such as intervertebral discs, ligaments, the spinal cord and nerve roots, but MRI is well suited for assessing these structures.
A number of electrophysiological techniques can be used to assess SCI impact on nerve function as well.

Question 18

ASIA Impairment Scale

Answer 18

The scale is used to determine the grade of spinal cord injury (SCI), which ranges from ASIA Impairment Scale grade A (the most severe injury with complete sensorimotor loss) to ASIA Impairment Scale grade E (the least severe injury with no neurological deficit)

A - complete
B - Sensory incomplete
C - Motor incomplete
D - Motor incomplete
E - Normal

Question 19

Spinal cord injury syndromes

Answer 19

The major descending motor tracts are in yellow and the major ascending sensory tracts are in
green (part a). The patterns of sensorimotor loss exhibited in patients with spinal cord injury (SCI) syndromes can be explained by damage to specific spinal cord tracts with sparing of other tracts. For example, anterior cord syndrome (part d) results in complete motor paralysis due to damage to the corticospinal tract, loss of pain and temperature sensation secondary to damage of the spinothalamic tract, but preservation of light-touch sensation and proprioception.

Posterior cord syndrome (part e) results in the
reverse, with loss of light touch and proprioception but preservation of motor function, and pain and/or temperature sensation.

Question 20

Neurological recovery prognosis

Answer 20

Neurological recovery in patients with SCI is typically observed within the first 6 months after injury, but continued improvements can be seen up to 5 years later. The prognosis for neurological recovery is variable and depends primarily on the initial severity of neurological injury; a more severe degree of initial injury portends a worsened prognosis at 1 year.
The neurological level of injury can also determine neurological recovery; in general, thoracic injuries (particularly complete injuries) are associated with reduced potential for motor recovery compared with injuries in the cervical or lumbar spinal cord. This is thought to exist because neurological recovery is more difficult to clinically detect in the thoracic region.
In general, patients with ASIA Impairment Scale grade A injuries are generally predicted to have a <5% chance of walking 1 year post-injury, regardless of the neurological level of injury. Ambulatory rates are substantially higher for patients with incomplete injuries but are variable and depend on the initial level of neurological injury.

Question 21

Prehospital and hospital care settings

Answer 21

• For any patient with suspected spinal trauma and/or traumatic SCI, complete immobilization of the cranio–spinal axis should be maintained. In the prehospital setting, this should involve transport with the use of a rigid spine board and application of a cervical collar.
• After rapid transport to the hospital, precautions, including flat bedrest with a cervical collar, should be maintained until confirmation or restitution of spinal stability.
• Current AANS/CNS SCI guidelines state that management of acute patients with SCI, particularly those with complete cervical injuries, should be performed in an intensive care unit (ICU) with continuous cardiac, haemodynamic and respiratory monitoring.
• Care in the ICU is more important when considering concomitant injuries that can accompany SCI, including traumatic brain injury, intra-abdominal injury, thoracic injuries, pelvic or long bone fractures and facial trauma.

Question 22

Medical Management - haemodynamics

Answer 22

In the ICU, one of the most essential components of acute SCI management is the maintenance of adequate spinal cord perfusion, through the avoidance of systemic hypotension and support of mean arterial pressure.
Hypotension is common post-SCI; and maintaining a mean arterial pressure between 85 and 90 mmHg for the first 7 days post-injury is a priority.
In addition, oxygen saturation should be maintained at ≥90% and prophylaxis to prevent deep venous thrombosis should be administered as soon as possible.

Question 23

Medical management - methylprednisolone

Answer 23

Somewhat controversial as there are positive, negative and possibly no effects, methylprednisolone can be given high-dose IV as an anti-inflammatory medication in the acute phase within 8 hours of surgery.

Current recommendations are for decision to be best made by physician involved, balancing the potential for benefit with the potential for complications, given the characteristics of the presenting patient.

Question 24

Medical management – decompressive surgery

Answer 24

Surgery aims to realign the spinal column, re-establish spinal stability and decompression (that is, relief of bony or ligamentous compression) of the spinal cord.
Surgery typically involves open reduction and decompression paired with an instrumented fusion (for example, using implanted metal hardware) to stabilize the spinal column in an anatomical position.
The extent of surgery is tailored to the anatomical site, as well as the severity and extent of injury.

Question 25

Systemic complications for QOL long-term - cardiovascular

Answer 25

∼60% of patients experience symptomatic orthostatic (or postural) hypotension (for example, dizziness, weakness and syncope (fainting)). These symptoms occur consistently initially but gradually resolve over weeks to months, although they can persist for longer in some patients.

Treatment includes the use of lower extremity compression stockings, abdominal binding or medical management, including volume augmentation (such as the use of hydration, salt tablets or fludrocortisone) and/or peripheral vasoconstriction.

Question 26

Systemic complications for QOL long-term - Autonomic dysreflexia

Answer 26

An urgent condition that most commonly occurs in patients with injuries at or above T6 (particularly, in those with complete injuries), caused by the presence of a noxious stimulus below the level of injury (such as bladder distension, bowel impaction or pressure sores), which causes a reflex overstimulation of spinal sympathetic neurons, leading to vasoconstriction and dangerous acute hypertension.

As a response, parasympathetic outflow increases above the injury level and sympathetic outflow can be inhibited, depending on the injury level, which leads to vasodilation, headache, sweating and sinus congestion. Prompt treatment requires upright positioning of the patient, removal of the triggering stimulus and pharmacological anti-hypertensives for refractory cases.

Episodes of life-threatening autonomic dysreflexia can occur in both acute and chronic stages of injury, making long-term prevention key by avoiding noxious stimuli (for example, by frequent bowel and bladder care and repositioning to avoid pressure sores).

Question 27

Systemic complications for QOL long-term - respiratory

Answer 27

Paralysis of the phrenic nerve, intercostal muscles and/or abdominal muscles leads to reduced lung capacity, ineffective cough and accelerated fatigue with respiratory demand. As a consequence, patients experience recurrent pneumonia, atelectasis (that is, alveolar collapse) and pleural effusion (fluids around the lungs), and are more likely to have sleep apnoea and respiratory failure.

Whereas long-term rehabilitation, which promotes cardiorespiratory conditioning, may be beneficial, the respiratory defects themselves restrict rehabilitation capacity and long-term independence.

Owing to this, respiratory complications are the leading cause of mortality in patients with chronic SCI.
In individuals with high cervical injuries, or those with poor respiratory reserve, lifelong ventilator dependency can also result.

Question 28

Systemic complications for QOL long-term - Secondary immunodeficiency

Answer 28

Disruption of CNS input to immune organs can result in the systemic dysfunction of macrophages, T cells, B cells and natural killer cells in a process known as immune paralysis.

The clinical manifestation of this is an increased susceptibility to infections, such as pneumonia, urinary tract infections and wound infections.

Although the cause of immune paralysis continues to be investigated, and no accepted management for secondary immunodeficiency exists.

Question 29

Systemic complications for QOL long-term - Genitourinary and gastrointestinal

Answer 29

Dysfunction of the genitourinary and gastrointestinal systems increases care requirements, the risk of infection and can be a source of substantial social and psychological stress in patients with SCI.

Injuries at or above L1–L2 interrupt innervation of the detrusor, or the bladder muscle, and urinary sphincters, which can cause an inability to empty the bladder, acontractile bladder, urinary incontinence and recurrent infections.

Management includes urethral catheterization every few hours, the surgical creation of a urinary stoma, and pharmacological therapies (such as anticholinergics or α-blockers).

Approximately 39% of patients with SCI report that bowel dysfunction significantly reduces their QOL.

SCI can interrupt the voluntary control of the anal sphincter (causing faecal retention) and/or the parasympathetic innervation of the bowel. Both cases lead to constipation, an increased risk of infection and stress for patients.

Treatments can range from dietary fibre intake, digital rectal stimulation or disimpaction and the use of suppositories, to implantation of an electrical stimulator or colostomy.

Question 30

Systemic complications for QOL long-term - Neuropathic pain

Answer 30

Neuropathic pain is experienced by up to 40% of patients with chronic SCI, has a mean onset of 1.2 years after injury and can have a substantial effect on the psychological well-being and QOL of patients.
The mechanism underlying injury-level pain is thought to be sprouting of spinal cord fibres around damaged nerve roots, leading to inappropriate activation of primary afferent fibres and the initiation of pain by normally non-noxious stimuli.
Neuropathic pain can be treated pharmacologically (for example, using antidepressants, anticonvulsants and/or opioids), surgically (such as implanted spinal cord stimulators, deep brain stimulators and dorsal root entry zone lesioning) or using other treatments such as acupuncture, massage and cognitive–behavioural therapy.

Question 31

Rehabilitation

Answer 31

Rehabilitation requires an interdisciplinary approach involving nurses, physicians, dieticians, psychologists, physiotherapists, social workers, recreation therapists, speech therapists, orthotists and child life specialists.
Rehabilitation can have significant effects on long-term health by helping patients to recover as much function as possible, prevent secondary complications, understand the extent of their injuries, cope with loss of independence and address other practical challenges, such as vocational and financial concerns.

Question 32

Rehabilitation focus

Answer 32

Physical rehabilitation is focused on regaining function, enhancing any remaining function and preventing complications. Key components of rehabilitation are strength training, cardiovascular- focused exercise, respiratory conditioning, transfer or mobility training and stretching to prevent muscle contractures (that is, the permanent shortening of muscle).

The patient’s progress helps to dictate the level of ongoing care that is needed in the community and the use of assistive devices for daily living.
Interestingly, physical rehabilitation can induce significant changes in cellular signalling and growth factor expression.

However, in clinical practice, ventilator dependence, poor vascular tone, neuropathic and somatic pain, psychosocial challenges and resource limitations in acute care institutions can make early mobilization challenging.

Question 33

Life post rehab - OT

Answer 33

Occupational therapy focuses on integrating adaptive devices into people’s daily lives to maximize functional independence at home and at work.
Devices might include wheelchairs, lifts, braces, orthoses, environmental control units (such as lights, television or phones), bathroom equipment (such as showering or toileting), vehicle modifications for driving and others.

Question 34

Future vista

Answer 34

• Neuroprotective treatments to reduce apoptosis and reducing local inflammation
• Neuroregenerative treatments
• Cell transplantation
• Neuromodulation and robotics