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≥ 92% of participants will know how to assess and manage different common causes of traumatic spinal cord injuries.
This course includes the more common and important causes of traumatic spinal cord disorders. This course will consist of the risk factors, clinical presentation, diagnosis, treatment, and prognostic outcomes of traumatic spinal cord injuries and conditions.
Upon completion of this course, the participant will be able to:
A spinal cord injury (SCI) occurs when there is damage made to the cells and nerves in the spinal cord that sends and receives signals to and from the brain to the rest of the body (National Institute of Neurological Disorders and Stroke [NINDS], 2021). This life-changing neurological condition comes with substantial implications for both patients and caregivers. There have been medical advancements in caring for individuals with SCIs, but there is still a lack of neurological treatment options. The outcome of a SCI largely depends on the severity of the lesion and the location of the lesion. Partial or complete loss of both motor and/or sensory function below the level of injury can occur, complicating the SCI diagnosis. The complex pathophysiology of a SCI increases the burden placed on patients (Alizadeh et al., 2019).
A 72-year-old male fell backward while fishing, hitting his back on the boat dock. The patient denies loss of consciousness. The fall was witnessed, and witnesses called 911. The patient complains of back pain all over.
Spinal cord injury (SCI) is a life-changing injury with neurological manifestations. Besides having significant implications for the patient, SCI places a considerable burden on healthcare resources.
There are roughly 330 million people in the United States (US). The annual incidence of SCIs is approximately 54 cases per one million people in the US, or about 17,700 new SCI cases each year (Kazim et al., 2021).
The number of individuals living in the US with an SCI is roughly around 300,000, but it could be nearly 400,000.
The average age of onset for a SCI is 43 years old. This is an increase, as in the 1970s, it was 29 years old.
SCIs are uncommon in young children, accounting for 1%-10% of all SCIs (Mehdar et al., 2019). However, the fragility of their spine means they are vulnerable to SCIs.
Roughly 80% of individuals with a SCI are male.
The length of stay in the hospital and rehab largely depends on the individual’s condition and the severity of the injury. In acute care settings, the average length of stay is 11 days, which has decreased significantly over the years (Mehdar et al., 2019). The length of stay in rehab facilities has also decreased and is generally around 34 days.
Approximately 30% of persons with SCI are re-hospitalized more than once following injury. Among those hospitalized for a second time, the length of hospital stay averages about 22 days (Mehdar et al., 2019).
In a 2019 study, the most common causes of SCI were automobile crashes (31.5%) (Bennett, 2021). After car accidents, falls (25.3%) were the second most common cause of a SCI. Gunshot wounds (10.4%), motorcycle crashes (6.8%), and diving incidents (4.7%) all accounted for SCIs (Bennett, 2021). Medical/surgical complications (4.3%) were least likely to result in an SCI. They all collectively accounted for 83.1% of total SCIs since 2005 (Bennett, 2021).
Car accidents were the leading cause of SCI until around age 45 (Bennett, 2021). After age 45, falls were the leading cause of a SCI. SCIs in males were often caused by motorcycle accidents, diving mishaps, and gunshot wounds. The only difference in race and ethnicity was among those who had a gunshot wound.
After one receives a SCI injury, swelling of the spinal cord occurs in the area of the damage. The swelling that occurs cuts off the nerves’ blood supply, decreasing the amount of oxygen. This then causes the spinal tissue that is injured to die. The immune system then attacks and causes further damage.
The blood flow at the injury site becomes sluggish and is reduced in adjacent spinal cord areas, affecting the entire body. The body can no longer self-regulate, which causes a drop in both blood pressure and heart rate.
Once there is a SCI, there is an accumulation of neurotransmitters and biochemicals. Both of these overexcite the nerve cells, which kill them through excitotoxicity. Excitotoxicity also destroys the oligodendrocytes that protect the spinal axons that allow the spinal nerves to transmit information.
After a SCI, the immune system sends many cells to the damaged spinal area. These cells promote inflammation by releasing many toxic cytokines to nerve cells (U.S. Department of Health and Human Services, 2022).
The inflammation of the spinal cord unleashes free radicals that then damage healthy nerve cells in the spinal cord.
Programmed cell death, called apoptosis, occurs at the injury site. After this, oligodendrocytes die, which reduces the integrity of the spinal cord (U.S. Department of Health and Human Services, 2022).
Many risk factors can predispose patients to a SCI. Age, gender, risky behavior, and some preexisting conditions can increase the chances of a SCI.
Risk factors can include (Ikpeze, 2017):
Risky behaviors that increase the chances of a SCI include (Ikpeze, 2017):
Some underlying spinal diseases can predispose patients to SCI. These conditions include (Ikpeze, 2017):
The most important structure between the body and the brain is the spinal cord. It extends from the foramen magnum, where it stays continuous to the level of the second lumbar vertebrae. The spinal cord is between 40 to 50 cm long and around 1.5 cm in diameter. There are two consecutive rows of nerve roots on each side of the spinal cord (Figure 1). The nerve roots join distally to form 31 different pairs of spinal nerves (Dafny, 2020).
The spinal cord, a cylindrical shape, is composed of gray and white matter and is divided into four different regions. These regions include (Dafny, 2020):
Each of these regions comprises several segments, and each spinal cord segment innervates a dermatome (Dafny, 2020).
Figure 1: Spinal Cord Matter
The spine, divided into four sections, does not include the tailbone. The vertebrae are as follows (Figure 2)(American Association of Neurological Surgeons [AANS], 2021):
Some discs act as a support system for the spine between the vertebral bodies. Some ligaments are attached to the vertebrae, serving as a supportive structure. The discs are oval-shaped with a tough outer layer called annulus fibrosus. The discs surround a soft layer called the nucleus pulposus and act as a shock absorber for the spine (American Association of Neurological Surgeons [AANS], 2021).
Figure 2: Anatomy of the Spinal Cord
There are two parts to the cervical spine. The first region is the upper cervical region (C1 and C2) (Bridwell, K & Rodts, 2022). The lower region is the second cervical region and comprises C3 through C7. C1 is named the Atlas, and C2 is the Axis.
The atlas is the first part of the cervical vertebrae and is called C1 (Figure 3). This is the vertebrae that aid in supporting the head and skull. C1, or the atlas, comprises bone and two lateral masses joined by both the anterior and posterior arch (Bridwell, K & Rodts, 2022).
Figure 3: Atlas of the Spinal Cord
The second cervical vertebrae are C2 or the axis. The axis is a blunt tooth-shaped process that points upward. The axis provides a pivot-like ability to move, allowing the head to rotate.
The atlantoaxial joint is located between C1 and C2. This particular joint does not have an intervertebral disc (Figure 4). A thick and strong ligament secures this joint, called the transverse ligament (Dickerman, 2019).
Figure 4: The Atlas and the Axis
The gray and white matter of the spinal cord appears in a cross-section pattern. The gray matter is full of motor and sensory neurons, neuropils, and interneurons. Fiber tracks make up the white matter that interconnects and are myelinated motor and sensory axons. The gray matter makes up the left and right dorsal horns and the left and right ventral horns. The central canal runs longitudinally and is continuous with the ventricles in the brain, and is filled with cerebrospinal fluid (Tenny & Varacallo, 2021).
The white matter is organized into tracts (Tenny & Varacallo, 2021). The ascending tracts carry information from the sensory receptors to the central nervous system.
Descending tracts carry information from the central nervous system to the rest of the body (Tenny & Varacallo, 2021).
The dorsal column contains the cuneate fasciculus and the gracile fasciculus which form the dorsal funiculus (Clark et al., 2021). The dorsal column is responsible for vibration sensation, pressure, and two-point discrimination (Clark et al., 2021). The dorsal column forms at the superior portion of the medulla oblongata.
The lateral spinothalamic carries temperature and pain information (Tenny & Varacallo, 2021). The lateral spinothalamic tract forms two segments above the spinal cord at the anterior commissure (Tenny & Varacallo, 2021).
The anterior spinothalamic carries pressure and touch information. It forms similar to the lateral spinothalamic tract (Tenny & Varacallo, 2021)(Figure 5).
The ventral and dorsal spinocerebellar transmit sensory information to the cerebellum (Tenny & Varacallo, 2021). The ventral spinocerebellar tract and the dorsal spinocerebellar tract are both ipsilateral.
Figure 5: Tracts of the Spinal Cord
The anterior and lateral corticospinal are involved with conscious control of the skeletal muscle. Most of the lateral corticospinal tract fibers form at the interior portion of the medulla oblongata (Tenny & Varacallo, 2021). The anterior corticospinal descends into the spinal cord and forms at the segmental level. The lateral corticospinal tract innervates the limbs’ muscles, also called the pyramidal tract. The anterior tract innervates the muscles of the trunk.
The vestibulospinal carries essential information from the ear that controls the position of the head and is involved with muscle tone to aid in maintaining balance and posture.
The rubrospinal is involved in the movement of the extensor and flexor muscles. This tract originates from the midbrain and forms a pathway (Tenny & Varacallo, 2021).
The reticulospinal is housed in the brainstem and influences and facilitates the corticospinal tract (Harrow-Mortelliti et al., 2022).
The vertebral column is divided into the thoracic, sacral, lumbar, cervical, and coccygeal regions. The peripheral nerves are also called the segmental or spinal nerves and innervate much of the body (Figure 6):
These peripheral nerves originate from the 31 segmental pairs in the spinal cord (Leijnse & D'Herde, 2016):
Figure 6: Vertebrae
The spine consists of 24 articulating vertebrae and nine fused vertebrae in the coccyx and sacrum. The vertebrae consist of the vertebral arch and vertebral body. Together, these contain the spinal cord and enclose the vertebral foramen. The vertebral arch is formed by laminae and pedicles, a pair of each. A spinous process is posterior to the vertebral body and has two transverse processes (Solmaz et al., 2015).
The spinous process projects posteriorly, while one transverse process projects to the right and the other to the left. The spinous process in the lumbar and cervical region can be felt through the skin. Above and below each vertebra are facet joints. These facet joints restrict the range of movement. Two small openings called intervertebral foramina sit between each pair of vertebrae (Cadotte et al., 2015).
Injuries to the spinal column may cause spinal cord and brain injuries through many different causes.
Transection:
Compression:
Contusion:
Vascular Compromise:
Vertebral artery injuries are usually associated with many spinal fractures. This can cause permanent disability and stroke if treatment is delayed.
There are some areas of concern when fractures are involved. Fractures of the atlas and the axis, transverse foramen displacement, transverse foramen fractures, and subluxation of cervical vertebrae are causes for concern (Shavelle et al., 2015).
Spinal cord injuries can be classified as either compression or acute impact.
A spinal cord concussion classifies as an acute compact injury. There is a cascade of events after this injury occurs and is on the gray matter, resulting in hemorrhagic necrosis. Hypoperfusion of the gray matter results. There is an increase in reperfusion injury and the amount of intracellular calcium. Both of these increases occur after injury and affect the cells.
The amount of necrosis in a SCI is based on the initial force of the trauma a patient receives. Trauma can lead to spinal compression, which alters blood flow and pressure (Anjum et al., 2020).
The spinal cord becomes compressed very early on after trauma. Compression occurs from a mass leaning on the spinal cord, which causes increased pressure in the parenchyma. The body responds with the loss of axons in the white matter of the spinal cord. If compression is critical, vasogenic edema will occur. This edema increases the pressure in the spinal cord and will increase the rate of dysfunction (Khorasanizadeh et al., 2019).
Spinal cord vascular supply interruption, hypoperfusion, and hypotension may occur directly after an injury. These clinical manifestations can produce bradycardia, neurogenic shock, and hypovolemia. Neurogenic shock and extensive bleeding lead to ischemia of the spinal cord. Leukocyte and red blood cell extravasation are promoted by rupturing capillaries and small blood vessels. Pressure on the damaged spinal tissues occurs because of the extravasations at the site of injury and can disrupt blood flow, potentially causing vasospasm. This can happen for 24 hours after injury. The occurrence of vascular ischemia, hypovolemia, and hyper-perfusion eventually leads to cell death and tissue destruction (O'Shea et al., 2017).
Ionic, vasogenic, and cytotoxic edema is caused by ischemia of the spinal cord. The influx of sodium occurs because of a passive influx of chloride. Because of this, molecules of water influx through aquaporin channels. The water and solute influx balance is disturbed, causing cell swelling and loss of cytoskeletal integrity and promoting cell death. Increased permeability of the blood and spinal cord barrier causes ionic edema because of the loss of water and ions from the interstitial spaces. There is an increase in inflammation and endothelial injury, which increases pore size and allows large molecules to pass through the cell membrane. This results in vasogenic edema (Dimitrijevic et al., 2015). This acute secondary injury phase continues from 2 h to 48 h. Continuous hemorrhage, edema, and inflammatory stage lead to substantial necrosis indicated by the increased concentration of specific inflammatory and structural biomarkers, e.g., glial fibrillary acidic protein (GFAP) or IL-6 in cerebrospinal fluid (CSF).
Injury of the spinal column in the cervical region is classified by location, injury, and mechanism (Table 1).
| Mechanisms of Spinal Injury | Stability |
|---|---|
| Flexion | |
| Anterior wedge fracture | Stable |
| Flexion teardrop fracture | Extremely unstable |
| Clay shoveler's fracture | Stable |
| Subluxation | Potentially unstable |
| Bilateral facet dislocation | Always unstable |
| Atlanto-occipital dislocation | Unstable |
| Anterior atlantoaxial dislocation with or without fracture | Unstable |
| Odontoid fracture with lateral displacement | Unstable |
| Fracture of transverse process | Stable |
| Flexion-Rotation | |
| Unilateral facet dislocation | Stable |
| Rotary atlantoaxial dislocation | Unstable |
| Extension | |
| Posterior neural arch fracture (C1) | Unstable |
| Hangman's fracture (C2) | Unstable |
| Extension teardrop fracture | Usually stable in flexion; unstable in extension |
| Posterior atlantoaxial dislocation with or without fracture | Unstable |
| Vertical Compression | |
| Burst fracture of vertebral body | Stable |
| Jefferson fracture (C1) | Extremely unstable |
| Isolated fractures of articular pillar and vertebral body | Stable |
When assessing the stability of the cervical spine, it is generally viewed as two columns.
Intervertebral disks and vertebral bodies form the anterior column. The posterior column is formed by the transverse processes, the pedicles, facets, spinous processes, and laminae. The nuchal ligament complex holds the posterior column together and in alignment.
If there is a malfunction in both the anterior and posterior columns, the cervical spine can become two independent columns. This means there is an increased risk of exacerbating an injury. If only one of the spinal columns malfunctions, there is a decreased risk of spinal cord injury (Torlincasi & Waseem, 2021).
The following image (Figure 7) will illustrate the sections of the spinal cord and where on the body the innervations of sensation and motor control occur. Notice the color-coded areas.
Figure 7: Innervations
Spinal innervations include (Kiehn, 2016):
There are 12 nerve roots in the thoracic spine (T1-12) (Yezak, 2018). They are located on each side of the spine. The nerve roots branch from the spinal cord and aid in sensory and motor signals from the back, the abdomen, and the chest. The thoracic spinal nerves are named for the vertebra above it. The T3 nerve root runs through the T3 and T4 vertebra. Twelve thoracic spinal nerve pairs start at T1-T2 and go down to T12-L1 (Yezak, 2018)(Figure 8).
There is a bony hole in the spinal canal where each thoracic nerve exits. This bony hole is called the intervertebral foramen. The size and shape of the vertebrae can differ.
The thoracic nerve root branches from the spinal cord and travels through the foramen. It then branches into two nerve bundles. These nerve bundles feed into the body's ventral ramus (front) and dorsal ramus (back). The ventral ramus travels through T1 to T11 and becomes an intercostal nerve. This intercostal nerve follows the path of the ribs (Yezak, 2018). When the ventral ramus meets T12, it becomes a subcostal nerve that lies below the twelfth rib. The dorsal ramus helps to provide skin sensation feelings in the back muscles through T1 to T12 (Yezak, 2018).
Its vertebral level determines the motor and sensory functions provided by a thoracic nerve root.
The functions are different for each person, but the typical functions include (Yezak, 2018):
Figure 8: Thoracic Cord
The lower back is comprised of the lumbar spine. The lumbar spine is formed by muscles, nerves, ligaments, blood vessels, intervertebral discs, and vertebral bodies. The top of the lumbar spine is where the spinal cord ends, and the remaining nerve roots, called the cauda equina, descend the remainder of the spinal canal (Beasley, 2020)(Figure 9). The lumbar spine is very resilient to pressure and is considered sturdy. However, the lumbar spine can be subjected to high stress and heavy load, resulting in pain.
The lower back performs the following essential functions (Beasley, 2020):
Many potential problems can occur in the lumbar spine. It is easier to understand these potential problems if they are divided by the segments. A lumbar motion segment is made up of (Cuellar et al., 2017):
Figure 9: Lumbosacral Cord
Spinal innervations include (Kiehn, 2016):
There are sacs, or nerve roots, at the lower end of the spinal cord called the cauda equina. These specific nerve roots cause the ability to feel or move in the legs and the bladder.
The cauda equina is sometimes called the “horse’s tail,” as the nerves near the end of the spine resemble exactly that. They extend through the spine in the lumbar area, are located over the sacrum, and follow down the back of each leg (Villavicencio, 2016).
There are 10 pairs of nerve roots in the cauda equina. Some of these nerve roots are combined in the lower body from larger nerves. An example of this would be the sciatic nerve.
Motor and sensory innervation in the lower limbs and the pelvis is possible due to the cauda equina and aids in bladder and bowel function. Sudden and severe symptoms usually develop if the cauda equina becomes inflamed or there is lower back compression. Early medical attention is essential for a full recovery (Dias et al., 2015).
Atlanto-occipital dislocation (AOD) is increasingly identified as a potentially survivable injury. This injury is now survivable because of increased awareness, more aggressive treatment, and earlier diagnoses. Though treatable and despite improved outcomes, there is still significant morbidity and mortality with AOD.
Damage to the bony structures of the skull in the cervical spine and damage to the ligaments results in AOD, which includes a craniocervical injury that is highly unstable. The increased morbidity and mortality associated with AOD are usually secondary to upper cervical spinal cord injury and brainstem injury. AOD, which only represents 1% of cervical spine injuries, is the most common cervical spine injury and fatality in motor vehicle accidents (Rief et al., 2019).
Bony fractures do not often accompany an AOD injury. The injury is usually located between the upper cervical spine and the occiput. It is more easily missed than traumatic fractures of the cervical spine (Hall et al., 2015). Proper identification and treatment of this injury requires a decent understanding of the anatomy of the craniocervical junction (CCJ) (Hall et al., 2015).
Different traumatic mechanisms may cause AOD. Excessive force to the CCJ is common to all traumatic mechanisms. This leads to ligamentous disruption. Hyperflexion, hyperextension, lateral flexion, or a combination of all are among the most common mechanisms.
Some predisposing conditions can increase the risk of AOD even when there is minor trauma. Some of these conditions include congenital, neoplastic, and inflammatory disorders. Rheumatoid arthritis of the spine, especially in the CCJ, can cause the transverse ligament to be weakened. This weakening increases the risk of subluxation of the C1. In 30% of cases of Down Syndrome, there is craniocervical ligament laxity. The fulcrum-life effect of some congenital vertebral fusion syndromes can also predispose patients to AOD (Hall et al., 2015).
Patients with AOD are often left with neurological impairments. These impairments can include unilateral or bilateral weakness, lower cranial nerve deficits, and quadriplegia. Some patients can be completely asymptomatic, while others may depend on life-support or life-saving measures. If simultaneous injuries to the chest, brain, abdomen, or extremities occur, this can mask weakness and neurogenic shock.
A regular neurological examination may occur in nearly 20% of patients with an AOD. Sometimes, the only symptom is severe neck pain. This and the lack of neurological findings can delay the diagnosis and treatment of AOD. Most patients with an AOD will present with respiratory arrest and even unconsciousness. There may also be lower cranial nerve involvement (Figure 10).
Spinal cord injury, hyperreflexia with clonus, motor, and sensory deficits, abnormal sphincter tone, and a positive Babinski sign may be seen in more severe cases of AOD. The neurological deficits present in AOD may be unilateral or bilateral and include the entire affected side. A reflex examination should be interpreted cautiously, given the possibility of spinal shock (Tobert et al., 2018).
Figure 10: Atlanto-Occipital Joint
Atlantoaxial dislocation (AAD) is rare but can be fatal. AAD results when something disrupts the anatomy of the occipital-cervical region. If AAD is not treated quickly, permanent deficits or deformities may occur.
Inflammatory, idiopathic, congenital, and traumatic abnormalities can cause loose articulation of the atlantoaxial joints. There is no precise mechanism of injury, but it can occur in all age groups. However, AAD is usually seen in adolescents (Tao, 2022).
A subluxation can occur in several ways (Tao, 2022; Ghailane et al., 2019):
Diagnosis: Subluxation of the atlantoaxial region can usually be diagnosed with plain X-rays. If subluxation is intermittent, flexion views may be required to get a visual. If this x-ray does not show any abnormalities or further images are required, an MRI would be the next test of choice. MRIs are able to provide sensitive evaluation of the spine, including compression and subluxation (Moley, 2022).
Treatment:
If patients with this form of subluxation are experiencing any pain, deficits, or instability, treatment is necessary. Treating the symptoms and a rigid cervical collar are the first steps in treatment. The urgency of treatment is based on the severity of the symptoms as well as the MRI results. Surgery may be necessary depending on the amount of instability (Moley, 2022).
A buckling force causes a bilateral facet dislocation and results in an unstable flexion type of dislocation. This bilateral facet dislocation is often called a 'doubly-locked' vertebral injury giving the impression of stability (Baba, 2021). Since there is complete ligamentous disruption, this is an unstable injury.
Radiographic features include (Baba, 2021):
Unilateral facet dislocations are the most frequently missed cervical spine injury on plain X-rays (Forsthoefel et al., 2021). These are associated with monoradiculopathy that improves with traction. The inferior facet of the cephalad vertebrae encroaches on the neuroforamina (Forsthoefel et al., 2021).
A burst fracture of the atlas is also called a Jefferson fracture. This can be a double fracture through both the anterior and posterior arches. Three-part and four-part fractures are also possible (Figure 11)(Worsley, 2021).
50% of Jefferson fractures are associated with other C-spine injuries.
Most Jefferson fractures are caused by diving headfirst, usually in shallow water (Worsley, 2021). The occipital condyles are driven into C1 because of the axial loading in the cervical spine axis. Spinal cord injury is possible if there is a retropulsion fragment in the cervical cord.
The Gehweiler classification system is used to describe injuries of the atlas. These injuries can occur with a Jefferson fracture or a type 3 injury. Transverse Atlanta ligament disruptions can also help classify these injuries (Worsley, 2021).
Diagnosis: An x-ray will show asymmetry. From an odontoid view, there will be a lateral mass displacement. Ligamentous injury is usually seen at greater than 6 mm. A CT scan usually demonstrates the fracture line, which involves anterior and posterior arches. The atlantodental interval (ADI) increases if the transverse atlantal ligament is injured. The normal ADI in the adult population is less than 3 mm; in pediatric populations, the average distance is less than 5 mm (Worsley, 2021). The localized soft-tissue injury will be apparent. Pre-vertebral hemorrhage or edema will identify damage at the level of C1/2 (Worsley, 2021). A ligamentous injury will also be demonstrated. A fat-sat T2 sequence is helpful in the trauma setting to help distinguish abnormal soft-tissue injury from normal fat (Worsley, 2021).
Treatment: Conservative treatments are typically used in Jefferson fractures. A rigid collar immobilization can be used to make sure the transverse atlantal ligament is intact. There should be no widening of the ligaments seen on MRI scans (Worsley, 2021). If there is disruption of the ligament, it is then considered unstable. More aggressive management is required if this injury is unstable. More aggressive management includes posterior C1-C2 lateral mass internal fixation, halo mobilization, and transoral internal fixation (Worsley, 2021; Mead et al., 2016).
Figure 11: Burst Fracture
A posterior neural arch fracture can occur due to forced neck extension if compression of the posterior elements near C1 occurs, between the spinous and occiput processes. This fracture can be potentially dangerous. If there is anterior displacement of the atlas >1 cm, the adjacent areas of the spinal cord can be injured.
The first and most common injury is odontoid fractures. Cervical spine trauma causes odontoid fractures. Odontoid fractures in younger patients usually occur from high-energy trauma from a motor vehicle or diving accident. Low energy impacts, such as a fall from a standing position in the elderly population, can cause trauma. Hyperextension of the cervical spine, which pushes the C1 vertebrae and the head backward, is the most common cause of injury. Suppose the energy mechanism and resulting force are high enough (or the patient's bone density is compromised secondary to osteopenia/osteoporosis). In that case, the odontoid will fracture, with varying displacement and degrees of comminution (Tenny & Varacallo, 2021; Gornet & Kelly, 2016).
Hyperflexion of the cervical spine can also cause an odontoid fracture. The transverse ligament runs behind the odontoid process and attaches to C1 on the lateral masses on either side. The transverse ligament can cause significant anterior force to the odontoid process if the cervical spine is excessively flexed, causing a fracture (Figure 12).
There are three major types of Odontoid fractures (Tenny & Varacallo, 2021):
Figure 12: Odontoid Fractures
The second most common axis injury is traumatic spondylolisthesis. This fracture has been called the Hangman’s Fracture because of the similarity seen in judicial hangings. Hangman’s fracture is most often caused by falls and motor vehicle accidents (Sirkis, 2020).
Hangman’s fracture is defined as the avulsion of the neural arches bilaterally from the vertebral body (Sirkis, 2020). Subluxation may or may not occur. The fracture occurs through the adjacent area of the articulating facet or through the pars of C2. The fracture may extend into the vertebral artery foramen or the posterior vertebral cortex (Sirkis, 2020).
Parts of the neural arch lying between the inferior and superior articular facets define the pars interarticularis. With traumatic spondylolisthesis, this is the site of the fracture (Schleicher et al., 2015).
Forced hyperflexion with compression and hyperextension with vertical compression is the usual mechanism of injury. There are many facial injuries due to the dashboard and windshield with this hyperextension injury.
Diagnosis: Lateral radiographs, mainly the cervical spine, reveal this fracture in most cases (Sirkis, 2020). Extension and flexion views should be taken to evaluate for displacement or angulation. Computed tomography (CT) detects displaced fractures, extends into the vertebral foramina, and localizes displaced fragments.
Since the spinal canal is decompressed, neurologic injury with this fracture does not usually occur—however, the more severe the injury, the greater the chance of neurological damage. Angiography can exclude vertebral artery dissection of the fracture extends into the transverse foramina (Sirkis, 2020).
Treatment: There are different types of treatment options for this type of injury (Sirkis, 2020):
A vertebral compression fracture that occurs laterally or anteriorly is called a wedge fracture because the injured vertebrae resemble a wedge. A wedge fracture is usually found in the thoracic spine because of the rigidity and a small degree of extension and flexion. The thoracic spine can rotate in a wide range of torsions. The thoracic spine does not respond well to hyperflexion.
When wedge fractures occur without neurologic involvement, they are generally stable. When the wedge fractures affect adjacent vertebrae, they are considered severe fractures (Bell, 2021). The more anterior wedging there is, there will be severe kyphosis and bone fragments should be suspected in the spinal canal. Myelopathy and spinal cord dysfunction may also be present (Bell, 2021).
Immediate care is required when a wedge fracture is suspected. Evaluation will include assessing sensory, motor, and reflex responses (Bell, 2021).
Diagnosis: X-rays should include lateral and AP views of the affected portion of the spine. A CT scan, both with and without contrast, may help to identify a wedge fracture, the stability of the spine, and if there are any fragments.
Treatment: The height of the vertebral body is affected by a wedge fracture. The exact height reduction is determined to help guide the course of treatment. If there is a vertebral height loss of 10-30%, conservative treatment will occur (Bell, 2021). Treatment includes bed rest with the spine hyperextended for seven to ten days, followed by a brace for eight weeks. After three weeks post-injury, the patient may participate in physical therapy and try to walk (Bell, 2021).
Traction with radiologic control is the conservative management for this type of fracture. This reduces the fracture when the height loss is less than 50% (Bell, 2021). After traction, the patient must wear a plaster jacket for 45 days. After the plaster jacket, the patient may be in a brace for two months to maintain reduction. The patient is enrolled in physical therapy. When height loss is more than 50%, surgery is required. Spinal fusion and instrumentation may be used to restore the loss of height (Zdeblick & Kalfas, 2016).
Flexion teardrop fractures are a pattern in the cervical spine's severe axial/flexion injury (Guapo, 2021).
These fractures are essential to recognize because they indicate an extensive underlying ligamentous injury and spinal instability (Guapo, 2021). Associated spinal cord injury may occur in the anterior cervical cord with resulting quadriplegia (Guapo, 2021).
Extension teardrop fractures are different as they occur higher in the spine and are less severe.
Compression forces (such as diving and motor vehicle accidents) and severe flexion are the causes of injury in this fracture. There is a pattern that these fractures typically follow.
A compression or shearing fracture occurs along the anterior body, anteriorly. The triangular anterior fragment may be isolated, and the anterior longitudinal ligament may rupture (Guapo, 2021). The fracture continues through the vertebral inferior subchondral plate (endplate), with shearing/rotational injury of the posterior discoligamentous complex and rupture of the posterior longitudinal ligament. The rotational force causes distraction in the posterior elements and the rupture of the posterior ligaments (Guapo, 2021).
There is often kyphotic deformity due to the posterior translocation in the lower cervical column. These are characteristic markings of an anterior spinal cord injury (Maharaj et al., 2016).
The extent of this injury is variable. If the injuries are less severe, there is a decreased chance of neurological damage.
Diagnosis: The typical characteristics and findings of this injury include (Guapo, 2021):
Treatment: The degree of injury of the flexion teardrop fracture guides the treatment and prognosis. This fracture is often unstable due to the ligamentous structures and both osseous being damaged. Most patients require internal fixation and decompression.
The degree of neurological injury will guide the long-term prognosis after this fracture occurs. Mild cord injuries can be asymptomatic. However, if the posterior column is injured, quadriplegia and paralysis can occur (Guapo, 2021).
Forced extension of the neck with avulsion of the vertebral body causes an extension teardrop fracture. These are often stable in flexion but unstable in extension as the longitudinal ligament is damaged and disrupted (AlJahdali, 2020). These are not as severe as flexion teardrop fractures.
Forced extension of the neck, such as in hyperextension, causes an extension teardrop fracture.
Radiographic features include (AlJahdali, 2020):
Part of the vertebral body, the lamina, or the pedicles being fractured is considered a major fracture. It is deemed major because it helps carry the load and distributes movement. The vertebral lineup will be altered. With this type of fracture, there is an increased risk of nerve damage. Since the lamina and pedicles provide stability, the spine may become unstable (Highsmith, 2019).
The three columns include the anterior, middle, and posterior columns.
The anterior column includes (Divi et al., 2019):
The middle column includes (Divi et al., 2019):
The posterior column includes (Divi et al., 2019):
These types of injuries can be divided into four injury patterns (Divi et al., 2019):
These fractures can result in these mechanisms of injury (Divi et al., 2019):
A Spine Trauma Group in 2005 created the thoracolumbar injury classification and severity score (TLICS), also sometimes known as the thoracolumbar injury severity score (TISS). This scoring system was developed due to trouble classifying fractures (Hacking, 2021; Divi et al., 2019).
Classification:
Three major categories or parameters make up the classification score. There are two different radiologic categories and a clinical assessment evaluation. It is divided into (Hacking, 2021):
Morphology:
Morphology of the injury is divided into three different patterns. Points are given to parameters or categories (Hacking, 2021):
A suspected injury is 2 points.
Being injured is 3 points.
Neurologic Involvement:
Treatment and Prognosis:
The total number of points helps surgeons and physicians to determine a management plan depending on other comorbidities and injuries.
Patient with a score of (Hacking, 2021):
The bottom of the thoracic spine, T11, and T12, and the first vertebrae of the lumbar spine are often affected by compression fractures (University of Maryland Medical System [UMMS], 2022).
Too much pressure on the vertebral body causes a compression fracture of the spine (Figure 13). Bending forward with increased downward pressure on the spine adds compression. Examples of this fracture can be falling from a chair in a sitting position which causes the head to go forward. The spine bends forward, and pressure is concentrated in the front part of the spin or vertebral body. The fracture occurs when the bone collapses and the vertebral body's front (anterior) part forms a wedge shape. The vertebral body is then compressed or crushed. If the injury is severe, the back of the vertebral body may protrude into the spinal canal, compressing the spinal cord (UMMS, 2022).
There is no single cause of compression fractures, though the word compression would indicate that the fracture occurs because of too much pressure placed on the bone. The vertebral body may collapse if the bone is weak. Healthy bones can withstand the pressure. However, even healthy bones can break if the pressure on the vertebrae is too great (UMMS, 2022). The way a vertebra collapses/fractures depends on the amount of pressure it can withstand.
Osteoporosis is a common cause of compression fractures. Osteoporosis thins the bones making them too weak to bear even normal amounts of pressure. The thin bones can collapse even during regular activity, leading to a compression fracture. The most common type of osteoporotic fracture is spinal compression fractures (UMMS, 2022). Nearly 40% of women will experience one of these fractures before 80 years old (UMMS, 2022). Compression fractures can alter the strength and shape of the spine.
Severe pain in the back, the legs, and the arms can occur if the injury is forceful and sudden.
If the fracture injures the spine's nerves, patients might also feel weakness or numbness in these areas (UMMS, 2022). If the collapse of bone is gradual, such as bone thinning, the pain may not be as severe.
Decreased activity, bracing, and pain medications are the most common thoracic compression fracture treatments (Donnally et al., 2022).
Figure 13: Thoracic Compression Fracture
Approximately 90% of spinal fractures are that of the thoracolumbar spine, followed by cervical and lumbar spine fractures. This area comprises T11 to L2 vertebrae, and it is considered the weakest point in the spine biomechanically (Cahueque et al., 2016).
Around 80% of bony lesions in the spine can be identified by lateral X-rays. However, if a CT scan is available, it should be used first (Cahueque et al., 2016).
The most sensitive method in evaluating soft tissues is the MRI. The MRI is the best image of disc structures, ligaments, and neurologic status. MRI is valuable when an X-ray or CT does not provide the evidence of injury the provider wants to see.
Roughly 25% of patients with neurological deficits in the initial evaluation with cervical or thoracic lesions will change their treatment plan (Cahueque et al., 2016).
Compression fractures (A1, A2) can occur without neurological dysfunction. Surgical treatment may not be an option for some patients due to their medical conditions. Patients with a neurological deficit or dysfunction typically have a great improvement rate (Cahueque et al., 2016).
Patients with this injury will first receive conservative treatment. Bedrest for up to 12 weeks and rehabilitation are essential treatments for these patients (Cahueque et al., 2016).
Seat belt injuries are also called chance fractures or flexion-distraction fractures and are located in the thoracolumbar spine. Thoracolumbar fractures comprise up to 15% of spinal fractures. These types of fractures are most often caused by a motor vehicle accident.
Failure of the spinal column in tension is caused by a seat belt acting as an axis of rotation. Compression or tension may result if the anterior portion of the spinal column is involved in the center of rotation.
Horizontal splitting of the vertebrae at the spinous process or lamina consists of a traditional chance fracture. This type of fracture usually extends through the vertebral body and pedicles.
Evaluation begins with assessing the bony anatomy using plain-film radiography or computed tomography (CT). Lateral and AP views on plain film may show interspinous widening. There may be some degree of segmental kyphosis seen on a lateral view film. Any level of translation would be consistent with significant instability.
If there is a high suspicion of a flexion-distraction injury, a CT scan should be performed to examine the disruption pattern. If there is any evidence of neurologic impairment, an MRI should be obtained. The MRI can detect compression and examine the integrity of the facets, ligaments, fascia, and other soft-tissue structures (Weerakkody, 2021).
Nonoperative treatment is possible if there is less than 15° of kyphosis. The patient must also be neurologically intact. A simple extension cast or orthotic can create fair results in these patients. Patients should be seen monthly and have an X-ray done at each visit to assess the maintenance of sagittal alignment.
Surgical stabilization is recommended for injuries presenting greater than 15° of kyphosis, neurologic deficit, or the posterior ligamentous complex disruption.
Surgery is performed to restore the tension band. A rod or screw is placed two levels above the injury and two levels below the injury during surgery. Long-segment stabilization may be necessary if the injury includes a ligament injury (Themes, 2016).
Severe injuries that are characterized by rotation or horizontal displacement of a vertebral body represent a translation-rotation spine injury. The leading cause of a translation-rotation spine injury is shear and torsional forces. This severe damage usually involves the posterior ligamentous complex (PLC).
Translation-rotation spine injuries are characterized by (Badhiwala et al., 2019):
Lateral radiographs, MRI, or sagittal CT will best show translational injuries. Coronal images will show mediolateral instability.
Posterior ligamentous complex injuries include the following:
Three points are given for the morphology, and three points are given for the PLC. With a total of 6 points, using the thoracolumbar injury classification and severity score (TLICS), there is a need for surgical stabilization (Murphy, 2021).
Pain near the spinal fracture of spinal cord injury is common. However, it is not a reliable feature when excluding traumatic spinal cord injuries. Brain and systemic injuries are often in patients with SCIs, including extremity fractures, hemothorax, and intra-abdominal injuries. This may alter the patient’s ability to report pain. These various injuries can also complicate the assessment, evaluation, and management of SCIs.
About half of SCIs involve the cervical cord and, as a result, present with quadriparesis or quadriplegia. The severity of cord syndromes is classified using the American Spinal Injury Association (ASIA) Scale (Table 2).
| American Spinal Injury Association Scale (ASIA) | |
| A | Complete cord injury. No motor or sensory function is preserved in the sacral segments S4-5. |
| B | Sensory incomplete. Sensory but not motor function is preserved below the neurologic level and includes the sacral segments (light touch or pinprick at S4-5 or deep anal pressure), AND no motor function is preserved more than three levels below the motor level on either side of the body. |
| C | Motor incomplete. Motor function is preserved below the neurologic level, and more than half of key muscle functions below the neurologic level of injury have a muscle grade <3 (Grades 0 to 2). |
| D | Motor incomplete. Motor function is preserved below the neurologic level, and at least half (half or more) of key muscle functions below the neurologic level of injury have a muscle grade ≥3. |
| E | Normal. Sensation and motor function are graded as normal in all segments, and the patient had prior deficits. |
Complete cord injuries demonstrate loss of pain sensation, bilateral loss of motor function, loss of temperature sensation, vibratory sensation, proprioception, and tactile sensation below the injury level (Downey, 2018; Bennett et al., 2021).
Loss of sensation in the lower extremities and paralysis occur in lumbosacral injuries. Loss of bowel and bladder control may occur, as well as sexual dysfunction.
The same deficits are seen in thoracic injuries and may also include loss of muscle function in the torso, leading to the inability to maintain posture (Bennett et al., 2021).
Cervical injuries present with the same deficits as above. However, tetraplegia or loss of upper extremity muscle function may occur. If the injury is above C5, respiratory compromise may happen (Downey, 2018; Bennett et al., 2021).
An incomplete spinal injury is categorized by ASIA grades B through D (Downey, 2018). The sensation is usually preserved more than motor function because the sensory tracts are less vulnerable due to location. The anal sensation and the bulbocavernosus reflex are often present.
The most common form of incomplete spinal cord injury is called central cord syndrome.
This syndrome is characterized by impairment in the hands, the arms, and sometimes the legs. The ability of the brain to receive and send signals from the body below the site of injury is reduced. The large nerve fibers that carry information to and from the cerebral cortex and spinal cord are damaged. Arm and hand function is dependent upon these nerves (NINDS, 2021).
There may be loss of fine movements in the hands, arms, and sometimes legs with central cord syndrome. Paralysis is possible. Loss of sensory control below the injury and loss of bladder control may also occur. The patient may feel sensations such as an ache, burning, or tingling. The type and amount of functional loss depend on the nerve damage severity (NINDS, 2021).
Central cord syndrome results from damage to the neck vertebrae or herniation of the vertebral discs. Gradual weakening of the discs and vertebrae as patients age can cause this syndrome as the spinal column narrows and the spinal cord compresses (NINDS, 2021).
When the anterior 2/3 of the spinal cord is affected, it is called anterior cord syndrome. This incomplete cord syndrome results in motor paralysis below the injury. There will also be loss of temperature and pain sensation before the level of injury.
There can be symptom variability depending on the area of the spinal cord affected. Other symptoms include back pain, neurogenic bowel or bladder, hypotension, and sexual dysfunction. There is usually resulting paraplegia or quadriplegia (Pearl & Dubensky, 2021).
Ischemia of the anterior spinal artery (ASA) causes anterior cord syndrome. The ASA supplies most of the blood to the anterior portion of the spinal cord. The vertebral arteries at the foramen magnum from the ASA run within the anterior median sulcus to the conus medullaris in the spinal cord (Pearl & Dubensky, 2021).
Severe spinal cord injury causes spinal shock. High-impact and direct trauma causes severe spinal cord injury. Those with spinal shock usually present as a trauma case. Spinal shock can also be caused by ischemia. Traumatic spinal shock and ischemic spinal shock are treated differently (Ziu & Mesfin, 2021).
The ABCD prioritization mnemonic: Airway, Breathing, Circulation, Disability can be used to assess a patient with a potential spinal cord injury.
A traumatic spinal injury should be assumed if the patient:
A brief neurological status assessment should be performed. A global evaluation of the level of response from the patient and the patient’s posture should be recorded. Any posturing and pupil asymmetry should be noted.
A recommended system is the AVPU mnemonic (Kaplan, 2021):
The Glasgow Coma Scale (GCS) and the patient's mental status should be assessed (Table 3).
Providers should also be aware of a spinal cord injury or severe head injury. Spontaneous respiratory effort and movement of extremities should be observed (Romanelli & Farrell, 2021).
| Test | Response | Score |
|---|---|---|
| Eye Opening | Never | 1 |
| To Pain | 2 | |
| To Verbal Stimuli | 3 | |
| Spontaneously | 4 | |
| Best Verbal | No Response | 1 |
| Incomprehensible Words | 2 | |
| Inappropriate Words | 3 | |
| Disoriented and Converses | 4 | |
| Oriented and Converses | 5 | |
| Best Motor | No Response | 1 |
| Extension Abnormal (Decerebrate Rigidity) | 2 | |
| Flexion Abnormal (Decorticate Rigidity) | 3 | |
| Flexion Withdrawal | 4 | |
| Localizes Pain | 5 | |
| Obeys Commands | 6 | |
| Total Score | 3 - 15 | |
There are some signs that indicate impending herniation due to a mass or edema. Signs and symptoms include impaired or absent light reflexes, pupillary asymmetry or dilation, and weakness.
If these symptoms are found, they indicate a traumatic brain injury (TBI). There is an emergent need for the treatment of intracranial hypertension. This form of hypertension can be treated by hypertonic saline, IV mannitol, muscle relaxants, and sedatives. Urgent neurological and neurosurgical consult is needed.
Spinal cord injury is indicated by paraplegia or quadriplegia but without a depressed level of consciousness. Complete spinal immobilization is necessary if a spinal cord injury is suspected. Endotracheal intubation should be performed if inspiratory efforts are weak, or a high cervical cord lesion is suspected.
Continuous GCS assessment should be performed.
There should be minimal movement of the spine. There are some techniques to minimize spine movement and include:
When patients are triaged, they are grouped based on their injury and the severity of the injury.
The patient with a spinal cord injury can be triaged based on the anatomy, physiology, and mechanism of injury.
Physiology (Ahuja & Fehlings, 2016):
Anatomy (Ahuja & Fehlings, 2016):
Mechanism of Injury (Ahuja & Fehlings, 2016):
There has been rapid development in imaging technology which has increased successful diagnosis and management of spinal cord injuries. MRIs truly allow for a noninvasive visualization to aid in diagnosing an SCI. Both acute and chronic SCIs can benefit from imaging due to their prognostic significance (Goldberg & Kershah, 2010).
The initial value of MRI in detecting and evaluating fractures was thought to be limited. CTs have also been perfected and are the first-line modality for evaluating the traumatized vertebral column (Kurpad et al., 2017; Goldberg & Kershah, 2010).).
Initial diagnosis of spinal trauma is recorded on multiplanar views. Coronal reconstruction can also be helpful when viewing the craniocervical junction to check for scoliosis. Usually, a CT angiography is performed to rule out cervical fractures. CTs are also used when there is penetration involved.
CTs are like plain radiography or X-rays in that they detect differences in tissue. MRIs show varying degrees of potential injury due to the power of the magnetic field. It is pertinent to know that the scanning parameters are altered when generating weighted images (Goldberg & Kershah, 2010). T1- weighted images show fat, fluid, and possible hemorrhages. T2-weighted images will show similar findings but will have hyperintense images. Short inversion recovery (STIR) imaging has been used to suppress fat for better visualization. Gradient-echo imaging aids in showing if bleeding is present (Kumar & Hayashi, 2016).
Diffusion-weighted imaging (DWI) uses echo-planar sequences that show changes by the movement of protons (Goldberg & Kershah, 2010). DWI is often used in traumatic brain injury and cerebral ischemia. DWI may not be the choice test when evaluating the spinal cord due to motion and pulsations.
Safety is a requirement when performing an MRI. The magnetic field in an MRI is so powerful. Any objects on the patient must be compatible with an MRI. Caution should be given to neurostimulator devices, pacemakers, intravascular stents, and implanted devices. Hemodynamic monitoring, blood pressure, and pulse oximeter measurements should be monitored. The patient should be stabilized on a slider board when performing an MRI, as this helps minimize neck movement (Goldberg & Kershah, 2010). The patient should be observed via video during scanning as well (Kumar & Hayashi, 2016).
We will now review each imaging modality separately.
There is a category of spinal cord injury without radiographic abnormality, and it is titled SCIWORA(Cao et al., 2022). It is described as neurologic deficits without a bony injury showing on an x-ray or CT scan. When using an MRI, it can detect spinal cord injuries without the absence of bony abnormalities. However, some patients have SCIWORA and no detectable damage on MRI.
This phenomenon can be explained by transient ligamentous deformation with spontaneous reduction. This injury is usually seen in children as they have weak and elastic muscles, which do not always adequately protect the spinal cord.
Other potential causes of SCIWORA include epidural or intramedullary hemorrhage, fibrocartilaginous emboli from an intervertebral disc ruptured into the radicular artery, radiographically occult intervertebral disc herniation, and traumatic aortic dissection with spinal cord infarction (Cao et al., 2022). An MRI can detect these.
Suppose a patient has severe and persistent pain, paresthesia, or focal neurologic findings (upper extremity weakness) without an obvious fracture on an x-ray or CT. In that case, a cervical ligamentous injury should be suspected. These injuries can be unstable but are not usually associated with permanent neurologic injury.
X-rays can provide visualizations of fractures, alignment, and soft tissue swelling.
X-rays are the first method of evaluation of a SCI. A complete cervical X-ray includes later open-mouth odontoid views and the anteroposterior view. Oblique views help to visualize facet injuries or lateral mass. The top of T1 and the cervical vertebrae must be seen.
If a male patient is muscular and presents with a neck injury, pulling the shoulders and wrist down in a straight line downwards toward the feet may help visualize the lower cervical vertebrae. If the top of T1 and the lower cervical levels are not visualized, a swimmer’s view should be performed.
If there are neurologic signs and symptoms, further studies besides X-rays may be needed. Anteroposterior, lateral, and oblique X-rays may be required if there is pain in the lumbar and thoracic areas.
Helical CT scanning with sagittal and coronal views may be used instead of X-rays. These images are more sensitive than X-rays, especially in cervical spine fractures. Patients can get this study done in a prone position. If there is a suspected head injury, it may be most cost-effective and time-efficient to use CT as the initial imaging study of the neck.
A more detailed CT with 2 mm cuts should be used to follow up on injuries seen on the x-ray. Because CT is more sensitive than plain X-rays, patients suspected of having a spinal injury and having normal plain X-rays should also undergo CT.
The CT can better assess the spinal cord patency over X-rays. The CT can also visualize the paravertebral soft tissues of the spine. However, the CT is still inferior to the MRI.
Myelography is not often used when an MRI is available. However, myelography can be used if CT and MRI are unavailable and suspected spinal canal compromise.
The indications for MRI in evaluating acute TSCI have not been defined. MRI helps to determine the extent of the spinal cord injury. It should be performed on patients who are stable.
MRI has an advantage as it provides a detailed image of the spinal cord, including the intervertebral discs, ligaments, and paraspinal soft tissues. It is superior to CT scans and is more sensitive in detecting epidural hematomas. The CT, however, is better for assessing bony structures.
The chief disadvantages of MRI include (Fehlings et al., 2017):
If the patient’s medical status allows, an MRI can provide valuable information that can complement a CT scan regarding the mechanism of injury and the extent of the damage, which can influence treatment and prognosis.
An MRI is also indicated when the patient suspected of having an SCI has a negative CT scan. An MRI is used to detect an epidural hematoma, disc injury, or occult ligamentous injury. Patients who are not alert require an MRI in addition to CT to exclude various spinal cord injuries. If obtunded patients have grossly normal motor movement in all extremities, a CT scan should be sufficient in this population (Fehlings et al., 2017).
Patients with spinal cord injuries require intense medical care and continuous monitoring. Monitoring cardiac rhythm, vital signs, neurologic signs, and arterial oxygenation should occur. Neurologic and systemic complications are common in the first days to weeks after injury. These complications can change the patient’s prognosis and can be avoidable if caught and treated early.
Medical issues management specific to spinal cord injury include the following:
Neurologic findings can be most helpful in patients with normal blood glucose levels, normal blood pressure, and no sedation (Clark et al., 2021). This is essential as any of these issues and sedation can alter the exam's signs and symptoms and utility.
When a patient has experienced trauma, a neurologic exam should be focused on assessing the central nervous system. Testing the cranial nerves, mental status, reflexes, and sensory and motor function is essential. If a patient is unconscious, reflexes and the cerebral input level should be monitored closely. All basal functions should be tested (Clark et al., 2021).
A more detailed exam of the cognitive function is performed by examining alertness or consciousness level. Awareness of both the external and internal environment is essential. Patients should be alert (respond appropriately), awake, and oriented (know who they are). Patients may experience mild sleepiness or even be completely unarousable in a coma. Properly describing the patient's awareness and consciousness is essential (Novick et al., 2018).
Such descriptions can include (Clark et al., 2021):
In patients who are awake and alert, cognitive function can be assessed (Clark et al., 2021). Obtaining a medical history and having the patient describe the traumatic events aid in testing language and memory function. Having the patient recall three simple objects (apple, house, car) immediately and after 5 minutes is specific to memory function. Asking patients to spell a simple word both forward and backward (e.g., life) or subtracting 7 serially from 100 (e.g., 100, 93, 86, 79, etc.) tests the cortical function.
Speech and language issues should be evident in conversation (Clark et al., 2021). If patients have had significant head trauma, they may speak in a monotone voice or have a flat affect. They may also appear devoid of emotion and have no inflection in their voice at all.
Twelve cranial nerves are tested (Clark et al., 2021). Examination of these cranial nerves shows brainstem dysfunction in acute trauma (Assir & Das, 2021).
The only nerve not tested due to no significance is the olfactory nerve (CN #1).
The “blink-to-threat” test for comatose patients can be assessed to determine the optic nerve function (CN #2) (Clark et al., 2021). The patient should blink in response to rapid hand movement in front of the eyes in different directions if the patient is awake and responsive. Patients who are awake and responsive can vocalize findings and have their visual acuity tested by a Snellen eye chart. Defects and blind spots in the visual field should be assessed. To assess this, the patient should fixate on an object straight ahead and report when they can see a finger move into the four visual quadrants. Testing both eyes separately is essential.
Eye vision, position, and movements are vital in assessing the function of the CNs (Clark et al., 2021). Pupillary responses are among the most important parts of the neurologic exam in patients with impaired consciousness. If the patient has a normal pupillary response, the optic nerve and oculomotor nerve (CN#3) are intact. The pupil shape and size should be noted while the patient is at rest. Pointing a light near the patient's eyes, each done twice should occur to assess the response of the illuminated pupil and then again to evaluate the consensual response of the non-illuminated pupil. Typically, the pupil should constrict or shrink in response to light (Clark et al., 2021).
Having the patient close one eye and focus on a finger while it is moved can test the oculomotor nerve (CN #3), the trochlear nerve (CN #4), and the abducens nerve (CN #6) (Clark et al., 2021). With one eye closed on the patient, move the finger in different directions from a central point. Move the finger vertically, diagonally, and horizontally. While doing so, examine each eye closely to look for abnormal or weak eye movements. The conjugate gaze functions can be assessed if the same steps are completed with the eyes open. Note any dysconjugate gaze (failure of the eyes to move in the same direction), nystagmus (repetitive, uncontrolled eye movements), or fixed deviation of the eyes in a particular direction (Clark et al., 2021).
CN 3, 4, and 6 can also be assessed when patients are comatose by eliciting a normal physiological response called the “oculocephalic reflex.” This reflex can be performed by holding the patient’s eyes open and rotating the head up and down and from side to side (Clark et al., 2021). If there are head and neck injuries, this should not be performed. The normal oculocephalic reflex is present if the eyes move in the opposite direction of the head movement (e.g., turning the head rightward causes leftward deviation of the eyes to maintain fixation of gaze, sometimes termed “doll’s eyes” movement) (Clark et al., 2021).
Touching each cornea gently with a cotton wisp can test the corneal reflex should elicit a bilateral blinking reflex (Clark et al., 2021). If there is any facial grimacing, it should be noted. Check for facial grimacing by rubbing vigorously on the supraorbital ridge or the bony prominence above each eye. These can be used to assess the trigeminal nerve's function (CN #5) and facial nerve (CN #7).
The trigeminal nerve can be tested by evaluating the mastication muscles and symmetric sensation in the face. Patients who are alert and awake can also demonstrate facial nerve function by puffing out their cheeks, smiling, wrinkling their eyebrows, and clenching their eyes tight. If there is asymmetry, it should be noted (Clark et al., 2021; Mount Sinai Health System, 2021).
Alert patients can also have the vestibulocochlear nerve (CN #8) tested (Clark et al., 2021). This can be tested partially through conversation. Still, direct testing can be done by rubbing fingers together right beside the individual’s ear. While performing this action, the patient should note if the sound is symmetric in both ears.
The vagus nerve (CN #10) and the glossopharyngeal nerve (CN #9) can be tested in an unresponsive patient through the gag reflex (Clark et al., 2021). This reflex can be elicited by touching the base of the tongue or the posterior pharynx with a cotton swab. The patient’s mouth should be opened, and a light shone in to evaluate and visualize the symmetric elevation when responding to the tactile stimulus. If the patient has an endotracheal intubation setup, this response can be elicited by using a suction tube (Clark et al., 2021).
Asking patients to shrug their shoulders against resistance and asking them to rotate the head in lateral directions against resistance and opposition tests the accessory nerve (CN #11) (Clark et al., 2021). Asking the patient to stick their tongue out, push it forcefully against the inside of each cheek, and move the tongue side to side tests the hypoglossal nerve (CN #12) (Clark et al., 2021). Note any weakness or deviation.
A sensory exam can be performed in responsive patients (Clark et al., 2021). It cannot be done in unresponsive patients as it relies on the ability of patients to report what they are feeling. This also causes some uncertainty in patient reports. Different types of sensations are brought to the brain from different pathways. Patterns of sensory impairment can help diagnose the nature or location of an injury. The surface of the skin should be systematically tested in all extremities to determine any deficits (Clark et al., 2021).
A light touch is assessed by applying a cotton swab, but a soft finger touch will often suffice (Clark et al., 2021).
Pain sensation can be assessed by using a safety pin (Clark et al., 2021). The sensation of “dull pain” can be tested using the rounded/dull portion, while the sensation of “sharp pain” can be tested using the pinprick end.
When the provider grasps the sides of the distal phalanx of a toe or finger and slightly displaces the joint up or down, this tests the joint position sense (Clark et al., 2021).
Vibration sensations and temperature are not urgently tested in most trauma situations (Wang, 2020).
Palpation, inspection, and functional testing of strength and tone make up a motor examination. Before beginning, observe, inspect, and palpate to detect visible abnormalities (Clark et al., 2021). Involuntary movements, muscle cramps, and tenderness should be noted. The patient’s injuries should be assessed before this examination so as not to worsen any existing injuries.
Some functional tests should be performed before testing strength (Clark et al., 2021):
Palpating the muscles of the extremities helps to judge muscle tone. If there is any movement resistance, it should be noted.
Muscle strength should be assessed in the extremities, neck, and trunk.
Provide resistance to the movement of the different muscles in either direction and assess if any of the strength is diminished (Clark et al., 2021). There is a scale that describes muscle strength and is rated on a scale of 0/5 to 5/5 as follows (Clark et al., 2021; Galgano et al., 2017):
When the deep tendon reflexes are tested, the motor and sensory fibers at their spinal level are tested (Clark et al., 2021). A percussion or reflex hammer can be used to assess the stimulus of a stretching muscle. The left and right side responses should be compared, noting any asymmetry.
Reflex responses to stimuli can be expected. Deep tendon reflexes often are rated according to the following scale (Clark et al., 2021):
Some reflexes are more commonly tested than others. There are specific ways to test these reflexes. Testing does require a percussion hammer (Clark et al., 2021).
To test the biceps reflex (C5/C6), one should hold the patient’s elbow at a right angle, flexed, with their palm facing upward. The examiner should place their thumb on the biceps tendon on the medial side. The examiner would then strike the thumb to elicit a slight flexion at the elbow (Clark et al., 2021).
To test the triceps reflex (C7), the patient’s elbow should be supported in the examiner’s hand (Clark et al., 2021). The forearm of the patient should hang downward towards a right angle. The examiner should strike the triceps tendon above the bony prominence. There should be a small extension of the arm.
To test the knee reflex (L2/L3/L4), the patient should be sitting at the edge of a table with the legs dangling or hanging loosely. The examiner should strike the patellar tendon with a percussion hammer. The knee should extend slightly (Clark et al., 2021).
The ankle reflex can be tested by holding the patient’s foot while the leg hangs loosely. The Achilles tendon should be struck, and there should be a slight plantarflexion (Ng & Lee, 2019).
Coordination and gait are usually tested separately. This is because cerebellar damage can disrupt coordination or gait even if other motor functions are still intact (Clark et al., 2021).
If the patient can walk, that should be assessed first. Observe the patient’s ability to walk in a straight line when walking. Also, observe the gait, posture, and coordinated automatic movements (swinging arms). Any abnormal motions or asymmetric movements should be noted (Clark et al., 2021).
To conduct the Romberg test, the patient should stand with their eyes closed and their heels and toes together (Clark et al., 2021). The examiner should be at the bedside and prepared to catch the patient if it goes wrong. If there is specific brain damage, the patient may fail to maintain posture, or they may sway.
When performing the finger-to-nose test, the patient places the tip of a finger on their nose and then touches the examiner’s finger, which is placed at arm’s length distance away (Clark et al., 2021). This performance should be repeated rapidly while the examiner changes the finger's location. The heel-to-shin test is the same test for the lower extremities. In this test, the patient places a heel on the opposite knee and then moves the heel along the shin, up and down. Each extremity should be tested separately in both the finger-to-nose and heel-to-shin tests.
A fundoscopic exam should be performed to visualize the retina and other structures of the eye. It should be noted if there is a blurred or swollen optic disc named papilledema. Direct head trauma may cause an intraocular collection of blood or a subhyaloid hemorrhage and should be noted.
Respiratory status and function can be evaluated for clues to neurologic function (Clark et al., 2021). Any irregular or abnormal breathing patterns should be noted.
Several findings may be present as a result of direct head trauma (Clark et al., 2021; James et al., 2019):
The cardiovascular effects in spinal cord injuries depend on the degree of injury and the level of trauma (Calvo-Infante et al., 2018). Patients with cervical injuries are at an increased risk of ventricular and atrial arrhythmias, cardiac arrest, and other cardiac complications (Calvo-Infante et al., 2018). These cardiovascular complications usually occur in the first month or so. Directly after a spinal cord injury, smooth muscle loss in the arteries causes vasodilation and hypotension (medullary shock). Given the mechanisms of trauma, this can be confused with hypovolemia. The parasympathetic tone may also be increased and become sensitive to stimuli (Calvo-Infante et al., 2018). Stimuli such as nasogastric tubes, hypoventilation, or endotracheal tubes can trigger a vagal response causing abnormal cardiovascular responses. This occurs more in patients with complete injuries and can be permanent. In patients with incomplete injuries, it usually disappears within a month.
These are the most common cardiovascular complications after trauma to the spinal cord (Calvo-Infante et al., 2018):
An orthostatic maneuver is defined as a decrease of at least 20 mm Hg in the systolic blood pressure and/or a decrease of at least 10 mm Hg in diastolic blood pressure. This is more common in patients with upper thoracic or cervical spinal cord injuries. There is a lack of sympathetic innervation in the cardiac system, which means hypotension could be severe in the acute phase (Calvo-Infante et al., 2018). This presents a challenge for treating spinal cord injuries. If hypovolemia secondary to trauma is noted, it will also challenge treatment.
Symptoms accompanying orthostatic hypotension include fatigue, dizziness, blurred vision, and agitation. These symptoms are due to cerebral hypoperfusion. The time span between the injury and the surgery may correlate with the number of cardiovascular complications. Arterial pressure should be between 85-90 mm Hg for the first week after a spinal injury occurs. Patients should be kept hydrated to prevent hypovolemia (Yarar-Fisher et al., 2017).
Patients with cervical or high thoracic injuries may have sudden episodes of peripheral vasoconstriction with dysautonomia. This is usually in response to hyperstimulation below the injury level. Intestinal or bladder distention is the most common stimuli. Other signs and symptoms include dizziness, headache, vomiting, nasal congestion, increased heart rate, and a 20% increase in basal blood pressure. Patients are treated conservatively by eliminating what is harming the patient. Alpha 1 blockers, calcium antagonists, ACE inhibitors, or intravenous nitrates could be used to treat hypertension.
In patients with spinal cord injuries, cardiac arrhythmias are higher after the acute phase of injury. The risk decreases as time passes on. The first few weeks are usually the most critical. The most common arrhythmia is bradyarrhythmias. Coupled with hypotension, bradyarrhythmias can lead to hemodynamic instability. Chronically, bradyarrhythmias are more common in patients with tetraplegia.
Tachyarrhythmias occur when dysautonomic dysreflexia is present and immediately requires treatment. Patients with spinal cord injuries are at risk for conduction disorders such as atrial and/or ventricular extrasystoles, branch blocks, and ST-segment elevation, to name a few (Calvo-Infante et al., 2018). Providers must be careful when performing maneuvers that could increase vagal tones, such as tracheal suction and laryngoscopy (Calvo-Infante et al., 2018). They could easily trigger bradyarrhythmias or even asystole.
The first-line treatment for bradycardia is dopamine. If there is no response to dopamine, transcutaneous pacemakers and atropine is usually used. A transvenous pacemaker may be used if the bradycardia is prolonged and severe. Preventive treatment should occur and provides should avoid maneuvers that create an increase of the parasympathetic tone (Calvo-Infante et al., 2018).
Approximately 20% of deaths from spinal cord injuries are associated with coronary heart disease (Calvo-Infante et al., 2018). This disease increases due to obesity, diabetes, hyperlipidemia, insulin resistance, and being physically inactive. In the chronic phase of a SCI, patients exhibit increased LDL cholesterol and decreased HDL. This could be due to an inappropriate diet, adrenergic dysfunction, and lack of exercise (Yarar-Fisher et al., 2017).
Eliminating the stimulus that causes dysautonomic dysreflexia improves tension and symptomatology (Calvo-Infante et al., 2018).
Prevention measures should be taken to prevent new stimuli from causing the same problem. Place the patient upright to redistribute the blood flow to the lower body (Calvo-Infante et al., 2018). Most cases of dysautonomic dysreflexia are solved without the use of medications. However, there are some cases where pharmacological management is necessary, especially in patients with cervical or high thoracic injuries. Nitrates are commonly used, both topically and orally. Intravenous sodium nitroprusside is reserved for patients with extremely high blood pressure. Dihydropyridine calcium antagonists are also widely used, but evidence suggests it could cause hypotension and medullary ischemia (Calvo-Infante et al., 2018). Prazosin, an alpha-1 blocker, is sometimes prescribed prophylactically to prevent dysautonomic dysreflexia from occurring.
Many nonpharmacological and pharmacological treatments must occur with deep vein thrombosis. Physical therapy, early limb immobilization, and intermittent compression measures should be taken. Low molecular weight heparins are often used to prevent thrombi formation as they do not increase the risk of bleeding. Mechanical prophylaxis has been shown to be less effective (Calvo-Infante et al., 2018). If a patient does develop a DVT, patients should be treated with intravenous heparin as soon as possible and are continued with oral anticoagulants for at least three months. Some studies show oral anticoagulants should be taken for six months in patients with spinal cord injuries. A lower vena cava filter may be used if there is a DVT in a patient who cannot take anticoagulants.
Treating cardiovascular disease and dyslipidemia includes reducing risk factors. These risk factors include obesity, physical activity, smoking, increased blood pressure, and poor cholesterol management. Statins are effective as secondary prevention for cardiovascular disease (Calvo-Infante et al., 2018). Still, atorvastatin has shown neuroprotective effects, decreases pain at 3-6 months, and the molecular level causes a significant decrease in IL-1 β, IL-6, etc., and lipid peroxide (Calvo-Infante et al., 2018). Patients benefit from lipid-lowering activity and the pleiotropic effects of statins, such as improving endothelial dysfunction, reducing platelet activity, stabilizing atherosclerotic plaques, and others (Calvo-Infante et al., 2018).
A neurogenic shock is defined as a systolic blood pressure <100 mm Hg and a heart rate of less than 80 beats per minute (Calvo-Infante et al., 2018). There is a sudden loss in autonomic tone due to a spinal cord injury with neurogenic shock. There is a decrease in systemic vascular resistance and vasodilation caused by an altered vagal tone. Managing neurogenic shock should focus on prevention. It should start immediately with identifying if a patient has a spinal cord injury (Moscote-Salazar et al., 2018).
Respiratory problems are the most common cause of mortality after a spinal cord injury (Ameer et al., 2021). Patients are most vulnerable in the first year. Respiratory complications suffered during admission and immediately following will more influence the length of hospital stay than the level of spinal cord injury will (Ameer et al., 2021). The ability of a patient to take a deep breath and cough is usually impaired depending on the spinal cord injury.
Directly after an SCI, patients tend to experience spinal shock that results in flaccid paralysis below the injury that could last for months. Flaccid paralysis of the intercostal muscles could create an unstable chest wall causing paradoxical inward depression of the ribs (Ameer et al., 2021). This means there is not efficient ventilation, but there is an increased work of breathing and an increased risk of microatelectasis and airway collapse. Airway secretions can back up due to increased production or the inability to cough effectively. If this occurs, ventilation and respiratory support may be necessary.
The tendons, ligaments, and joints in the rib cage tend to stiffen due to weakness and a reduction in chest wall movement (Berlowitz et al., 2016; Ameer et al., 2021). This can help stabilize the rib cage since this is a lower absolute lung volume. The resolution of spinal shock may also improve lung volumes as the thoracic and abdominal muscles begin to develop increased spasticity (Berlowitz et al., 2016).
The risk of respiratory failure is associated with the level of injury. Cord swelling and bleeding occur rapidly, which makes the patient very high-risk. Patients with a complete cord injury above C5 usually have impaired diaphragm function and require mechanical ventilation through endotracheal intubation (Ameer et al., 2021). A C5 injury may also cause diaphragm weakness, but patients can generally breathe independently. Patients also lack cough effort, have impaired inspiration, and exhibit no extremity movement. A patient with a complete T12 injury will have full upper body strength and balance, no observable inspiratory or expiratory impairment, but also no lower limb movement (Berlowitz et al., 2016; Ameer et al., 2021).
Patients with a spinal cord injury are at risk for many factors that could induce respiratory impairments. Patients with incomplete injuries have some feeling and movement preserved below their injury level (Ameer et al., 2021). These patients will improve the remaining function of the muscles and systems below the injury. Since traumatic brain injury often occurs in spinal cord injury patients, maintaining the airway is essential. Patients with an SCI will often have internal organ damage, rib fractures, and thoracic cage trauma.
Nearly 50% of patients with tetraplegia have pulmonary edema. Causes can be multifactorial but most often are caused by excessive fluid resuscitation in the presence of hypotension (Ameer et al., 2021). The risk of pulmonary embolism increases after a SCI. In the first month post-injury, SCI patients have 500 times the risk of death from pulmonary embolism (Ameer et al., 2021).
Lung function and respiratory muscle pressure decrease over time (Berlowitz et al., 2016). Ventilation patterns change within the first year after a spinal cord injury. Flaccid paralysis of the abdomen may occur after injury, which results in up to 90% of paraplegia. The residual capacity of the lungs also decreases and is associated with fibrosis and atelectasis (Berlowitz et al., 2016).
Moving from upright to supine affects the tetraplegic and high paraplegic individuals' respiratory function differently from non-disabled people (Berlowitz et al., 2016). Postural changes can cause specific symptoms in patients with a SCI. Patients with a high spinal cord injury report less breathlessness when supine than sitting (Berlowitz et al., 2016). The weight of the abdomen and internal organs forces the diaphragm to rest higher when in the prone position. This produces a greater excursion of the diaphragm.
The ability to produce an effective cough is severely impaired in patients with cervical or high thoracic SCI (Berlowitz et al., 2016). Patients may lose the ability to produce expiration forcefully if there is a loss of innervation in the internal intercostals and abdominal muscles. If patients have an injury between C5-C8, they may be able to utilize the clavicular portion of the pectoralis major to generate an expulsive force.
People with SCI have marked impairment of respiratory function and strength after injury (Berlowitz et al., 2016).
After a spinal cord injury, obstructive sleep apnea is the most common problem. It usually appears in up to 80% of cervical injury cases within a year after a SCI. Patients with this form of apnea are also prone to impaired cognition and cardiac disease (Berlowitz et al., 2016).
Observing the patient’s breathing pattern to identify unequal chest wall movement of paradoxical breathing is essential in patients with a SCI (Berlowitz et al., 2016). View the patient in a supine position at the foot end of the bed to view whether there is asymmetry with deep inspiration. Other assessments include simple spirometry, respiratory muscle strength, and sniff nasal inspiratory pressure which can all be done at the bedside.
Patients are stabilized early after a spine injury. Patients are usually intubated for surgery, admitted to an ICU, and surgically stabilized. After this, patients can be sat up and out of bed. This upright position may lead to increased work of breathing and hypotension (Ameer et al., 2021).
Restoring lung volume in patients with high paraplegia is essential. Intermittent positive pressure breathing (IPPB) by a mouthpiece may be used to increase the volume and flow of the lungs (Ameer et al., 2021).
Insufflation using a noninvasive ventilator can be used to boost inspiratory volumes before assisted coughing.
When a resuscitation bag is used with a facemask or mouthpiece, it is called breath stacking. Two or more breaths before exhalation are delivered to augment lung volume. This treatment can easily be provided at home (Ameer et al., 2021).
Glossopharyngeal breathing (GPB) can increase lung volumes and assist secretion clearance in people with high tetraplegia (Ameer et al., 2021).
A large inspiratory effort followed by a quick and forceful expiration is needed to achieve a successful cough (Berlowitz et al., 2016). A compressive force directed inwards and upwards under the diaphragm may provide manual expiratory assistance and replace the work of the abdominal and internal intercostal muscles (Berlowitz et al., 2016; Ameer et al., 2021). The applied pressure must be synchronized with the patient’s breathing effort (Berlowitz et al., 2016).
Respiratory muscle training (RMT) can help improve respiratory muscle strength, endurance, and function (Berlowitz et al., 2016; Ameer et al., 2021). RMT can increase maximal expiratory pressure, maximum voluntary ventilation, inspiratory capacity, and vital capacity.
Elasticated abdominal binders can minimize postural hypotension effects. This binder restores pressure transference across the thorax and abdomen and decreases abdominal compliance (Berlowitz et al., 2016; Ameer et al., 2021). This allows the diaphragm to assume a more normal resting position in the upright posture.
Secretion and ventilation management efforts are different in individuals with pulmonary dysfunction. Secretions can accumulate due to poor cough, increased production, and aspiration of saliva. Atelectasis can lead to impaired aeration, infection, and pneumonia (Ameer et al., 2021).
Long-term ventilation may be required in nearly 8% of patients who survive a high SCI. Quality of life can suffer after a high SCI, but there are ways to increase the quality of life. However, the first year after a high SCI injury is usually stressful as it requires many life changes and coordination. Comprehensive training and peer support can aid in making this time easier (Berlowitz et al., 2016).
Venous thromboembolisms (VTE) are a very common occurrence after a SCI. They are, in fact, the leading cause of mortality. Most DVTs and VTEs occur within the first two weeks after a SCI (Godat, 2015). There are specific risk factors that place a patient at risk for a VTE. Three significant risk factors are venostasis, hypercoagulation of the blood, and endothelial injury, causing pressure on the veins. This is called the Virchow's Triad (Eichinger et al., 2018).
Doppler ultrasonography (DUS) may monitor if a VTE is forming. Leg compression devices and stockings can help prevent VTEs (Eichinger et al., 2018).
Patients followed long-term after a SCI show a lower risk of a VTE. Long-term research studies show that effective prevention of VTEs is essential. After the first year of an SCI, the mortality risk due to a pulmonary embolism is 210 times greater than that of a patient without an SCI. Each year that passes, the risk of a VTE decreases significantly.
Nearly 15% of patients die within the first year after a SCI due to a VTE. Thromboprophylaxis has decreased the risk of VTE significantly.
When using opiates with potential sedating properties, pain control must be balanced with the need for ongoing clinical assessment, particularly in patients with a concomitant head injury. Pain can be reduced by stabilizing and realigning the fracture by external orthosis or surgery.
Pressure sores commonly develop on the heels and buttocks and can develop quickly (within hours) in immobilized patients. To prevent pressure sores:
Urologic evaluation should occur regularly for all patients after SCI. An indwelling urinary catheter should be placed to avoid bladder distension. Urinary output should be monitored. Urine output should be more than 30 mL/h. Within a week after surgery, intermittent catheterization can be substituted, reducing the incidence of any type of infection.
Patients with cervical cord injuries are at high risk for stress ulcers. Proton pump inhibitors can be used to combat this and are recommended upon admission for four weeks.
Bowel motility can be slowed for a few days to weeks after a spinal cord injury. A nasogastric (NG) tube is essential to prevent aspiration. Patients should be monitored for bowel sounds and bowel emptying. Patients should not ingest food or liquid until motility is restored.
Patients are not always able to control their temperature after an SCI. This usually occurs in patients with high thoracic and cervical injuries. This is because there is reduced sensory input to thermo-regulating centers.
Hypothermia should be prevented. Patients with a SCI lack vasomotor control and cannot sweat below the lesion (Jayakumar et al., 2017). The patient’s temperature may vary with the environment and needs to be maintained (Jayakumar et al., 2017).
Temperature interventions may include (Jayakumar et al., 2017):
Occupational and physiotherapy should be started as soon as possible. Psychological counseling is also best offered to patients and relatives as early as possible.
Enteral or parenteral feeding should be provided within a few days after SCI.
Changes in sweat secretion are common after patients have a SCI. Absence of sweating (anhidrosis), diminished sweating (hypohidrosis), and excessive sweating (hyperhidrosis) may occur (Hagan, 2015).
Episodic hyperhidrosis usually occurs with other autonomic dysfunctions such as autonomic dysreflexia, post-traumatic syringomyelia, and orthostatic hypotension (Hagan, 2015). Patients typically experience profuse sweating over the level of injury, and minimal/abolished sweating under the level of injury. This is because of a compensatory increase in sweat secretion due to the loss of sympathetic stimulation below the level of injury. Sweating excessively may also occur below the injury level and is usually a symptom of a significant autonomic response.
Heterotopic ossification (HO) is irreversible and involves the para-articular formation of mature lamellar bone in soft tissues (Hagan, 2015). This occurs below the level of injury and usually in the first three weeks post-injury. Patients suffer from a reduction in the joint's range of motion. The hip and knee are the most affected.
Bladder dysfunction is common immediately after an SCI and is classified as either an upper or lower motor neuron syndrome in the chronic phase (Hagan, 2015).
Upper motor neuron syndrome, also called reflex bladder, involves loss of inhibition of the reflex arcs due to the disturbance of descending spinal tracts. This leads to detrusor hyperactivity, often combined with detrusor sphincter dyssynergia (Hagan, 2015).
Lower motor neuron syndrome is due to injury to the sacral (S2-S4) part of the autonomic nervous system (Hagan, 2015). This results in diminished motor stimulation of the bladder and the detrusor muscle's reduced or absent contractility. The bladder then becomes enlarged.
Almost 62% of patients with an SCI report bowel problems. Symptoms include distention, pain, and obstipation. Other symptoms include incontinence, autonomic dysreflexia, rectal bleeding, and hemorrhoids (Sezer et al., 2015).
Patients with a complete acute SCI may present with a spinal shock that includes muscle paralysis, absent tendon reflexes, and reduced muscle tone. Spasticity is usually established after nearly six months post-injury with increased muscle tone, muscle spasms, and exaggerated tendon reflexes.
Directly following a SCI, patients experience a range of feelings. Acute pain is almost guaranteed after this form of trauma. The amount of pain decreases as healing occurs. However, chronic pain is a frequent occurrence after a SCI. Nearly 80% of patients after an SCI will experience chronic pain in the form of nociceptive or neuropathic pain.
Minimizing neurological damage and preventing secondary injuries are key to decreasing the amount of chronic pain (Hagan, 2015; Sezer et al., 2015).
The blood-spinal cord barrier breaks down after a SCI due to excessive matrix metalloproteinases (MMP) activity. Leukocytes enter the cells and disintegrate them. MMPs can contribute to the pain felt after a SCI. It is possible to block the effects of MMPs with pharmacological management.
Patients with a SCI may struggle with sexual health, depending on the effects of the injury. It is essential to manage these feelings in the rehabilitation process.
Having a SCI causes psychological stress (Hagan, 2015). Even patients in good mental health are affected by the extent of injury. The patient’s current life situation plays a role in coping mechanisms. It is essential that providers look at the patient’s psychological status during care. Pain relief, proper sleep routine, and reducing overstimulation can increase a patient’s psychological health.
Patients with SCIs often experience damage to other organs and parts of the body. Extremity fractures are the most common secondary injury. Loss of consciousness, lung impairments, and traumatic brain injury are also common occurrences after an SCI (Hagen, 2015).
There is limited evidence that glucocorticoid therapy improves neurologic outcomes in patients with acute traumatic SCI, and major society guidelines do not endorse such therapy.
Methylprednisolone is a common and potent corticosteroid used to minimize inflammation. Methylprednisolone is the only treatment suggested in clinical trials to improve neurologic outcomes in patients with acute, nonpenetrating traumatic SCI (Hagan, 2015). Patients who present within eight hours of a nonpenetrating traumatic SCI should have intravenous methylprednisolone. The standard dose is 30 mg/kg IV bolus, followed by an infusion of 5.4 mg/kg per hour for 23 hours. A contraindication for the use of glucocorticoids includes the fact that it may increase mortality in moderate to severe traumatic brain injury (TBI) patients. Side effects of corticosteroids include nausea, vomiting, anxiety, and insomnia (Maher, 2021).
Many medications can treat pain. Most pain medications do come with side effects. Below are some common pain medications used in SCIs. In addition to treating pain, several of these medications are used for other complications related to SCI.
Pain after spinal cord injury can vary from mild to severe (Maher, 2021). Patients with mild to moderate pain will likely be recommended NSAIDs to help. NSAIDs may help relieve pain and swelling by slowing the production of prostaglandins, which play a huge role in reducing pain perception (Maher, 2021).
NSAIDs include naproxen, aspirin, and ibuprofen (Motrin®, Advil®). These are most commonly used to treat musculoskeletal pain. Side effects of these medications can include stomach upset or bleeding problems. These medications are easily accessible and can help relieve pain after SCI (Maher, 2021).
After SCI, individuals experiencing severe chronic pain may be prescribed narcotic analgesics or opioids. Narcotics (opiates) such as morphine, hydrocodone, codeine, and oxycodone treat neuropathic and musculoskeletal pain. These work by binding to opioid receptors in the brain and activating neurotransmitters that relieve pain and help regulate digestion, mood, movement, and reward perception. Individuals can develop tolerance and become addicted. Side effects include constipation, dizziness, sleepiness, and the fact that these medications may be habit-forming (Model Systems Knowledge Translation Center [MSKTC], 2009; Maher, 2021). While not the first consideration for chronic pain management, they should not be dismissed because of fears about dependency or side effects (MSKTC, 2009).
Muscle relaxants and anti-spasticity medications are used to treat spasm-related and musculoskeletal pain. Muscle relaxants and antispasmodics help block the transmission signals that cause muscle contractions. These medications can also help reduce the effects of bowel or bladder problems. Medications like these include diazepam (Valium®), baclofen (Lioresal®), and tizanidine (Zanaflex®) (MSKTC, 2009). These medications may be taken by mouth or delivered directly to the spinal cord through an implanted pump. The side effects of these drugs include sleepiness, sedation, decreased blood pressure, and confusion (MSKTC, 2009; Maher, 2021).
Antiseizure medications or anticonvulsants can reduce pain by suppressing the overactive transmission of pain signals below the injury level. Neuropathic pain is caused by damage to the nerves, which affects the hyperexcitability of pain signals.
Antiseizure medications such as gabapentin (Neurontin®) and Pregabalin (Lyrica®) treat this neuropathic pain (MSKTC, 2009). Side effects of these medications include dizziness, sleepiness, and swelling.
Antidepressants can be given to treat neuropathic pain in patients with a SCI (MSKTC, 2009). Such medications include selective serotonin-norepinephrine reuptake inhibitors (SNRIs), such as venlafaxine (Effexor®), and tricyclics, such as amitriptyline (Elavil®). Side effects may include dry mouth, sleepiness, dizziness, and nausea.
In addition to treating neuropathic pain, antidepressants are also prescribed for depression following SCI (Maher, 2021). Depression after a spinal cord injury is very common and can result in a lack of energy, loss of interest, inability to concentrate, and changes in sleeping and eating habits. Antidepressants like SSRIs and SNRIs, as mentioned above, can increase neurotransmitter levels in the brain responsible for regulating mood and perception of pain.
SSRIs (selective serotonin reuptake inhibitors) increase serotonin levels. They do this by blocking its reabsorption in the brain. Serotonin makes patients feel happy and helps regulate sleep and appetite (Maher, 2021). SNRIs (serotonin and norepinephrine reuptake inhibitors) work similarly to SSRIs. However, they also block the reabsorption of norepinephrine, which plays an essential role in regulating energy and alertness.
Much higher-level SCI patients have the low lung capacity and weak coughs due to paralysis or weakness of major breathing muscles like the diaphragm, intercostals, and abdominals (Maher, 2021). Patients may struggle to clear secretions in the lungs due to poor ability to cough. Patients also have a higher risk of pneumonia. Antibiotics kill bacteria to prevent the spread of infection and help clear the lungs of mucus buildup, so it is easier to breathe and cough (Maher, 2021).
Surgical management should be considered in patients who are likely to benefit from either fracture reduction, decompression, mechanical stabilization, and/or deformity correction (Wang et al., 2021). These interventions can eliminate the source of possible secondary injury and promote patient recovery (Wang et al., 2021).
The mechanism, type of injury, severity of other bodily injuries, and clinical exam are crucial in determining the appropriate timing of surgery following SCI (Wang et al., 2021). For example, timely surgery is imperative in cases of acute cord injury in which a herniated disc is causing ischemia secondary to anterior spinal artery (ASA) compression with evidence of exam deficits (Wang et al., 2021). Patients with stable neurological exams should undergo decompression within 24 hours to potentiate improved outcomes compared to late decompression (Wang et al., 2021).
Decompression surgery aims to relieve the pressure of the spinal cord and/or spinal nerves (Fehlings et al., 2019). This can be achieved by the removal of damaged structures such as a herniated disc, a bone fracture, or soft tissues pressing on the cord and nerves (Fehlings et al., 2019). This will then create space around these neural elements (Fehlings et al., 2019). Multiple decompression procedures exist, including laminotomy and laminectomy (Fehlings et al., 2019).
Spinal stabilization surgery often involves instrumentation (implantable devices) and fusion of the spine (Fehlings et al., 2019). The devices for instrumentation include rods, screws, plates, or interbody cages. While instrumentation provides an element of immediate spinal stabilization, the fusion is the “glue” holding it together. Spinal fusion entails autograft or allograft packed into and around the instrumentation to promote bony ingrowth and healing (Fehlings et al., 2019).
The goals for surgical intervention in SCI include (Lee et al., 2020):
Providers consider deteriorating neurologic function as an indication to perform surgery to decompress the spine. Cord compression with a neurologic deficit is an indication of cervical spine surgery. If patients are neurologically intact, they will be treated nonoperatively.
Penetrating injuries requires surgical exploration to ensure no foreign bodies are embedded in the tissue and thorough cleaning of the wound to prevent infection.
As mentioned above, not all surgical cases require decompression. The technical aspects of the surgery are tailored to the individual case and the patient's specific injury (Lee et al., 2020).
The amount of neurological injury after a SCI can predict the patient's long-term prognosis. Complete neurological function recovery may not be possible. Surgical intervention may limit the amount of neurological damage experienced.
Functional expectations and prognosis following a SCI depend on many individualized factors such as (Ahuja, 2017):
Most patients begin recovering function within 72 hours of injury. Most of the function of the spinal cord recovers in the first six months. If there is an incomplete tetraplegia injury, healing takes longer.
A poor prognosis after a SCI is typically due to older age, medical comorbidities, poor social support, and cognitive deficits. Patients with less severe injuries and who are younger have a greater outlook and overall prognosis.
Functional outcomes are of interest to most patients with a SCI. Patients with ASIA Impairment Scale grade A injuries are generally predicted to have a <5% chance of walking 1-year post-injury (Ahuja, 2017). Ambulatory rates are substantially higher for patients with incomplete injuries (Ahuja, 2017).
Most recovery in patients with incomplete SCI occurs in the first six to eight months. The general expectations for functional recovery based on the motor level are outlined below (Table 4). These levels of mobility and abilities to participate in activities of daily living (ADLs) assume an uncomplicated, complete SCI (ASIA grade A) followed by appropriate rehabilitation interventions in a healthy, motivated individual.
| Spinal Level | Activities of Daily Living | Mobility/Locomotion |
|---|---|---|
| C1-C4 | Feeding is possible with balanced forearm orthoses. Computer access by tongue, breath, and voice controls. Weight shifts with power tilt and recline chair. Mouth stick use. | Operate a power chair with tongue, chin, or breath controller. |
| C5 | Drink from a cup, feed with static splints, and set up. Oral/facial hygiene, writing, and typing with equipment. Dressing upper body possible. Side-to-side weight shifts. | Propel chair with hand rim projections short distances on smooth surfaces. Powerchair with a hand controller. |
| C6 | Feed and dress upper body with setup. Dressing lower body possible. Forward weight shifts. | Bed mobility with equipment. Level surface transfers with assistance. Propel indoors with coated hand rims. |
| C7 | Independent feeding, dressing, bathing with adaptive equipment, built-up utensils. | Independent bed mobility, level surface transfers, Wheelchair use outdoors (power chair for school or work). |
| C8 | Independent in feeding, dressing, and bathing. Bowel and bladder care with setup. | Propel chairs, including curbs and wheelies. Wheelchair-to-car transfers. |
| T1 | Independent in all self-care. | Transfer from floor to wheelchair. |
| T2-L1 | Independent in all self-care. | Stand with braces for exercise. |
| L2 | Independent in all self-care. | Potential for swing-to-gait with long leg braces indoors. Use of forearm crutches. |
| L3 | Independent in all self-care. | Potential for community ambulation. Potential for ambulation with short leg braces. |
| L4-S1 | Independent in all self-care. | Potential for ambulation without assistive devices. |
After a patient with an SCI becomes stable, rehabilitation should take place to prevent secondary complications. Objectives of rehabilitation include improving independence in activities of daily living (ADLs), helping the patient accept a new lifestyle, and reintegrating a patient into society (Fehlings et al., 2017).
Rehabilitation after a SCI can be acute, subacute, and chronic. In the acute phase of rehab, neurorecovery is promoted. Compensatory actions are performed in the chronic phase of recovery. Rehabilitation is critical to ensure patients heal as well as possible.
Rehabilitation can be challenging due to outcome measures, spontaneous recovery, and a lack of standard protocols (Fehlings et al., 2017).
The diagnosis of spinal cord injury is based on the patient’s presentation. However, when the time of injury and preceding events are less clear, a broader differential for motor and sensory deficits should be considered (Bennett et al., 2021):
Central Nervous System Pathologies:
Peripheral Nerve Pathologies:
Neuromuscular Junction Pathologies:
In order to prevent SCI (SpinalCord.com, 2020):
Sometimes it is impossible to prevent a spinal cord injury. However, some general safety practices can make them less likely (Spinal Cord Inc., 2020).
Life can completely change after a traumatic SCI. There are many changes for patients and their caregivers. Medically managing a SCI can increase the survival rate and well-being of a SCI.
Neurological outcomes in SCIs are often challenging to treat. This is due to the pathophysiology of a SCI. Severity and location of a SCI guides the treatment, outcome, and prognosis of a SCI.
SCI is a problem that primarily affects young male adults because of falls, motor vehicle accidents, and violence. Blunt trauma, particularly motor vehicle collisions, accounts for most spinal column injuries. Elderly patients who fall are also at increased risk.
Most SCI occurs with injury to the vertebral column. This produces compression or distortion of the spinal cord. Secondary injuries often result from either ischemic or inflammatory pathways.
The cervical spine is the most commonly injured part of the spinal column, and the most common injury sites are around the second cervical vertebra (C2, or axis) or in the region of C5, C6, and C7.
The spine is susceptible to dislocations, ligamentous injuries, and fractures. The most common thoracolumbar spinal injury is a compression fracture.
Most patients with a SCI have associated injuries to the brain and limbs. The neurologic injury produced by traumatic SCI is classified according to the spinal cord level and the severity of neurologic deficits. Nearly half the injuries associated with SCI involve quadriparesis or quadriplegia.
ABCDs (airway, breathing, circulation, and disability) should be initially evaluated and managed in patients with a SCI.
Patients need continued immobilization until imaging studies exclude an unstable spine injury if they have neurologic deficits or neck pain. All patients with suspected SCI should have spinal imaging with plain x-rays or helical CT scans. Patients may need a follow-up CT if there is a negative or abnormal screening. MRIs are useful to help define the extent of a SCI and help decide the treatment plan. Patients who have a SCI require efforts to manage stabilization and decompression.
Patients who have a SCI require ICU admission to monitor the injury. They also need treatment for potential acute, life-threatening complications, including cardiovascular instability and respiratory failure.
CEUFast, Inc. is committed to furthering diversity, equity, and inclusion (DEI). While reflecting on this course content, CEUFast, Inc. would like you to consider your individual perspective and question your own biases. Remember, implicit bias is a form of bias that impacts our practice as healthcare professionals. Implicit bias occurs when we have automatic prejudices, judgments, and/or a general attitude towards a person or a group of people based on associated stereotypes we have formed over time. These automatic thoughts occur without our conscious knowledge and without our intentional desire to discriminate. The concern with implicit bias is that this can impact our actions and decisions with our workplace leadership, colleagues, and even our patients. While it is our universal goal to treat everyone equally, our implicit biases can influence our interactions, assessments, communication, prioritization, and decision-making concerning patients, which can ultimately adversely impact health outcomes. It is important to keep this in mind in order to intentionally work to self-identify our own risk areas where our implicit biases might influence our behaviors. Together, we can cease perpetuating stereotypes and remind each other to remain mindful to help avoid reacting according to biases that are contrary to our conscious beliefs and values.
