This course describes injuries to the cervical, thoracic, and lumbosacral spinal column, including fractures, dislocations, and subluxations of the vertebrae, and injuries to the spinal ligaments. The importance of recognizing and appropriately managing injuries to the spinal column is underscored by their association with SCI. Management via medical and/or surgical care with appropriate interventions and prevention of complications of SCI will be discussed with, hopefully, a return to maximal level of functioning.
Upon completion of this course, the participant will be able to:
Spinal cord injury (SCI) has become epidemic in modern society. SCI remains a devastating event, often producing severe and permanent disability despite advances made in the understanding of the pathogenesis and improvements in early recognition and treatment. With a peak incidence in young adults, traumatic SCI remains a costly problem for society. Direct medical expenses accrued over the lifetime of one patient range from 500,000 to 2 million US dollars.1
Approximately 3% of patients who experience blunt trauma sustain a spinal column injury, such as a spinal fracture or dislocation, and 1% sustain a spinal cord injury (SCI).2 Spinal column injury rates reported in other studies range from 2 to 6%.3 The incidence is likely to be significantly higher in patients with head trauma and those who are unconscious at presentation. Fracture of the thoracolumbar spine, including spinous and transverse process fractures, may occur in as many as 8 to 15% of blunt trauma patients cared for at major trauma centers.4 Additional noncontiguous spine fractures are common in patients diagnosed with a spine fracture following high-energy blunt trauma.5,6 A review of over 83,000 patients from the United States National Trauma Data Bank diagnosed with a spine fracture reported that 19% sustained a noncontiguous spine fracture.
A systematic review of 13 international studies found great variation (up to a threefold difference) in the rate of spinal column injury among nations, particularly between developed and developing nations.7,8 Most studies demonstrate a bimodal age distribution where the first peak is found in young adults between 15 and 29 years of age and a second peak in adults older than 65 years of age. Mortality is significantly higher in elder patients.9 Spinal column injuries are more common in males.
It is of importance to note that statistics from trauma registries can be incomplete and inaccurate, depending on the inclusion criteria, and may underestimate the number of patients with spinal column injury. For examples, victims who die at the accident scene and patients whose neurologic deficits rapidly improve are often excluded.
The human spine consists of 33 bony vertebrae: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral (fused), and 4 coccygeal (usually fused).20 The vertebral column provides the body's basic structural support and protects the spinal cord, which extends from the midbrain caudally to the level of the second lumbar vertebra and then continues as the cauda equina (Figure 1).
Spine Anatomy Overview
A "typical" vertebra cross section
The 3rd-6th cervical vertebrae have a "typical" structure. The 1st, 2nd, and 7th cervical vertebrae are "atypical." Typical vertebrae demonstrate rectangular bodies with articular uncinate processes on their lateral aspects, triangular vertebral foramina, bifid spinous processes, and transverse foramina.
Vertebra C1 (Atlas)
Vertebra C2 (Axis)
T1 has a vertebral foramen and body like a cervical vertebra. T5-T9 vertebrae have typical characteristics of thoracic vertebrae. T12 has bony processes and a body size like a lumbar vertebra. The planes of the articular facets of thoracic vertebrae define an arc that centers on an axis vertically traversing the vertebral bodies.
Superior and inferior costal facets (demifacets) on the vertebral body, costal facets on the transverse processes, and long sloping spinous processes are characteristic of thoracic vertebrae.
Due to its exposed location above the torso and its inherent flexibility, the cervical spine is the most commonly injured part of the spinal column. Within the cervical spine, the most common sites of injury are around the second cervical vertebra (C2, or axis) or in the region of C5, C6 and C7.3
The thoracic spine, in contrast, is rigidly fixed, since the thoracic ribs articulate with the respective transverse processes and sternum. As such, a great amount of force is necessary to damage the thoracic spine of an otherwise healthy adult. In older adults with osteoporosis or patients with bone disease or metastatic lesions, minor trauma may be sufficient to cause a compression fracture.
The second most commonly injured region is the thoracolumbar (TL) junction. The orientation of the facet joints at the TL junction may concentrate forces created from traumatic impact at this level.21 At the TL junction, the spinal column changes from a kyphotic to a lordotic curve. Ninety percent of all TL spine injuries occur in the region between T11 and L4. However, these injuries rarely result in complete cord lesions as the spinal canal is relatively wide at this level.22
The vertebral column (and the spinal cord within it) is divided into cervical, thoracic, lumbar, sacral, and coccygeal regions. The peripheral nerves (called the spinal or segmental nerves) that innervate much of the body arise from the spinal cord's 31 segmental pairs.
The segmental spinal nerves leave the vertebral column through the intervertebral foramina that lie adjacent to the respectively numbered vertebral body. Sensory information carried by the afferent axons of the spinal nerves enters the cord via the dorsal roots, and motor commands carried by the efferent axons leave the cord via the ventral roots. Once the dorsal and ventral roots join, sensory and motor axons (with some exceptions) travel together in the segmental spinal nerves.
Because the spinal cord is considerably shorter than the vertebral column, lumbar and sacral nerves run for some distance in the vertebral canal before emerging, thus forming a collection of nerve roots known as the cauda equina. This region is the target for a “lumbar puncture” that allows for the collection of cerebrospinal fluid by placing a needle into the space surrounding these nerves to withdraw fluid for analysis. In addition, local anesthetics can be safely introduced to produce spinal anesthesia. At this level, the risk of damage to the spinal cord from a poorly placed needle is minimized.
The spinal cord is divided longitudinally into four regions:
The spinal cord extends from the base of the skull and terminates near the lower margin of the first lumbar vertebral body (L1). Below that level, the spinal canal contains the lumbar, sacral, and coccygeal spinal nerve roots that comprise the cauda equina.
Because the spinal cord is shorter than the vertebral column, vertebral and spinal cord segmental levels are not necessarily the same.
Longitudinal Organization of Spinal Cord Innervation
The first cervical vertebra (the atlas) and the second cervical vertebra (the axis), upon which the atlas pivots, support the head at the atlanto-occiput junction. The interface between the first and second vertebra is called the atlanto-axis junction.
Cervical spinal segments innervate the skin and musculature of the upper extremity and diaphragm:
The thoracic vertebral segments are defined by those that have an attached rib. The spinal roots form the intercostal nerves that run along the inferior rib margin and innervate the associated dermatomes, as well as, the intercostal abdominal wall musculature. These muscles are the main muscles of expiration. The thoracic cord also contains the sympathetic nerves that innervate the heart and abdominal organs.
The lumbosacral spinal cord contains the segments that innervate the muscles and dermatomes of the lower extremity, as well as, the buttocks and anal regions. Sacral nerve roots S3 through S5 originate in the narrow terminal part of the cord, called the conus medullaris.
Sacral nerve roots also provide parasympathetic innervation of pelvic and abdominal organs. Lumbar nerve roots L1 and L2 contain sympathetic innervation of some pelvic and abdominal organs.
In adults, the spinal cord ends at the level of the first or second lumbar vertebral bodies. The filum terminale, a thin connective tissue filament that descends from the conus medullaris with the spinal nerve roots, is connected to the third, fourth, and fifth sacral vertebrae. Its terminal part is fused to the periosteum at the base of the coccygeal bone.
Pathology at the T12 and L1 vertebral level affects the lumbar cord. Injuries to L2 frequently damage the conus medullaris. Injuries below L2 usually involve the cauda equina and represent injuries to spinal roots rather than to the spinal cord.
Spinal column injury may result in spinal cord or brain injury through many mechanisms:23
The primary injury refers to the immediate effect of trauma which includes forces of compression, contusion, and shear injury to the spinal cord. In the absence of cord transection or frank hemorrhage (both relatively rare in nonpenetrating injuries), the spinal cord may appear pathologically normal immediately after trauma. Penetrating injuries (e.g., knife, gunshot injuries etc.) usually produce a complete or partial transection of the spinal cord. An increasingly described phenomenon, however, is a spinal cord injury following a gunshot wound that does not enter the spinal canal.24 Presumably, the spinal cord injury in these cases results from kinetic energy emitted by the bullet.
A secondary, progressive mechanism of cord injury usually follows, beginning within minutes and evolving over several hours after injury.1,25-28 The phenomenon of secondary injury is sometimes clinically manifest by neurologic deterioration over the first 8 to 12 hours in patients who initially present with an incomplete cord syndrome. The processes propagating this phenomenon are complex and incompletely understood.29,30
Possible mechanisms include:1,29,31
Because of these secondary processes, spinal cord edema develops within hours of injury, becomes maximal between the third and sixth day after injury, and begins to recede after the ninth day. This is gradually replaced by a central hemorrhagic necrosis.32
Acute cervical spinal column injury may be classified according to the stability of the injury, its location, or the mechanism (flexion, flexion-rotation, extension, and vertical compression) (Table 1).33,34
|Mechanisms of Spinal Injury||Stability|
|Anterior wedge fracture||Stable|
|Flexion teardrop fracture||Extremely unstable|
|Clay shoveler's fracture||Stable|
|Bilateral facet dislocation||Always unstable|
|Anterior atlantoaxial dislocation with or without fracture||Unstable|
|Odontoid fracture with lateral displacement||Unstable|
|Fracture of transverse process||Stable|
|Unilateral facet dislocation||Stable|
|Rotary atlantoaxial dislocation||Unstable|
|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|
|Burst fracture of vertebral body||Stable|
|Jefferson fracture (C1)||Extremely unstable|
|Isolated fractures of articular pillar and vertebral body||Stable|
The spine is viewed as consisting of two columns when assessing the stability of cervical spinal column injuries below C2:
If both the anterior and posterior columns are disrupted, the cervical spine can move as two independent units, and there is a high risk of causing or exacerbating a spinal cord injury.34 In contrast, if only one column is disrupted, and the other column maintains structural integrity, the risk of spinal cord injury is lessened considerably.
Pure flexion injuries involving the atlas (C1) and the axis (C2) can cause an unstable atlanto-occipital or atlanto-axial joint dislocation, with or without an associated odontoid fracture.
Several measurements are used to determine the presence of atlanto-occipital joint dislocation on plain lateral x-rays of the cervical spine. Their accuracy and interobserver reliability, however, are not well studied in trauma patients.35 These measurements are called the:
Rotary atlanto-axial dislocation is an unstable injury, caused by a flexion-rotation mechanism, best visualized on open-mouth odontoid x-rays or CT scan. The interpretation of odontoid x-rays warrants careful attention, since there may be false positive asymmetry between the odontoid process and the lateral masses of C1 if the skull is rotated. When the radiograph reveals symmetric basilar skull structures, a unilaterally magnified lateral mass confirms a C1-C2 dislocation.
Cervical Vertebrae Dislocation
The Jefferson fracture of C1 is highly unstable and occurs when a vertical compression force is transmitted through the occipital condyles to the lateral masses of the atlas. This force drives the lateral masses outward, resulting in fractures of the anterior and posterior arches of the C1, with or without disruption of the transverse ligament. Disruption of the transverse ligament determines instability.
Prevertebral hemorrhage combined with disruption of the transverse ligament may cause an increase in the predental space between C1 and the odontoid (dens) seen on the lateral x-ray. A predental space greater than 3 mm in adults is abnormal.36 In the anterior-posterior (AP) projection (open-mouth or odontoid view), the masses of C1 lie lateral to the outer margins of the articular pillars of C2. The Jefferson fracture may be difficult to recognize on plain x-rays if there is minimal displacement.37
The transverse ligament is presumed to be disrupted if the interval between the atlas and the dens is increased on a lateral x-ray, or the lateral masses of the atlas extend laterally beyond those of the axis on the odontoid x-ray. In such instances, clinicians should obtain a computed tomography (CT) scan of the cervical spine.
A posterior neural arch fracture of C1 results from compression of the posterior elements between the occiput and the spinous process of C2 during forced neck extension.Although mechanically stable because the anterior arch and the transverse ligament remain intact, this fracture is potentially dangerous because of its location. Anterior displacement of the atlas greater than 1 cm can injure the adjacent spinal cord.
Traumatic spondylolysis of C2 is an unstable injury that occurs when the cervicocranium (the skull, atlas, and axis functioning as a unit) is thrown into extreme hyperextension because of abrupt deceleration (i.e., forced extension of an already extended neck).Bilateral pedicle fractures of the axis may occur with or without dislocation in this circumstance. Although this lesion is unstable, spinal cord damage is often minimal because the AP diameter of the neural canal is greatest at C2, and bilateral pedicle fractures permit spinal canal decompression.38
Forceful flexion or extension of the head in an anterior-posterior orientation (i.e., sagittal plane), as might occur with a forward fall onto the forehead, may result in a fracture of the odontoid process, also called the dens.
Fractures can occur:
Forceful, extreme flexion of the cervical spine can compress the anterior portion of a vertebral body, creating an anterior wedge fracture.
Spinal instability can result if anterior wedge fractures are severe (loss of over half the height of the anterior vertebral body) or multiple adjacent wedge fractures occur.
In pure flexion injuries below C2, the strong nuchal ligament complex usually remains intact, and most of the force is expended on the vertebral body anteriorly, causing a simple wedge fracture.38 On x-ray, the height of the anterior border of the vertebra is diminished, and prevertebral soft tissue swelling is present. Because the posterior column remains intact, this injury is usually stable and rarely associated with spinal cord injuries.
A flexion teardrop fracture results when severe flexion and compression cause one vertebral body to collide with the body below, leading to anterior displacement of a wedge-shaped fragment (resembling a teardrop) of the antero-inferior portion of the superior vertebra. They usually occur in the lower cervical spine.
On plain lateral x-rays, the fractured vertebra appears to be divided into a smaller anterior fragment and a larger posterior piece. The larger piece displaces posteriorly as a unit with the superior cervical spine relative to the vertebrae below. The anterior fragment typically remains aligned with the inferior cervical vertebrae. If there is no posterior displacement of the superior column, widening of the interlaminar and interspinous spaces supports the diagnosis of a flexion teardrop fracture.40
The severe anterior flexion involved in this injury creates distraction forces at the posterior cervical spine and disruption of the posterior longitudinal ligament. Thus, flexion teardrop fractures are highly unstable. They are associated with acute anterior cervical cord syndrome.
An extension teardrop fracture occurs when abrupt neck extension causes the anterior longitudinal ligament to pull the antero-inferior corner from the remainder of the vertebral body, producing a triangular-shaped fragment.
This unstable injury is found most often at C2 but can also occur at C5 to C7 with diving accidents and can be associated with a central cord syndrome.23
Although similar in x-ray appearance to the flexion teardrop fracture, the vertebra involved in an extension teardrop injury generally does not lose height. In contrast, a vertebra with a flexion teardrop fracture may lose height from compression.40
The clay shoveler's fracture, an isolated fracture of one of the spinous processes of the lower cervical vertebrae, is a stable injury.
Vertical compression injuries occur in the cervical and lumbar regions when axial loads are exerted on the spine.
Such forces are applied from above (via the skull) or below (via the pelvis or feet) and may cause one or more vertebral body end-plates to fracture.
When the nucleus pulposus of the intervertebral disk is forced into the vertebral body, the body shatters outward, resulting in a burst fracture.
Although technically burst fractures are "stable" since all ligaments remain intact, posteriorly displaced fracture fragments may impinge on the spinal cord, causing an anterior cord syndrome.
To reflect this risk of spinal cord injury, burst fractures can be classified as unstable if any of the following are present:
Associated neurologic deficits including41:
Most laminar fractures of the cervical spine are associated with other fractures, such as burst fractures or fracture dislocations, which usually determine the stability of the injury.42
The pattern of the fracture often reflects the mechanism of injury. Vertical lamina fractures are thought to result from axial loading. Transverse fractures often represent avulsion fractures from hyperflexion.
Although rare, isolated lamina fractures, which are generally not associated with instability, can be treated nonoperatively with cervical collar immobilization.43
In contrast to the two-column scheme for cervical spinal column injury, a three-column scheme may be used to describe injuries of the thoracic and lumbar (TL) spinal column.45 The three columns are anterior, middle, and posterior.
The anterior column includes the:
The middle column includes the:
The posterior column includes the:
According to the three-column scheme, stability is based upon the integrity of two of the three spinal columns. Spinal instability may be inferred when plain x-rays demonstrate a loss of 50% of vertebral height or excessive kyphotic angulation around the fracture.46 The angle is determined by the intersection of two lines, one measured along the superior endplate of the vertebral body one level above the fracture and the other along the inferior endplate of the vertebral body one level below.47 Compression fractures with greater than 30 degrees and burst fractures with greater than 25 degrees angulation are generally considered unstable. The presence of a neurologic deficit also indicates spinal instability, since the spinal column has failed to protect the spinal cord.48
Few studies have been performed to validate the three-column scheme. In a biomechanical study of cadaveric human spines, researchers found the middle column to be the major determinant of spine stability when axial or flexion stress was applied.49
TL injuries can be divided into four injury patterns:
All these fractures result from one or more of three mechanisms of injury:45,50
A widely used classification for TL spinal column injury combines a distinction between major and minor fracture patterns using the three-column scheme and the four injury patterns.
In 2005, the Spine Trauma Study Group introduced a classification system for thoracolumbar injuries called the Thoracolumbar Injury Classification and Severity Score (TLICS). This score assigns numeric values to each injury based upon morphology, neurologic status, and integrity of the posterior ligamentous complex, which includes the supraspinous ligament, interspinous ligament, ligamentum flavum, and facet joint capsules.51 Scoring of the TLICS is as follows:
Cord, conus medullaris:
Posterior Ligament Complex
The total numerical score is used to guide treatment.52
Wedge, or anterior, compression fractures account for 50 to 70% of all TL fractures.50,53 They usually result from compressive failure of the anterior column under an axial load applied in flexion. Injuries that do not disrupt the posterior ligament complex are stable. An additional rotational force is necessary to cause an unstable fracture pattern. If there is severe compression (>50% of vertebral height), significant fracture kyphosis (>30 degrees), a rotational component to the injury, or compression fractures at multiple levels, then the posterior ligamentous complex may fail and progress to involve the middle column, resulting in spinal instability. Fractures with any of these characteristics or a TLICS score ≥ 4 warrant imaging with computed tomography (CT).
Thoracic Compression Fracture
Compression fractures that exhibit between 10 and 40% compression are managed on a case-by-case basis in consultation with a spine surgeon. Neurologic findings or concomitant injuries warrant a thorough evaluation.
Simple wedge fractures demonstrate less than 10 to 30% compression and generally cause no neurologic impairment, since the middle column remains intact. These fractures generally result from falls, motor vehicle crashes, and occasionally generalized tonic-clonic seizures.54 Associated injuries are common, and fractures frequently occur at other spinal levels.
Simple wedge compression fractures are best seen on lateral x-rays, which demonstrate anterior compression of the vertebral body without disruption of the posterior cortex. The AP x-ray may demonstrate a subtle increase in the interspinous distance if there is a kyphotic deformity.
It is important to confirm that the posterior elements remain intact (i.e., no vertebral subluxation), since the integrity of the posterior cortex is what distinguishes the stable wedge compression fracture from the unstable burst fracture. Standard x-rays may not be adequate to evaluate the integrity of the posterior vertebral cortex.
In an analysis of 67 thoracolumbar x-rays reviewed by two radiologists and two orthopedists, 20% of CT-confirmed burst fractures were initially misdiagnosed as wedge fractures.55 Thus, CT should be performed when plain x-rays suggest any possible involvement of the posterior cortex in what appears to be a wedge compression fracture. Such findings include fracture lines that extend into the posterior cortex and any compression of the posterior cortex. Other suggestive features include loss of posterior vertebral height and widening of the interpedicular distance.
Burst fractures comprise approximately 14% of all TL injuries.53 They are caused by compressive forces that fracture the vertebral endplate and pressure from the nucleus pulposus upon the vertebral body. Spinal cord injury from retropulsion of bony fragments into the spinal canal can occur.
Burst injuries can occur with or without injury to posterior elements. Posterior element involvement increases the risk for neurologic deficits.54 Burst fractures are most commonly associated with falls and motor vehicle collisions. All burst fractures should be considered unstable, since neurologic deficits are seen in 42 to 58% of patients.53
Burst fractures can be difficult to visualize and are often misdiagnosed by plain x-rays because posteriorly displaced bone fragments often lie at the level of the pedicles.56 Lateral x-rays of burst fractures may demonstrate a loss of anterior and posterior vertebral height and may show a distorted posterior longitudinal ligament line. AP x-rays may demonstrate a widening of the interpedicular distance (>1 mm difference between the vertebrae above and below).
Unstable burst fractures are often misdiagnosed as stable anterior wedge fractures. In one retrospective trial, 6 experienced radiologists correctly identified only 30 of 39 burst fractures among 53 thoracolumbar x-rays reviewed.57 A CT scan should be obtained if there is vertebral compression greater than 50% or a burst fracture is suspected for any reason.
Flexion-distraction injuries account for 10% of all TL spinal column injuries and occur most frequently in patients wearing only a lap belt (i.e., no chest restraint) during vehicular trauma.58 While neurologic deficits are rare, associated intraabdominal injuries, such as small and large intestinal perforations, are more common. A seatbelt sign may be present.
Chance fractures are representative of a TL flexion-distraction injury. Classically the patient is wearing only a lap belt, positioned incorrectly above the pelvic bones. Sudden deceleration during a collision causes forceful flexion at the lap belt, leading to compressive failure of the anterior and middle columns and a tear in the posterior longitudinal ligament. Chance fractures are often misdiagnosed as compression fractures. Pure ligamentous disruptions also occur and account for 10 to 25% of flexion-distraction injuries.54
In contrast to the cervical region, where articular processes are small, flat, and almost horizontal, articular processes in the lumbar region are large, curved, and nearly vertical, and thus, unilateral facet dislocations are rare. Instead, one or both articular processes fracture, and the upper vertebra swings forward, resulting in an unstable fracture-dislocation pattern.
X-ray findings of flexion-distraction injuries include compression fractures of the vertebral body and increased posterior interspinous spaces caused by distraction. A characteristic finding is increased length of the vertebral segment because of distraction. Displacement is unusual, since the mechanism does not involve a significant rotational or translational component.
Flexion-distraction injuries may be missed on routine axial CT scans since the disruption is oriented in the horizontal plane. Thus, it is important to obtain sagittal reconstructions of CT images if a lap belt mechanism is known or a flexion-distraction injury is suspected for other reasons (e.g., presence of abdominal seat belt sign, known bowel injury).22 A systematic review found that reformatted CT images from visceral studies demonstrated greater sensitivity and specificity than plain TL x-rays in detecting spinal column injury.59
Massive direct trauma to the back can cause failure of all three columns of the TL spine resulting in translational injuries. Several injury patterns can occur, including rotational fracture-dislocations, shear injuries, and pure vertebral dislocations. The thoracolumbar junction (T10 to L2) is the most common site.60 Patients with a complete vertebral dislocation from massive trauma almost invariably demonstrate neurologic deficits.
Among patients rendered paraplegic from TL trauma, the majority have sustained a fracture-dislocation injury. Approximately 26 to 40% of these result in permanent neurologic deficits.60 Most patients also sustain multiorgan system trauma.
Shear fractures and pure dislocations result in severe neurologic injury, causing complete paraplegia in nearly all patients. Pure dislocations appear as a complete displacement of the superior vertebrae relative to the one below. Fracture fragments created by shearing forces may lodge in the spinal canal. CT scan is helpful in evaluating these injuries because it quantifies the extent of spinal cord impingement.
Minor spinal fracture patterns account for 14% of all TL injuries and include isolated transverse process fractures, spinous process fractures, facet or laminar fractures, bipedicular fractures, and fractures of the pars interarticularis. Most minor spinal fractures occur in the lumbar region and are caused by direct blows. Sudden contraction of the psoas muscles can result in avulsion of a transverse process.
While transverse process fractures are considered stable, in high velocity trauma they frequently do not occur in isolation. In one retrospective analysis of 28 patients who initially appeared to have isolated transverse process fractures by plain x-rays, three patients were subsequently found to have compression and burst fractures by CT scan.61 High thoracic spinous process fractures may be associated with brachial plexus injury, while lumbar and sacral spinous process fractures may cause lumbosacral plexus injury. To ensure appropriate diagnosis and management of spinal column injury, a CT should be obtained when transverse process fractures are seen on plain x-rays.
When associated with a burst fracture, the presence of thoracic or lumbar laminar fractures indicates potential instability and a greater severity of injury, due to the greater chance of damage to the posterior dural sac and compression of neural structures between the laminar fragments.62 In an observational study of 146 patients, the presence of a laminar fracture was associated with greater narrowing of the spinal canal (47% versus 28%) and a higher mean injury severity score (ISS) (17% versus 12%).63
A patient with a spinal cord injury typically has pain at the site of the spinal fracture. But this is not always a reliable feature to exclude traumatic spinal cord injury (TSCI). Patients with TSCI often have associated brain and systemic injuries (e.g., hemothorax, extremity fractures, intra-abdominal injury etc.) that may limit the patient's ability to report localized pain.1,17 These associated injuries also complicate the initial evaluation and management of patients with TSCI and affect prognosis.
About half of TSCIs involve the cervical cord and as a result present with quadriparesis or quadriplegia.15,17 The severity of cord syndromes is classified using the American Spinal Injury Association (ASIA) Scale (Table 2):64
|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 pin prick 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.|
Muscle function is graded using the International Standards for Neurologic Classification of Spinal Cord Injury.
For an individual to receive a grade of C or D (i.e., motor incomplete status), he/she must have either:
(1) Voluntary anal sphincter contraction or
(2) Sacral sensory sparing with sparing of motor function more than three levels below the motor level for that side of the body.
Patients without an initial spinal cord injury do not receive an AIS grade.
In a complete cord injury (ASIA grade A), there will be a rostral zone of spared sensory levels (e.g., the C5 and higher dermatomes spared in a C5-6 fracture-dislocation), reduced sensation in the next caudal level, and no sensation in levels below, including none in the sacral segments, S4-S5. Similarly, there will be reduced muscle power in the level immediately below the injury, followed by complete paralysis in more caudal myotomes. In the acute stage, reflexes are absent, there is no response to plantar stimulation, and muscle tone is flaccid. A male with a complete TSCI may have priapism. The bulbocavernosus reflex is usually absent. Urinary retention and bladder distension occur.
In incomplete injuries (ASIA grades B through D), there are various degrees of motor function in muscles controlled by levels of the spinal cord caudal to the injury. Sensation is also partially preserved in dermatomes below the area of injury. Usually sensation is preserved to a greater extent than motor function because the sensory tracts are located in more peripheral, less vulnerable areas of the cord. The bulbocavernosus reflex and anal sensation are often present.
The relative incidence of incomplete versus complete spinal cord injury has increased over the last half century.1 This trend has been attributed to improved initial care and retrieval systems that emphasize the importance of immobilization after injury.
An acute central cord syndrome, characterized by disproportionately greater motor impairment in upper compared with lower extremities, bladder dysfunction, and a variable degree of sensory loss below the level of injury, is described after relatively mild trauma in the setting of preexisting cervical spondylosis.65,66
Lesions affecting the anterior or ventral two-thirds of the spinal cord, sparing the dorsal columns, usually reflect injury to the anterior spinal artery. When this occurs in TSCI, it is believed that this more often represents a direct injury to the anterior spinal cord by retropulsed disc or bone fragments rather than primary disruption of the anterior spinal artery.
Immediately after a spinal cord injury, there may be a physiological loss of all spinal cord function caudal to the level of the injury, with flaccid paralysis, anesthesia, absent bowel and bladder control, and loss of reflex activity.67,68 In males, especially those with a cervical cord injury, priapism may develop. There may also be bradycardia and hypotension not due to causes other than the spinal cord injury. This altered physiologic state may last several hours to several weeks and is sometimes referred to as spinal shock.
It is believed that this loss of function may be caused by the loss of potassium within the injured cells in the cord and its accumulation within the extra-cellular space, causing reduced axonal transmission. As the potassium levels normalize within the intracellular and extra-cellular spaces, this spinal shock wears off. Clinical manifestations may normalize but are more usually replaced by a spastic paresis reflecting more severe morphologic injury to the spinal cord.
A transient paralysis with complete recovery is most often described in younger patients with athletic injuries. These patients should undergo evaluation for underlying spinal disease before returning to play.
The primary assessment of a patient with trauma in the field follows the ABCD prioritization mnemonic: Airway, Breathing, Circulation, Disability (neurologic status).
A traumatic spinal injury should be assumed if the patient:
During the acute resuscitation period which begins at the scene of the trauma, a brief assessment of disability (neurologic status) should be performed. This assessment should include a global assessment of the trauma patients level of responsiveness, as well as, the patient's posture (i.e., any asymmetry, decerebrate or decorticate posturing), pupil asymmetry and pupillary response to light.
A recommended system is the AVPU mnemonic:
A = Patient is awake, alert and appropriate
V = Patient responds to voice
P = Patient responds to pain
U = Patient is unresponsive
The disability of the acute trauma patient should be assessed by determining:
|To Verbal Stimuli||3|
|Disoriented and Converses||4|
|Oriented and Converses||5|
|Extension Abnormal (Decerebrate Rigidity)||2|
|Flexion Abnormal (Decorticate Rigidity)||3|
|3 - 15|
Pupillary asymmetry or dilation, impaired or absent light reflexes and hemiplegia or weakness suggest impending herniation of the cerebrum through the tentorial incisura due to an expanding intracranial mass or diffuse cerebral edema.69 These findings are indicative of traumatic brain injury and mandate the need for emergency treatment of intracranial hypertension, including administration of IV mannitol, hypertonic saline, sedatives and muscle relaxants, after obtaining a definitive airway. Urgent neurosurgical consultation is mandatory.
The absence of a depressed level of consciousness but the presence of paraplegia or quadriplegia indicates spinal cord injury. The possibility of a spinal cord injury requires full spinal immobilization. If inspiratory efforts are weak or when a high cervical cord lesion is suspected, an endotracheal intubation should be performed.70,71
Continuous assessment using the GCS should be made at the scene, during the primary survey and resuscitation phase and where indicated throughout the remainder of hospitalization should the trauma patient’s mental status appear to change.
Extreme care should be taken to allow as little movement of the spine as possible to prevent more spinal cord injury. Techniques to minimize spine movement include:72
Triage is the process of grouping trauma victims according to risk of death or other adverse outcomes. EMS personnel should be trained to carry out this process according to a predetermined checklist of criteria or a system of injury severity scoring. Triage for the suspected TSCI patient usually depends on three simple groups of factors:
Mechanism of injury:
Management in the emergency department continues to prioritize assessment and stabilization following the ABCD mnemonic. Life-threatening priorities related to other injuries, such as systemic bleeding, breathing difficulties, or a hemopneumothorax etc., should take precedence over the spinal cord injury.
Management of the suspected TSCI patient in the ED includes:
Interventions should include:
Interventions may include:
Hypotension may occur due to blood loss from other injuries or due to blood pooling in the extremities lacking sympathetic tone because of the disruption of the autonomic nervous system (neurogenic shock). Prolonged hypoperfusion may adversely affect prognosis.
Interventions may include:
Until spinal injury has been ruled out, immobilization of the neck and body must be maintained.Interventions may include:
A neurologic examination should be completed as soon as possible to determine the level and severity of the injury, both of which impact prognosis and treatment. An evaluation of mental status and cranial nerve function should be included, as many patients with TSCI have also suffered a head injury.
The patient must be checked for bladder distension by palpation or ultrasound. A urinary catheter should be inserted as soon as possible, if not done previously, to avoid harm due to bladder distension.
Patients with suspected TSCI because of neck pain or neurologic deficits and all trauma victims with impaired alertness or potentially distracting systemic injuries require continued immobilization until imaging studies exclude an unstable spine injury.
In many trauma centers, a full set of cervical spine x-rays are required on all trauma patients before a cervical collar can be removed. Data from the National Emergency X-Radiography Utilization Study (NEXUS) allow this requirement to be modified.76 Patients without neurologic deficits, who are alert and not confused, who are not intoxicated, and who have no neck or midline pain or tenderness or other injury that is distracting to the patient are unlikely to have a cervical spine injury. In the NEXUS study, these five criteria had a 99.8% negative predictive value for cervical spine injury (sensitivity 99%; specificity 12.9%.76 Similar results have been reported in other large series.77
Patients who are not clinically evaluable for SCI because of obtundation or confusion should be assumed to have a SCI until proven otherwise. In one meta-analysis of studies looking at such patients, the incidence of spine injury was 7.5%; 42% of these had unstable injuries.78
Plain x-rays provide a rapid assessment of alignment, fractures, and soft tissue swelling and are, in general, the first method of assessment of TSCI. A complete set of cervical x-rays includes anteroposterior, lateral, and open-mouth odontoid views. Oblique views may be necessary if one suspects a lateral mass or facet injury or damage. All cervical vertebrae and the top of T1 must be visualized. In muscular males with a neck injury, pulling the shoulders down by pulling down on the wrists in a straight line and downward towards the feet may better allow visualization of the lower cervical vertebrae. A swimmer's view should be performed if the lower cervical levels and the top of T1 are not adequately visualized. While there are reports of missed cervical spine injury with plain x-rays, it is rare to miss significant injuries with adequate performance and interpretation of plain x-rays of the occiput through the top of T1.79,80
Neurologic signs and symptoms of cervical spine injury in the setting of normal plain x-rays warrant further imaging studies.
Patients who have pain in the thoracic or lumbar areas, especially with an appropriate neurologic deficit, also require lateral, anteroposterior, and sometimes oblique plain x-rays of either the thoracic spine, lumbar region, or both. Such spinal injuries, especially with a neurologic deficit, require further imaging.
Helical CT scanning with coronal and sagittal reconstructions may replace plain x-rays for screening assessment in centers in which it is readily available.81 Prospective case series report a higher sensitivity for detecting spinal fracture when compared with plain x-rays. This is especially true for cervical spine fracture.80,82-86 This study can also be done without moving the patient out of the supine position. When a head CT is required to rule out head injury, it may be most cost and time efficient to use CT as the initial imaging study of the neck as well.
All abnormalities on screening x-rays or CT are followed up with a more detailed CT scan of the area in question, with fine, 2 mm cuts as needed. Areas not well visualized on plain x-rays should be further imaged as well. This test is very sensitive for defining bone fractures in the spine. Because CT is more sensitive than plain x-rays, patients who are suspected to have a spinal injury and have normal plain x-rays should also undergo CT. CT also has advantages over plain x-rays in assessing the patency of the spinal canal. CT also provides some assessment of the paravertebral soft tissues and perhaps of the spinal cord as well but is inferior in that regard to magnetic resonance imaging (MRI).
When MRI is available, myelography is rarely if ever used, but remains an alternative in combination with CT when an MRI cannot be performed, and spinal canal compromise is suspected.
The indications for MRI in the evaluation of acute TSCI have not been defined.87,88
MRI can be useful to further define the extent of TSCI and should be performed on stable patients with TSCI, as well as, on patients suspected to have TSCI (because of neck pain or neurologic deficits) despite a normal CT scan.
The chief advantage of MRI is that it provides a detailed image of the spinal cord, as well as, spinal ligaments, intervertebral discs, and paraspinal soft tissues that is superior to CT and is more sensitive for detecting epidural hematoma.87,89-92 CT, however, is better than MRI in assessing bony structures.
The chief disadvantages of MRI include:
Nonetheless, if the patient's clinical status permits, an MRI can provide valuable information that complements CT regarding the extent and mechanism of spinal cord injury, which can influence treatment and prognosis.87,93,94 MRI is also indicated in patients with a negative CT scan who are suspected to have TSCI, in order to detect occult ligamentous or disc injury or epidural hematoma.95 In a systematic review of reported case series, 5.8% of individuals with negative CT scan who went on to have an MRI were found to have a TSCI.96 While it has been suggested that nonalert patients require an MRI in addition to CT to exclude TSCI, one case series suggests that if obtunded patients are observed to have grossly normal motor movement in all extremities, CT scan is sufficient in this population.97
A category of TSCI defines spinal cord injury without radiographic abnormality (SCIWORA). It originated prior to the use of MRI and but it is often defined as the presence of neurologic deficits in the absence of bony injury on a complete, technically adequate, plain x-ray series or CT scan. Because an MRI provides superior imaging of the spinal cord, it can detect injuries to the cord that exist despite the apparent absence of bony abnormalities.98 Nevertheless, many patients with SCIWORA also have no detectable lesion on MRI.99
A common explanation for this phenomenon is transient ligamentous deformation with spontaneous reduction. This injury pattern is more common in children who have weak paraspinal muscles, elastic spinal ligaments, lax soft tissues, disc prolapse and cervical sponylosis which fail to protect the spinal cord from force but has also been described in adults.
Other possible mechanisms for SCIWORA include radiographically occult intervertebral disc herniation, epidural or intramedullary hemorrhage, fibrocartilaginous emboli from an intervertebral disc that has ruptured into the radicular artery, and traumatic aortic dissection with spinal cord infarction. MRI is invaluable for the diagnosis of these conditions.
Clinicians should suspect a cervical ligamentous injury in the injured patient who has persistent severe pain or paresthesias or focal neurologic findings (e.g., upper extremity weakness) in the absence of a fracture seen on plain x-ray or CT. Such injuries may be unstable, although they are rarely associated with permanent neurologic damage.
Patients with TSCI require intensive medical care and continuous monitoring of vital signs, cardiac rhythm, arterial oxygenation, and neurologic signs in the intensive care unit (ICU). 100,101 Many systemic, as well as, neurologic complications are common in the first days and weeks after TSCI, contribute substantively to prognosis, and are potentially avoidable or ameliorated with early intervention.101
The management of medical issues specific to spinal cord injury include the following:
Associated head injury occurs in about 25% of patients with spinal cord injury. A careful neurologic assessment for associated head injury is compulsory.
Neurogenic shock refers to hypotension, usually with bradycardia, attributed to interruption of autonomic pathways in the spinal cord causing decreased vascular resistance.
Patients with TSCI may also suffer from hemodynamic shock related to blood loss and other complications. An adequate blood pressure is believed to be critical in maintaining adequate perfusion to the injured spinal cord and thereby limiting secondary ischemic injury.
Guidelines currently recommend maintaining mean arterial pressures of at least 85 to 90 mmHg, using intravenous fluids, transfusion, and pharmacologic vasopressors as needed.101-104 Maintenance of blood pressure intraoperatively is also important.
Patients with multiple injuries often receive large amounts of intravenous fluids usually an isotonic crystalloid solution to a maximum of 2 L for various reasons. Excess fluids cause further cord swelling and increased damage and places the patient at increased risk for acute respiratory distress syndrome (ARDS).
Interventions include monitoring of:
Bradycardia may require external pacing or administration of atropine. This complication usually occurs in severe, high cervical (C1 through C5) lesions in the first two weeks after TSCI. 105,106
Autonomic dysreflexia is usually a later complication of TSCI, but may appear in the hospital setting, requiring acute management.107 This phenomenon is characterized by episodic paroxysmal hypertension with headache, bradycardia, flushing, and sweating.
Aspiration and pulmonary complications are the most frequent category of complications during acute hospitalization after TSCI which contribute substantively to early morbidity and mortality and both are related to the level of neurologic injury. 89,101,108-110 Respiratory complications include:
The incidence of these pulmonary complications is highest with higher cervical lesions (up to 84%), but they are also common with thoracic lesions (65%).
Weakness of the diaphragm and chest wall muscles leads to impaired clearance of secretions, ineffective cough, atelectasis, and hypoventilation.
Signs of impending respiratory failure, such as increased respiratory rate, declining forced vital capacity, rising pCO2, or falling pO2, indicate urgent intubation and ventilation with positive pressure support. 89,110,111
Rapid-sequence intubation with in-line spinal immobilization is the preferred method of intubation when an airway is urgently required.
If time is not an issue, intubation over a flexible fiberoptic scope may be a safer, effective option. Tracheostomy is performed within 7 to 10 days, unless extubation is imminent.
For patients with concomitant pneumothorax and/or hemothorax chest tube thoracostomy may be performed.
With a goal of preventing atelectasis and pneumonia, interventions include:
Deep venous thrombosis (DVT) is a common complication of TSCI, occurring in 50 to 100% of untreated patients, with the greatest incidence between 72 hours and 14 days. 112,113
The level and severity of TSCI does not clearly have an impact on the risk for DVT. All patients should receive prophylactic treatment.
Low-molecular-weight (LMW) heparin (considered the treatment of choice for patients with TSCI). 101,114-116 Combining LMW heparin with pneumatic compression stockings may provide additional benefits, but this has not been studied.
Use of either low-dose unfractionated heparin therapy or pneumatic compression stockings as monotherapy is considered inadequate protection117, but combination therapy with these two approaches may be considered an alternative to LMW heparin.
Inferior vena cava filters should be inserted for patients for whom anticoagulation is contraindicated.101
When using opiates with potential sedating properties, the need for pain control must be balanced with the need for ongoing clinical assessment, particularly in patients with concomitant head injury. Pain is often reduced by realignment and stabilization of the cervical fracture by surgery or external orthosis.
Pressure sores are most common on the buttocks and heels and can develop quickly (within hours) in immobilized patients.101
Initially, an indwelling urinary catheter must be placed to avoid bladder distension, to monitor urine output and to decompress the neurogenic bladder. Urine output should be more than 30 mL/h.
Rarely, inotropic support with dopamine or norepinephrine is required and should be reserved for patients who have decreased urinary output despite adequate fluid resuscitation. Usually, low doses of dopamine in the 2 to 5 mcg/kg/min range are sufficient.
Three or four days after injury, intermittent catheterization should be substituted, as this reduces the incidence of bladder infections.101
Urologic evaluation with regular follow-up is recommended for all patients after SCI.118
Gastrointestinal stress ulceration
Patients with TSCIs, particularly those that affect the cervical cord, are at high risk for stress ulceration.119 Prophylaxis with proton pump inhibitors is recommended upon admission for four weeks.109
Bowel motility may be silent for a few days to weeks after TSCI. Placement of a nasogastric (NG) tube is essential to prevent aspiration. Aspiration pneumonitis is a serious complication in the patient with a spinal cord injury with compromised respiratory function. Antiemetics should be used aggressively.
Patients should be monitored for bowel sounds and bowel emptying and should not ingest food or liquid until motility is restored.120
Prevent hypothermia. Patients with a cervical spinal cord injury may lack vasomotor control and cannot sweat below the lesion. Their temperature may vary with the environment and needs to be maintained.
Interventions may include:
There is limited evidence that glucocorticoid therapy improves neurologic outcomes in patients with acute TSCI, and such therapy is not endorsed by major society guidelines. Methylprednisolone is the only treatment that has been suggested in clinical trials to improve neurologic outcomes in patients with acute, nonpenetrating TSCI. However, the evidence is limited, and its use is debated.121
In 2013, based upon the available evidence, the American Association of Neurological Surgeons and Congress of Neurological Surgeons stated that the use of glucocorticoids in acute spinal cord injury is not recommended.122 Position statements from the Canadian Association of Emergency Physicians, and endorsed by the American Academy of Emergency Medicine, concur that treatment with glucocorticoids is a treatment option and not a treatment standard.123-125 A Consortium for Spinal Cord Medicine similarly concluded that "no clinical evidence exists to definitely recommend" the use of steroid therapy.126 In a 2006 survey of 305 neurosurgeons in the United States, 91% used glucocorticoids to treat patients with nonpenetrating TSCI within eight hours of injury.127 In contrast, a 2008 survey of Canadian spine surgeons found that 76% did not prescribe glucocorticoids even while 76% had reported administering methylprednisolone five years earlier.128
Indications for use of Methylprednisolone:
Contraindications to the use of glucocorticoids include:
There are little data regarding the use of methylprednisolone with penetrating spinal cord injuries since retrospective studies suggest a higher rate of complications and no evidence of benefit.129-131
Similarly, the results of NASCIS II and III studies may not apply to individuals with multisystem trauma, in whom the risk of complications is likely higher than those with isolated spinal cord injury.132
Patients with TSCI require urgent neurosurgical consultation to manage efforts at decompression and stabilization.
There are currently no standards regarding the role, timing, and method of vertebral decompression in acute spinal cord injury.31 Options include:
This technique involves use of longitudinal traction using skull tongs or a halo headpiece. An initial weight of 5 to 15 pounds is applied. This is increased in five-pound increments, taking lateral x-rays after each increment is applied. The more rostral the dislocation, the less weight is used, usually about three to five pounds per vertebral level. While weights up to 70 pounds are sometimes used, it is suggested that after 35 pounds is applied, patients be observed for at least an hour with repeat cervical spine x-rays before the weight is cautiously increased further. Administration of a muscle relaxant or analgesic, such as diazepam or meperidine, may help facilitate reduction. For cervical spine fracture with subluxation, closed reduction methods are a treatment option.
Thoracic and lumbar fractures do not respond to closed treatment methods.
Goals for surgical intervention in TSCI include:
Indications for cervical spine surgery include significant cord compression with neurologic deficits, especially those that are progressive, that are not amenable or do not respond to closed reduction, or an unstable vertebral fracture or dislocation.133 Neurologically intact patients are treated nonoperatively unless there is instability of the vertebral column.
Most penetrating injuries require surgical exploration to ensure that there are no foreign bodies imbedded in the tissue, and to clean the wound to prevent infection.
Defining surgical indications for closed thoracolumbar fractures has been somewhat more challenging, in part because of difficulties defining spinal instability in these lesions.
The timing of surgical intervention is not defined and remains somewhat controversial.101 Animal and some clinical studies suggest that early relief of spinal cord compression (within eight hours) leads to a better neurologic outcome.31,134-138 However, older clinical reports suggested that early surgery led to increased medical complications and poorer neurologic outcome, perhaps as a reflection of the vulnerability of the acutely injured cord.139-141 More contemporary studies suggest that medical complication rates are actually lower in patients who undergo early surgery, which allows for earlier mobilization and reduced length of ICU and hospital stay.142-148
Most clinicians consider deteriorating neurologic function after incomplete TSCI to be an indication to perform surgery as early as possible if there are no contraindications (e.g., hemorrhagic shock, blood dyscrasias).
In a 2010 survey of spine surgeons, the majority (>80% of 971 respondents) reported a preference to decompress the spine within 24 hours of TSCI.149 Shorter time intervals (within 6 to 12 hours) are preferred by most surgeons for certain lesions, including incomplete cervical TSCI. A 2011 report of an expert panel concurred with this approach.138
Not all surgical cases require decompression, and not all decompression cases require instrumentation and fusion. The technical aspects of the surgery are tailored to the individual case.
In the case of a cervical fracture with a cervical spinal cord injury, the anesthesiologist usually performs a fiberoptic intubation, done with the patient awake to reduce any further cord injury that potentially could be caused by a regular intubation with neck movement and extension.150 There is a risk for regurgitation and aspiration with the patient in a head-dependent position. Anesthetists are also usually involved in the postoperative care of patients with TSCI.151
Many strategies are being investigated as potential treatments of acute TSCI29 but are not currently recommended.147 Among others, these include:
Early death rates after admission for TSCI range from 4 to 20%. 1,159-163 The patient's age, level of spinal cord injury, and neurologic grade predict survival. Severe systemic injuries, traumatic brain injury, and medical comorbidity also increase mortality.162-164 Compared with spinal cord injuries in the thoracic cord or lower, patients with C1 to C3 injuries have a 6.6-fold increased risk of death, C4 to C5 injuries a 2.5 increased risk, and C6 to C8 a 1.5 increased risk.108 Survivors of TSCI have a reduced life expectancy as well.
Rates of motor score improvements are also related to the initial severity and level of injury.165-167 The greatest degrees of improvement are seen in those with incomplete injury and in those without significant comorbidities or medical complications, such as infection. 168,169
Among patients with complete TSCI (ASIA grade A):
Among patients with an initial ASIA grade B:
Among patients with an initial ASIA grade C and D
Most recovery in patients with incomplete TSCI takes place in the first six months.170 The general expectations for functional recovery based on motor level are outlined in the Table (Table 4).171 These assume an uncomplicated, complete SCI (ASIA grade A) followed by appropriate rehabilitation interventions in a healthy, motivated individual.
Activities of Daily Living
|C1-C4||Feeding possible with balanced forearm orthoses. Computer access by tongue, breath, voice controls. Weight shifts with power tilt and recline chair. Mouth stick use.||Operate power chair with tongue, chin, or breath controller.|
|C5||Drink from cup, feed with static splints and setup. Oral/facial hygiene, writing, typing with equipment. Dressing upper body possible. Side-to-side weight shifts.||Propel chair with hand rim projections short distances on smooth surfaces. Power chair with hand controller.|
|C6||Feed, 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, bathing. Bowel and bladder care with setup.||Propel chair, including curbs and wheelies. Wheelchair-to-car transfers.|
|T1||Independent in all self-care.||Transfer from floor to wheelchair.|
|T2-L1||Stand with braces for exercise.|
|L2||Potential for swing-to gait with long leg braces indoors. Use of forearm crutches.|
|L3||Potential for community ambulation. Potential for ambulation with short leg braces.|
|L4-S1||Potential for ambulation without assistive devices.|
Per EMS (1300): 65-YEAR-OLD FEMALE, Mrs. Joan Hutton, fell backwards while stepping out of the bathtub following her shower hitting her back on the side of the tub. Denies LOC. Patient was able to crawl to the phone and call 911. C/o generalized back pain.
Upon arrival in the emergency department, EMS reports:
HR: 120-130, sinus tachycardia without ectopy
RR: 30-40, rapid, shallow
You observe: Patient is on a backboard with a semi-rigid cervical collar in place. Patient alert, oriented, cooperative. PERRLA. MAE’s. 20 gauge peripheral IV placed in right antecubital with 1000ml Normal Saline infusing at 100ml/hr. Patient on 2L/NP.
Continue backboard and semi-rigid collar.
Continue monitoring GCS to monitor neurologic status.
Repeat temperature: continue monitoring.
Place EKG leads to cardiac monitoring: monitor cardiac rhythm.
Place pulse oximetry: monitor SaO2.
Place BP cuff: monitor BP.
Draw stat Hgb/Hct, serum electrolytes, coagulation studies, cell blood counts: send to lab.
Bedside fingerstick for blood glucose level.
Draw ABG for stat results.
Insert urinary catheter and send stat urine drug screen to lab.
Primary and secondary surveys should be conducted.
Chest x-ray: AP and lateral
Thoracic spine x-rays: AP and lateral.
Discussion of Outcomes
GCS continues at 15.
Chest AP and lateral x-rays: chronic fractures of the left 3rd, 4th, 5th, and 6th ribs.
Thoracic spine x-rays both AP and lateral projections: compression fracture of T5 with about 70% loss of the height of the vertebral body. A second compression fracture of T7 resulted in about a 15% loss of height of the vertebral body. Kyphosis of the thoracic spine of about 30% has resulted. Associated findings include mild osteopenia and chronic fracture of the left 3rd, 4th, 5th, and 6th ribs.
All laboratory tests WNL.All vital signs WNL. BP now 130-140/82-90. HR 80-90, NSR without ectopy.
Continuing GCS of 15 with imaging studies indicative of compression fracture of T5 with about 70% loss of the height of the vertebral body. A second compression fracture of T7 resulted in about a 15% loss of height of the vertebral body. Kyphosis of the thoracic spine of about 30% has resulted.
Chest AP and lateral x-rays: chronic fractures of the left 3rd, 4th, 5th, and 6th ribs.
A neurosurgeon should be consulted for evaluation in the emergency department.
TSCI is a problem that largely affects young male adults because of motor vehicle accidents, falls, or violence. Blunt trauma, particularly motor vehicle collisions, accounts for most spinal column injuries. Approximately 3% of blunt trauma patients sustain such an injury. Elderly patients who fall are also at increased risk.
Most TSCI occurs with injury to the vertebral column, producing mechanical compression or distortion of the spinal cord with secondary injuries resulting from ischemic, inflammatory, and other mechanisms.
The cervical spine is the most commonly injured part of the spinal column. Within the cervical spine, the most common sites of injury are around the second cervical vertebra (C2, or axis) or in the region of C5, C6, and C7.
Associated injury of the spinal cord or possibly the brain (due to vascular compromise) are critical clinical considerations and must be investigated immediately. In the absence of apparent spinal cord or brain injury, the degree of fracture stability is the most important feature of any spinal column injury. Differences in the structure and location of the cervical and thoracolumbar portions of the spinal column lead to different types of injuries, although there is some overlap.
The cervical spinal column is susceptible to a wide range of fractures, dislocations, and ligamentous injuries. Compression fractures are the most common injury of the thoracolumbar spinal column.
Most TSCI is associated with injury to brain, limbs, and/or viscera, which can obscure its presentation. The neurologic injury produced by TSCI is classified according to the spinal cord level and the severity of neurologic deficits. Half of TSCIs involve the cervical spinal cord and produce quadriparesis or quadriplegia.
The initial evaluation and management of patients with TSCI in the field and emergency department focuses on the ABCDs (airway, breathing, circulation, and disability), evaluating the extent of traumatic injuries, and immobilizing the potentially injured spinal column.
Patients with suspected TSCI because of neck pain or neurologic deficits and all trauma victims with impaired alertness or potentially distracting systemic injuries require continued immobilization until imaging studies exclude an unstable spine injury.
All patients with potential TSCI should receive complete spinal imaging with plain x-rays or helical CT scan.
Patients with abnormal screening imaging studies or in whom TSCI remains strongly suspect despite normal screening imaging studies should have follow-up CT scanning with fine cuts through the region of interest (based on localized pain and/or neurologic signs).
MRI can be useful to further define the extent of TSCI and should be performed on stable patients with TSCI, as well as, on patients suspected to have TSCI (because of neck pain or neurologic deficits) despite a normal CT scan. Patients with TSCI require urgent neurosurgical consultation to manage efforts at decompression and stabilization.
Patients with acute TSCI require admission to an ICU for monitoring and treatment of potential acute, life-threatening complications, including cardiovascular instability and respiratory failure. Patients with TSCI should receive prophylaxis to protect against the plethora of medical complications associated with TSCI. There is limited evidence that glucocorticoid therapy improves neurologic outcomes in patients with acute TSCI, and such therapy is not endorsed by major society guidelines.
Because the neurologic benefits are uncertain, glucocorticoid therapy is NOT recommended in cases when there are clear risks associated with such therapy, such as penetrating injury, multisystem trauma, moderate to severe traumatic brain injury, and other comorbid conditions associated with risk of complications from glucocorticoid therapy.
In other patients who present within eight hours of isolated, nonpenetrating TSCI, administration of intravenous methylprednisolone can be considered with knowledge of potential risks and uncertain benefits. The standard dose of intravenous methylprednisolone is 30 mg/kg IV bolus, followed by an infusion of 5.4 mg/kg per hour for 23 hours.
Braddom R. Physical medicine and rehabilitation. 2nd ed. Philadelphia,PA: WB Saunders Company; 2000: 1236.