Spine and Spinal Cord Injuries

Andrea L. Strayer

Joanne V. Hickey

A PERSPECTIVE

The following statistical information describes spinal cord injuries (SCIs) in the United States (US) as of February 2012.¹ There are an estimated 12,000 new SCIs per year and approximately 1,60,000 suffer traumatic spinal (vertebral) column injuries without SCI. The majority of these injuries are cervical and lumbar spine fractures with an additional 15% to 20% occurring at the thoracolumbar junction (T-11 to L-2) and 9% to 16% in the thoracic spine levels L-1 to L-10.¹ Because no overall incidence studies of SCIs in US have been reported since the 1970s, it is not known whether the pattern of incidence has changed in recent years. The estimated number of people living with SCIs is 2,70,000, with a range of 2,36,000 to 3,27,000 persons.

Historically, young adults were primarily affected by SCIs; the average age at injury was 28.7 years, (most occurring between the ages of 16 and 30). With the growth of the US geriatric population, since 2005 the average age of injury is now 41 years. Most significant has been the number of people older than 60 years of age at time of injury, which has increased from 4.7% prior to 1980 to 10.8% in 2005. However, the most common age at injury is 19 years of age, with 24.9% being injured between the ages of 17 and 22. Over 80% of SCIs occur among males. Since 2005, the major categories of cause of injury include motor vehicle crashes (39.2%), falls (28.3%), acts of violence (primary gunshot injuries, 14.6%), and recreational sports (8.2%). At discharge, the most common diagnosis is incomplete tetraplegia (40.8%), followed by complete paraplegia (21.4%), incomplete paraplegia (21.4%), and complete tetraplegia (15.8%). Less than 1% of persons experienced complete neurological recovery by hospital discharge. Nearly 60% of persons who sustain SCIs are employed at the time of injury. However, by 1 year post injury, only 11.7% of persons with SCI are employed. At discharge from the hospital, 89.3% of persons with SCIs return to noninstitutional settings such as their home. Only 6.6% are discharged to nursing homes. The length of stay in the hospital in 2005 was approximately 11 days and 37 days in acute rehabilitation. The average yearly expenses for SCIs are highest the first year, with higher costs for high-level (C-1 to C-4) tetraplegics. The estimated lifetime cost for a high-level tetraplegic who is 25 years old is $45,43,182, as compared to $24,96,856 for someone who is 50 years old. For paraplegics, the cost for the same age categories is $22,21,596 versus $14,57,967, respectively. The major causes of death among persons with SCIs are pneumonia, septicemia, and pulmonary emboli.

In summary, the SCI statistics reported from the National Spinal Cord Injury Statistical Center reflect SCI primarily affects young adults. However, there has been a significant increase in the number of elders suffering from SCI. Even though costs are high, the length of stay in the hospital and acute rehabilitation has decreased by over 50% since 1979.²

Regarding cervical spine-injured patients without SCI, the most often injured level is C-2 (38%).³ Elders are especially at risk from a number of factors including decreased mobility and postural instability; visual impairments; and sensorineural impairment, leading to falls.⁴ In addition, decreased bone quality and increased stiffness of the spinal column add to fracture risk from low impact events such as fall from standing or sitting height. The aging population will invariably lead to more elders with spine fractures and SCI.

Comprehensive Evidence-Based Practice

Created by congressional act in 1970, the Spinal Cord Injury Model System Program was established to develop evidence-based and best-practice models that are cost effective for the care of SCI patients across the continuum of care, from accident scene through rehabilitation. Funded by the National Institute on Disability and Rehabilitation Research, there are currently fourteen model SCI programs across the country. Each provides a major research- and evidence-based practice focus while providing exemplary patient care. The American Spinal Injury Association (ASIA) and the International Medical Society of Paraplegia (IMSOP) published the International Standards for Neurological and Functional Classification of Spinal Cord Injury.⁵, ⁶ Revised in 2011, the ASIA scale is the standard method for communicating neurological status following SCI. The Consortium of Spinal Cord Medicine has a very comprehensive and practical guideline for early acute management in adults with SCI.⁷ In addition to early acute management available through the Consortium are guidelines on topics such as autonomic dysreflexia (AD), neurogenic bowel and bladder management, sexuality, and depression. The American Association of Neurological Surgeons and the Congress of Neurological Surgery Section on Disorders of the Spine and Peripheral Nerves published in 2013, Guidelines for the Management of Acute Cervical and Spinal Cord Injuries⁸; previously published in 2002, these guidelines provide an up-to-date review of the medical literature on 22 topics regarding care, management, imaging, and treatment of patients with acute cervical spine and/or SCIs. Please refer to “Websites” at the end of this chapter for further information.

UNDERSTANDING THE SPINE AND SPINAL CORD INJURIES

Anatomic Considerations

To appreciate the potential for injury to the spinal axis and its surrounding structures, one must understand the interrelated function of the anatomic structures involved including the vertebral or (spinal) column, the ligaments, intervertebral discs, muscles, and the neural elements (the spinal cord and spinal nerves). The spinal column develops cervical and lumbar lordotic curves as one matures and gravitational forces of the weight of the head and upright posture occur. The vertebrae, stacked one upon another to form a column, provide stability and support as well as protection for the spinal cord and spinal nerves. There are 33 vertebrae in the vertebral column: seven cervical (C), twelve thoracic (T), five lumbar (L), five sacral (S) (fused as one), and four coccygeal (fused as one). The vertebrae of each area have a distinctive shape with inferior and superior articulating processes forming a facet joint, to fit into position with the support of structures called ligaments. The ligaments, muscles, and other supporting structures are considered to be soft-tissue components (Figs. 17-1 and 17-2; see also Chapter 5).

There are two main parts to a vertebra: the body (ventral/anterior) and the arch (dorsal/posterior). The vertebral bodies are separated by intervertebral discs that serve as shock absorbers as well as providing constraint and preventing excessive translation (sliding) during movement of the spinal column. The arch of the vertebra is created by two pedicles, two laminae, two transverse processes, and the spinous process posteriorly. The inferior and superior articulating processes form the facet joint, a synovial joint. The various projections of the vertebral arch allow for alignment, flexion, and movement of the vertebral column.

Figure 17-1 ▪ Level of spinal cord injury and functional loss; the higher the spinal cord injury, the more motor, sensory, and autonomic functional losses are incurred.

The C-1 (atlas) and C-2 (axis) vertebrae are unique from each other, as well as the rest of the spine. C-1 articulates with the cranium, along with highly structured ligamentous support, and provides significant flexion and extension of the head. C-2, articulating with C-1, provides the majority of cervical rotation and the stability of the upper cervical spine. The odontoid process of C-2 sits ventrally with C-1 pivoting around it, again, with intricate ligamentous support. Both C-1 and C-2 have transverse foramen on either side, for the vertebral artery to travel through. The soft, vulnerable spinal cord passes through the spinal canal formed by the vertebral body and posterior elements. The spinal cord ends with the conus medullaris, at approximately L-1 to L-2. Flowing below the conus medullaris are the lumbar and sacral nerves, called the cauda equina which is the Latin term for “horse’s tail.”

The close anatomic relationship and functional synergy of the spinal column, spinal cord, ligaments, and surrounding soft-tissue structures increases the probability that injury to any one of these structures can cause concurrent injury to any or all of the other structures. In other instances, injury to one structure, such as a vertebral fracture, can create the potential for injury to another structure, such as the spinal cord, if the primary injury is not treated promptly and effectively. Therefore, when discussing injury to the vertebral column and spinal cord, consider the interrelatedness of not only these two structures, but also the supporting softtissue structures and the intervertebral discs. (Note that spine and SCIs are discussed in this chapter, while intervertebral disc disease is the focus of Chapter 18).

Kinetics of Movement

The cervical spine, comprising of seven vertebrae, provides for movement in all directions including flexion, extension, rotation, and lateral bending while supporting the head that weighs 8 to 10 lbs (3.62 to 4.53 kg). The unique anatomy of the upper cervical spine (occiput to C-2) gives us significant motion of our head, allowing 40 degrees or 40% of the total unilateral axial rotation (turning your head left or right). In addition, a total of 45 degrees of combined flexion/extension occurs from occiput through C-2.⁹ Distributed throughout the mid and lower cervical spine, also termed the subaxial spine, is a total of about 60 to 75 degrees of flexion/extension. Beneath the cervical vertebrae are the 12 thoracic vertebrae, which move very little, owing to the anchoring of the ribs. The lumbar spine consists of five lumbar vertebrae that are quite substantial as compared to cervical vertebra. The cervicothoracic and thoracolumbar transition zones are at increased risk of injury because these areas are transitioning from mobile cervical and lumbar spine to immobile thoracic spine. Forces along the stiff highly supported thoracic spine are transferred to the mobile lumbar spine through the thoracolumbar junction. Biomechanically, this transition zone is susceptible to injury and is the most commonly injured portion of the spine.¹⁰ Because the cervical spine is mobile and not fixed like the thoracic spine, it is vulnerable to injury as a result of forces placed upon it.

Figure 17-2 ▪ A: Lateral radiograph of the cervical spine (AA-anterior arch of C-1). B: MRI scan of the thoracic spine. C: Lateral radiograph of lumbar spine. F, Facet joint; DS, Intervertebral disc space; IA, Inferior articular process; IV, Intervertebral foramen; P, Pedicle; SA, Superior articular process; SP, Spinous process. Vertebral bodies are numbered.

Responses to Forces Placed on the Spinal Column

Fracture patterns are a result of the alignment of the spine at the moment of impact and the direction and degree of the force (energy) applied. Most injuries are the result of a complex combination of forces. The following section provides an overview of description of injuries. Important to appreciate is that the injury is due to the forces or the energy exerted on the patient—their spine, spinal cord, and soft tissues. It is the role of the nurse to carefully and thoroughly assess the patient so that there is confidence in the neurological examination and current condition of the patient.

SPECIFIC CATEGORIES OF INJURIES

Soft-Tissue Injuries

Whiplash-Associated Disorders

Whiplash-associated disorders are a constellation of symptoms that may result from an acceleration-deceleration mechanism of energy transfer to the neck.¹¹ Typically, symptoms are triggered by a motor vehicle collision to the rear or back side. However, symptoms can
occur as a result of diving, sports, etc. Usual signs and symptoms include stiff neck, pain in the neck and shoulders, occasionally the arms, decreased cervical mobility, and muscle spasms. Other signs and symptoms may include headache that is generally described as occipital which may radiate to the forehead, paresthesias in the hands, nausea, dizziness, vertigo, and tinnitus. The findings on physical examination are normal except for the previously listed signs and symptoms. The radiologic examination is negative. If physical or radiographic examination reveals any abnormal findings, further evaluation is warranted. The diagnosis is based on the history of injury and the presence of the characteristic signs and symptoms. This is a common injury causing much pain and suffering to the patient, even though no abnormalities are noted on radiographic examination.

The pain caused by whiplash is thought to be multifactorial. Potentially involved are the epiphyseal joints and capsules, dorsal root ganglion, spinal ligaments, muscles, vertebral discs, and the vertebral artery. In addition, psychosocial and sociocultural factors are likely to play a role in the persistence of pain symptoms as a result of whiplash injury. Patients with pre-existing cervical spondylosis, increased spinal column rigidity, or central canal or neuroforaminal narrowing from other spine conditions put them at greater risk of developing neurological problems if a whiplash injury occurs.¹²

Management. Management of an acute whiplash-injured person is based on presenting clinical symptoms, and assuring no underlying pathology (spine fracture). Treatment involves education, pain management, physical rehabilitation, and psychological intervention. Literature synthesis reveals treatments ranging from immobilization with a collar to active mobilization.¹³ While the evidence lacks consistency, exerciseand mobilization-based therapies have the greatest support for reducing the duration and severity of whiplash symptoms. Education is best delivered in person, face to face; however, patient preference for method of delivery should be taken into account. Pain management includes nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen. Approximately 50% of patients who have suffered a whiplash injury continue to complain of pain 1 year after injury. For those with chronic symptoms, further treatment options including epidural steroid injections, trigger point injections, facet joint injections, and percutaneous radiofrequency rhizotomy may be offered.¹³

Ligamentous Injuries

Vertebral column stability highly depends on an intact ligamentous structure to resist hypermobility of the spine. Therefore, ligamentous injury that occurs with trauma can render the vertebral column unstable. Ligamentous injury without bony fracture is most common in the upper cervical spine, but does also occur in the subaxial cervical spine. The other soft-tissue injuries with significance for vertebral stability are discussed in this chapter in conjunction with vertebral injury and SCI.¹⁴

Vertebral Injuries

Classification

Numerous classification systems specific to particular segments of the spine (upper cervical, subaxial, thoracic, thoracolumbar, lumbar, and sacral) are available. These classification systems are based on factors such as mechanisms of injury, radiographic findings, injury severity, and neurological status. All classification systems have strengths and weaknesses, and many of the systems’ goals of care overlap. The impetus of all classification systems is to improve communication amongst care providers; aid the physician with appropriate treatment decision making and injury prognosis; and provide consistency between providers and institutions to facilitate outcomes research.¹⁵ While fracture classification is important for the previously stated reasons, astute nursing care of the patient who has suffered a spinal trauma with or without SCI relies on keen assessment of the patient’s clinical condition as a result of their trauma—not classifying their particular injury type. To provide the neuroscience nurse with the background for medical conversations and decision making, an overview of differing spinal injury classification approaches will be briefly discussed. These approaches of defining injury are different from each other, with one not necessarily better than another. Just as spine and SCI are highly complex, so is the language in attempting to describe their cause and resultant patient sequela. Vertebral (spinal) bony injury descriptive classification approaches include the following.

Mechanistic: flexion, extension, axial load, rotation, penetrating
Radiographic: compression, burst, teardrop, facet dislocation fractures
Stability or instability of injury: according to a two- or threecolumn framework
Segment of spinal column involvement: upper cervical, subaxial cervical, thoracic, thoracolumbar, lumbar, and sacral

Each category offers a special practical perspective and is discussed in the following section.

Mechanistic Classification of Vertebral Injury

Cervical spine injuries generally occur from rapid head deceleration, such as the head hitting a solid surface. Fracture patterns are a result of the alignment of the spine at the moment of impact and the direction and degree of the force (energy) applied. Spinal column injuries at any level are the result of a complex combination of forces. Mechanisms of injury include flexion, extension, axial loading, rotation, and penetrating injury of the spinal column.

Hyperflexion tends to produce compression of the vertebral bodies with disruption of the posterior longitudinal ligaments and the intervertebral discs. Motor vehicle crash is an example (Fig. 17-3).

Figure 17-3 ▪ Hyperflexion injury. With hyperflexion to the cervical spine, there may be tearing of the posterior ligamentous complex, resulting in anterior dislocation.

Figure 17-4 ▪ Burst fracture subsequent to axial loading.
Axial loading, also known as vertical compression, occurs when a vertical force is exerted on the spinal column. Axial loading is seen in injuries resulting from diving accidents, landing on the feet when jumping from a height, or landing on the buttocks when falling from a height (Fig. 17-4).
Hyperextension usually causes fractures of the posterior elements of the spinal column and disruption of the anterior longitudinal ligaments. Falling downstairs is an example of an event leading to a hyperextension injury.
Excessive rotation refers to turning of the head beyond the normal range on the horizontal axis. This can result in compression fractures, tearing or rupture of the posterior ligament, dislocation at the facet joint, and fracture at the articular processes.
Penetrating injuries occur when missiles, such as bullets or shrapnel, or impalement instruments (knives, ice picks) penetrate the spinal column. The object may shatter bone, create bone fragments, or transect a portion or complete plane of the spinal cord or soft tissue.

Radiographic Classification

Radiographic classification, complementary to the clinical examination, is a means to describe fracture type utilizing the visualized radiographic picture following injury. For the purposes of this discussion, vertebral fractures are subdivided into simple compression fractures, severe compression/burst fractures/axial compression injuries, teardrop fractures/severe compressive flexion injuries, cervical facet dislocations/distractive flexion injuries, hyperextension/distractive extension injuries, and dorsal element fractures.

Compression Fractures

Compression fractures are sometimes further subclassified as simple compression fractures, burst fractures, and teardrop fractures. They are caused by axial loading and hyperflexion.

A simple compression fracture is caused by forceful axial loading or flexion and may involve the upper or the lower vertebral end plates. With a more significant injury, may involve both upper and lower endplates. There is no ligament disruption, facet injury, or subluxation. No surgery is required. These fractures heal well with a semirigid collar immobilization for about 2 months.¹⁵
Burst fractures (severe compression/axial compression injuries) are the result of axial loading with various flexions under significant forces/high energy. The result is crush injury and possible retropulsion of bone into the spinal canal. The posterior bony arch and ligamentous complex remains intact. If there is no neurological damage and if the posterior ligaments are stable, wearing a hard collar for 2 months may be adequate therapy (Fig. 17-5). However, burst fractures may require neurosurgical procedure for the removal of bone fragments, cord decompression, and spinal stabilization. Stabilization is accomplished by insertion of instrumentation, such as rods and screws to hold the spine in alignment, so that bony healing can take place. See section on surgical management for further discussion.
Teardrop fractures (severe compression flexion injuries) are caused by extreme flexion with axial loading. With this fracture, a vertebral body is crushed by the vertebral body superior to it, causing the anterior portion of the compressed body to break away with disruption of the posterior elements at the same time. These unstable fractures have a high rate of neurological injury and require surgical decompression and stabilization¹⁵ (Fig. 17-6 A,B).
Cervical facet dislocations (distraction flexion injuries) can be unilateral or bilateral. Unilateral cervical facet dislocations usually result in approximately 25% subluxation of the upper vertebral body over the lower one. Bilateral facet dislocations often demonstrate 50% or greater subluxation. There may be associated facet fracture, disruption of the posterior ligaments, and musculature from the high-energy impact of this injury. This is an unstable injury with neurological injury common in bilateral facet dislocation. Subluxation is a partial or incomplete dislocation of one vertebra over another. Damage to the cord and supporting ligaments may or may not be present. With dislocation, re-establishment of alignment is necessary. This may be accomplished by traction followed by surgical stabilization with internal stabilization and fusion.¹⁵, ¹⁶
Hyperextension injuries (distraction extension injuries) demonstrate disruption of the anterior longitudinal ligament and disc from forced hyperextension. This is often seen in elderly patients who have a stiff spine, and a low energy fall places forces to the injury site. In more severe cases, there may also be posterior element disruption. Most require surgical stabilization¹⁵, ¹⁶ (Fig. 17-7).
Spinous process (dorsal element fractures) and other posterior bony fractures can be associated with more severe fractures, and require careful evaluation to rule out additional injury. The type and degree of these fractures is highly variable, as is the treatment.¹⁵, ¹⁶

Figure 17-5 ▪ Burst and compression fractures. A: Burst fracture. Axial compressive forces may result in severe vertebral body fractures involving the anterior and middle columns with a collapse of the entire vertebral body, often with retropulsion into the spinal canal. This is a potentially unstable fracture, often with accompanying spinal cord injury. B: Compression fracture. A compression fracture is a wedgeshaped fracture (also called wedge fracture) of the vertebral body involving the anterior column. It occurs in the thoracic and lumbar region, most often in the midthoracic and midlumbar region. Compression fractures can occur with minor trauma in older patients with osteoporosis and in younger people with significant trauma.

Stability of the Spine Classification

Stability or Instability of the Spinal Column. The concept of stability of the spinal column was classically addressed by White and Panjabi. Clinical stability, as per their definition is “the ability of the spine under physiologic loads to limit patterns of displacement so as to not damage or irritate the spinal cord and nerve roots and, in addition, to prevent incapacitating deformity or pain due to structural changes.”¹⁷ If the spinal column is unable to structurally support the load it must bear, the spinal column becomes unstable, which results in potential injury and predisposes the spinal column to further failure and the neural elements to injury. Therefore,
nurses will hear much discussion about the clinical stability or conversely instability of the spinal column, which influences the medical and surgical management of the patient.

Figure 17-6 ▪ 18-year-old unrestrained male involved in high-speed rollover crash. Suffered C-5 incomplete spinal cord injury as demonstrated by initial neurological exam of right tricep and hand grasp 2/5 with full strength in bicep and deltoid on the right. Right leg with 3/5 hip flexor, otherwise full strength. Left arm and leg full strength. Sensation intact to pain throughout. Reflexes 2/4 throughout. A: MRI scan, sagittal, T-2 weighted demonstrates anterior tissue edema, C-5 tear drop fracture, hyperintensity within the spinal cord, and ligamentous damage posteriorly. B: CT scan, sagittal reconstruction demonstrates very well the C-5 tear drop fracture caused by high-energy flexion injury.

Figure 17-7 ▪ Hyperextension injury in the subaxial spine is often related to falls where the head is forcefully hyperextended. This can cause rupture of the anterior longitudinal ligament, disc disruption, and stretching of the spinal cord that can lead to central cord syndrome.

It is critical when considering spinal trauma to distinguish between stable and unstable injuries. Medical decision making for this distinction includes evaluation of ligament integrity, the exact pattern of the fracture or dislocation, and the patient’s neurological examination. Many classification systems are utilized to determine spinal stability following trauma, one of those being the three-column theoretical framework.⁹ This approach is discussed in Chart 17-1. A stable spinal column is not apt to cause neural compromise and is able to resist the necessary loads, whereas an unstable spinal column is at risk of developing spinal deformity, which can lead to pain, and cause injury to the spinal cord and/or nerve roots. Internal immobilization or internal fixation (surgery) may be unnecessary for stable injuries, whereas it is essential for unstable injuries (Fig. 17-8).

Figure 17-8 ▪ A: C-6-C-7 fracture-dislocation with significant subluxation between C-6 and C-7; disruption of the anterior, posterior longitudinal, and interspinous ligaments as well as ligamentum flavum; severe cord compression at C-6-C-7 with signal change in the cord; small posterior epidural hematoma from C-6 to T-3. B: Surgery involved anterior decompression and instrumented fusion; posterior stabilization with instrumentation. At discharge his neurological exam revealed left tricep 4/5 and hand intrinsics 2/5. Right hand intrinsics 4/5. Leg strength full 9 months after injury, strength was full.

Classification According to Spinal Segment

Vertebral injuries can be divided into four groups based on the involved spinal region: upper cervical, subaxial cervical, thoracic and lumbar, and sacral.

Upper Cervical Spine

The four most commonly encountered upper cervical spine fractures are atlas fractures, atlantoaxial subluxation, odontoid fractures (Fig. 17-9), and so-called hangman’s fractures. Four less common injuries are occipital condyle fractures, atlanto-occipital dislocation, atlantoaxial rotary subluxation, and C-2 lateral mass fractures. A summary of upper cervical fractures and lower cervical fractures is presented in Table 17-1.

CHART 17-1 The Two- and Three-Column Frameworks: Spinal Stability and Instability

The purpose of defining the stability of a patient’s spine following injury is to delineate the most appropriate management for that individual. The two- and three-column frameworks are conceptual frameworks to use as a foundation for medical decision making. In clinical practice, the integrity of each component of the spinal segment must be carefully analyzed before making management decisions. Defining stability or instability is not simple, and requires in-depth knowledge of applied spinal anatomy and biomechanics of the spine. While many schemes for the classification of instability have been reported, the two- and three-column conceptual frameworks offer good foundations. The two-column approach consists of an anterior and a posterior column. The anterior column contains the anterior longitudinal ligament, intervertebral disc, vertebral body, and posterior longitudinal ligament. The posterior column consists of the posterior bony elements, facet joints, interspinous and supraspinous ligaments, and the ligamentum flavum. Anteriorly, the annulus fibrosis is the most important stabilizer. Posteriorly, the facet joints are the most important stabilizers. The three-column approach provides an anatomic framework for considering stability. The cross-section of the spine is organized into three anatomic columns. The anterior column consists of the anterior longitudinal ligament, anterior half of the vertebral body, annulus fibrosis, and disc. The middle column consists of the posterior half of the vertebral body, annulus, disc, and posterior longitudinal ligament. The posterior column consists of the facet joints, ligamentum flavum, posterior elements, and interconnecting ligaments. Applying this classification system to spinal injuries results in four classification categories, which are determined by the specific column(s) injured.
TYPE OF INJURY	COLUMNS INJURED
	Anterior	Middle	Posterior
Compression fractures	Yes	No	No
Burst fractures	Yes	Yes	No
Flexion-distraction fractures	Yes/No	Yes	Yes
Fracture-dislocations	Yes	Yes	Yes

The general rule of thumb is that when one column is injured, the spine is usually stable; when two or three columns are injured, the sustained injury is considered unstable.

Figure 17-9 ▪ Sagittal CT scan demonstrating Odontoid Type II fracture in a 72-year-old male who fell while intoxicated. He was neurologically intact. This fracture was managed in an external semirigid orthosis.

Subaxial Cervical Spine

Compared with the upper cervical segment, there is an increased risk of cervical cord damage in injuries to the lower cervical vertebrae (subaxial, i.e., below C-2). Two factors account for this: the size of the spinal canal is decreased in the lower cervical spine; and an increased prevalence of injuries that narrow rather than expand the canal. Mechanistic and radiographic classification as well as spinal stability all pertain to subaxial cervical vertebrae injuries, and have been discussed above.

The treatment options for subaxial cervical vertebral injuries include immobilization with sternal-occipital-mandibular orthotic device; halo vest; posterior fusion and stabilization with wires or instrumentation; anterior approaches for decompression; fusion with or without instrumentation; or a combination of these therapies.

Treatment choices depend on the specifics of the fracture or malalignment and on the stability of the ligaments.

Thoracic and Lumbar Spine

As with the cervical spine, there are many classification schemes for thoracic, thoracolumbar and lumbar vertebral fractures. The thoracic spine is a long stiff segment highly supported by the ribs. A combination of forces acts on the spine, resulting in different and diverse fracture patterns. The resultant fracture may or may not lead to neurological compromise. Assessment of fracture stability is key for the physician to ascertain. In addition, many of these fractures are caused by high-speed and very high-energy trauma, and careful attention to concomitant injuries (chest, abdomen, orthopedic) is warranted (Fig. 17-10).

Anatomically, the spinal cord begins tapering into a cone shape at T-11, ending at L-1 to L-2. As the cord tapers, it forms a cone called the conus medullaris, which continues at the filum terminale. The nerve roots coming off the lower segments of the spinal cord, termed the cauda equina, hang loosely and are susceptible to injury. Injury of the conus medullaris can occur with thoracolumbar spine fractures. These lesions can have confusing clinical presentations. Injury to the conus usually results in upper motor neuron symptoms (muscle spasticity, hyperreflexia), because of the disruption of the anterior gray horn cells, once past the initial period of spinal shock. Injuries involving the cauda equina produce single or multiple radiculopathies, lower motor neuron injuries. The sacral roots innervate bowel, bladder, and sexual function. The patient can present with highly variable clinical examination—from complete loss of function below the level of injury to mixed patterns of motor and sensory lumbar and sacral function to neurologically intact function. A conus medullaris syndrome generally involves symmetrical deficits, whereas cauda equina is generally asymmetric. Bowel and bladder dysfunction is unfortunately often permanent. Clinical examination will help differentiate injury and functional status. Decompression of the neural elements is necessary if there is compression¹⁸, ¹⁹ (Fig. 17-11).

Thoracic, Thoracolumbar, and Lumbar Spine Fractures

There are four general categories of vertebral fractures of the thoracic, thoracolumbar, and lumbar spine²⁰ (Table 17-2 and Fig. 17-12).

Wedge compression fractures, caused by axial load in flexion, are common in the thoracic and upper lumbar spine. Wedge compression fractures involve the anterior column. Typically, neurologically intact, bracing, and pain management is generally the treatment.
Burst fractures, caused by axial loads, involve the anterior and middle column with varying amounts of retropulsed bone fragments into the spinal canal. If the posterior column is also involved, the injury is unstable and warrants surgical intervention. Neurological injury is variable. If neurological deficits are present, emergent surgical decompression and stabilization is warranted.
Flexion-distraction injuries (also called Chance fractures) involve the middle and posterior columns with sparing of the anterior longitudinal ligament. The fracture can extend through the posterior elements, pedicle, and vertebral body or can be a ligamentous injury through the posterior ligamentous complex and the disc annulus complex. The mechanism of injury is acute flexion of the torso, for example, while restrained with only a lap belt. The flexion-distraction injuries (Chance fractures; Fig. 17-13) are classified according to the involvement of bone and soft-tissue components. These fractures are unstable and require surgical stabilization.
Fracture-dislocations are the result of high energy rotational forces, translational forces, or a combination of both. Fractures of this type are unstable, and involve all three columns. Patients generally suffer neurological sequela. In addition, abdominal organ and vascular injury are associated with this fracture type.

Sacral Spine

Fractures of the sacrum and coccyx typically result from highinjury impact, such as falls from a height. Increasingly, however,

low-energy falls from standing height have been implicated in sacral and coccyx fractures in the elderly and those with osteoporosis. Nerve injury in this region can range from a single nerve root to the entire cauda equina. Neurological sequela can cause bladder, bowel, or sexual dysfunction and saddle anesthesia.²¹

TABLE 17-1 CERVICAL VERTEBRAL INJURIES

TYPE	DESCRIPTION	TREATMENT
Upper Cervical Vertebral Injuries (Occiput to C-2)
Atlas (C-1) fractures	Result from vertical compression of the occipital condyles on the arch of C-1; cause single or multiple fractures of the C-1 ring; bony pieces thrust away from the center, increasing the space for the spinal cord; thus, neurological injury is rare. There are four types of atlas fractures. Isolated anterior arch fractures: avulsion from anterior part of ring (usually stable). Isolated posterior arch fracture (fx): hyperextension with compression of posterior arch of C-1 between occiput and C-2 (usually stable). Lateral mass fx: fx anterior-posterior to articular surface of C-1 with unilateral displacement; stable fx. Jefferson fx: burst fx into four pieces; can result in concurrent rupture of transverse ligament, resulting in instability.	Management of C-1 fractures based on integrity of transverse ligament. If the transverse ligament is intact, bracing with cervical collar or halo immobilization. If transverse ligament no longer intact, surgical stabilization is indicated. Posterior C-1-C-2 fixation with instrumentation generally preferred, but is surgeon preference.
Atlantoaxial subluxation	Caused by a weak or ruptured transverse ligament that stabilizes dens to anterior ring of atlas. Produces atlantoaxial instability; high risk for spinal injury due to compression of upper cervical cord against the posterior arch of C-1. Most common cervical spine fracture. Most often caused by hyperextension, but can occur from a number of mechanisms, especially fall from standing height in the elderly. Neurological injury rare. Odontoid fractures classified into three types. Type I: chip avulsion fx through the tip of the odontoid; stable fracture; heals well. Type II: fx through the base of the dens with separation, usually anteriorly, from the body of C-2; most common; poor blood supply to area; nonunion in 40-50%; treatment depends on severity and response to treatment options. Type III: fx line extends into the body of C-2.	Halo vest for 3 mos, only ligament injuries need a C-1-C-2 posterior fusion. Type I: cervical collar. Type II: can be difficult to heal, especially in the elderly; if fracture is stable, may be treated in cervical collar or halo immobilization with interval radiographic imaging to evaluate for healing; if unstable or does not heal with immobilization, surgical stabilization is indicated. This can be anterior with odontoid screw placement or posterior C-1-C-2 fixation. Type III: generally heal adequately in cervical collar.
Hangman’s fractures	Bipedicular fx with disruption of the disc and ligaments between C-2 and C-3 resulting from hyperextension and distraction. Named for injury seen in judicial hangings. Further classified according to amount of displacement and angulation of the C-2 body in relation to the posterior elements. Type I: fx of neural arch without angulation and with up to 3 mm of anterior C-2 displacement on C-3; stable fx. Type II: <5 mm anterior displacement or angulation of C-2 on C-3. Type IIA: severe angulation of C-2 on C-3 with minimal displacement because anterior longitudinal ligament is hinge. Type III: bipedicle fx associated with unilateral or bilateral facet dislocations; unstable; often neurological deficits present.	Type I: managed with a cervical collar or observation only. Type II: generally stable and managed in a collar. if significant displacement (>4-6 mm) halo immobilization may be indicated. Type IIA: likely unstable, surgical stabilization may be indicated. Type III: unstable, requiring surgical stabilization.
	Most types unstable; may or may not include neurological deficits depending on amount of displacement or angulation. Important to know type of fx to determine treatment.
Occipital condyle fractures	Rare injury caused by concurrent axial loading and lateral flexion. Can be associated with severe head injury. Two types: avulsion or comminuted compression fx.	Cervical collar.
Occipitocervical dislocations	Rare ligamentous injury caused by hyperflexion and distraction during high-impact blunt trauma. Highly unstable, results in an avulsion of the atlas (C-1) body from the occipital bone and all ligaments. Frequently fatal.	Traction contraindicated; surgical stabilization required; halo vest.
C-1-C-2 rotary subluxation	More common in children and adolescents. Present with neck pain and rotated head position.	Cervical traction for reduction and alignment, then often a halo vest for healing.
Lower Cervical Vertebral Injuries (C-3-T-1)
RADIOLOGIC CLASSIFICATION/MECHANISTIC CLASSIFICATION	DESCRIPTION	TREATMENT
Simple compression fracture of C-3 to T-1	Involves the upper or lower vertebral end plates (or both); results from forceful flexion and significant axial loading. Common in patients with osteoporosis and high-energy trauma in normal bone patients.	Immobilization in cervical collar for 6-8 wks. If no neck pain, flexion-extension cervical spine radiographs to rule out instability. If no motion, can wean from collar.
Severe compression/burst fractures/axial compression fractures	High-energy trauma that has been subjected to axial loading with variable amount of flexion. There may be bony fragments in the spinal canal. The posterior complex is intact.	If neurologically intact, immobilization in a cervical collar or halo orthosis may be adequate with close follow-up. If neurological deficit, decompressive surgery. Often with anterior approach.
Cervical facet dislocation/distractive flexion injuries of C-3 to T-1	Hyperflexion and posterior distractive forces are sustained. Seen in high-energy trauma such as diving accidents, falls from a height, motor vehicle crash. An unstable injury.	In the awake, alert patients, some advocate closed reduction with cervical traction and serial x-rays prior to surgery. Others advocate immediate surgical intervention and reduction in the operating room. Stabilization with instrumentation, generally posteriorly, is necessary.
Teardrop fracture/severe compressive flexion injury	Severe flexion and compressive forces on the spine; two-/threecolumn injury with high incidence of neurological deficits. MRI if completed, commonly demonstrates spinal cord compression, traumatic hemorrhage, and signal change within the spinal cord, along with posterior ligament disruption.	Surgical decompression and stabilization; may require anterior and posterior combination surgery.
Hyperextension/distractive extension injuries	Commonly involves elderly patients whose spine is stiff, less mobile. Can occur from fall from standing height or other lowenergy trauma. There is disruption of the anterior longitudinal ligament and disc. Although, in more severe injuries, there can also be posterior ligament disruption; often associated with central cord syndrome.	Most benefit from surgical stabilization procedures. May be anterior, posterior, or combination.
Dorsal (posterior) element fractures of C-3-T-1 Spinous process fractures	Also known as “Clay Shoveler’s” fractures; most commonly seen at C-6, C-7, and T-1. Caused by hyperextension with forceful compression of spinous processes, avulsion of the spinous process by hyperflexion, or direct blunt trauma.	Usually stable and treated with a cervical collar; flexion/extension radiographs to assure stability in approximately 8 wks.
Lamina, pedicle, and lateral mass fractures	Astute evaluation of radiographs is warranted to assess stability of the spine.	Treatment is variable depending on the exact fracture pattern.
Based on Sayadipour, A., Anderson, D., Miyavykh, S., Perlmutter, O., & Vaccaro, A. (2012). Subaxial cervical spine injuries. In E. Benzel (Ed.). Spine Surgery: Techniques, Complication Avoidance, and Management (3rd ed., pp. 611-624). Philadelphia: Elsevier.

Figure 17-10 ▪ Rotational injury. High-energy forces are applied from multiple directions creating a severe, unstable injury. Spinal cord and/or cauda equina injury often accompanies this injury.

Figure 17-11 ▪ Diagrammatic representation of an axial section of the midlumbar spinal canal and how the cauda equina nerves would be organized. The lower level nerves are placed most medially and those preparing to exit the spinal canal are most lateral.

Figure 17-12 ▪ Types of flexion-distraction (Chance) fractures. A: Disruption through the entire bony elements. B: Disruption through the entire ligamentous elements. C, D: Disruption through bony and ligamentous elements.

TABLE 17-2 THORACIC/THORACOLUMBAR/LUMBAR

Compression	Also referred to as “wedge” or “simple” compression fracture	May be observed or bracing with nonoperative treatment With osteoporosis, at risk for compression fractures and kyphosis
Multiple compression fractures		Treatment options are multiple and varied, including bracing, surgical stabilization.
Burst fractures	Retropulsion of bony fragments into the canal variable	Treatment options are multiple and highly variable depending on degree of fracture, ligament stability, and if neurological deficits are present. If neurological deficits: surgical decompression and fusion
Fracture-dislocation		Surgical decompression and stabilization
Flexion-distraction		Surgical decompression and stabilization
Transverse process fracture		Observation

Figure 17-13 ▪ Severe L-2 chance fracture in a teenage wearing a lap belt involved in a highway speed head on collision. She suffered multisystem trauma including bowel perforation and necrosis, abdominal wall degloving, pneumothorax, facial injury, and radial/ulna fractures. She was in critical/acute care for nearly 2 months. She remained paraplegic at discharge to acute rehabilitation. CT and MRI demonstrate an unstable injury with posterior and middle column disruption. A: CT scan, sagittal reconstruction. L-5 also demonstrates a teardrop fracture. B: MRI scan demonstrates severe disruption of posterior vertebral body, posterior longitudinal and posterior ligamentous structures. C: posterior stabilization with instrumentation

CASE STUDY: A 42-year-old man is admitted after falling asleep while driving, hitting an embankment at 55 mph (88.51 km/hr). Local emergency department (ED) providers found a lumbar spine fracture, transferring him to a tertiary care center via med flight. On presentation, lower extremity strength was full; sensation intact with normal rectal and perianal sensation as well as rectal tone. Foley catheter was placed en route, thus bladder function unknown. CT scan demonstrated an L-1 burst fracture with retropulsed fragment resulting in approximately 50% canal compromise. While bladder function cannot be determined, he is otherwise neurologically intact. Treatment options were discussed with the patient. In this circumstance, nonoperative external orthosis was a good option, supported by evidenced-based medicine. He remained on bed rest until fit with a Thoracolumbar Sacral Orthosis (TLSO) brace. Once fit with the brace, orders for mobilization and upright x-rays to assure stable alignment were written. Upright x-rays were obtained the evening the brace was placed, demonstrating increased compression deformity. The following morning, patient reported to the treating surgeon that his legs felt weak when standing. Strength appeared full to confrontation while supine. When assisted to standing (with the TLSO on), his legs buckled under his weight and he experienced bowel
incontinence. Further examination in bed demonstrated diminished rectal tone and perianal sensation. He underwent emergent L-1 corpectomy to decompress the conus medullaris and cauda equina, and stabilization with instrumentation spanning T-12 to L-2. At discharge, he had continued weakness in bilateral lower extremities with hip strength 3/5; knee extensors, dorsiflexion and plantarflexion 4/5. His sensation was intact, however, he had continued urinary retention. At 2 weeks after surgery, lower extremity strength was full, he was ambulating without difficulty. Bowel management was improved, however, a self-catheterization program continued. At 1 year after injury, he was working full time at his usual with adequate sexual and bowel function. However, self-catheterization continued to be necessary (Fig. 17-14).

Figure 17-14 ▪ L-1 Burst fracture demonstrated on (A) sagittal and, (B) axial CT scans. B also demonstrates retro pulsed bone fragment. C: Postoperative decompression, reconstruction, and stabilization.

The velocity and angle of impact, as well as the type of exaggerated mechanical movement produced, influence the type of injury sustained. Patients who have anatomic abnormalities or disease processes of the spinal column are much more vulnerable to SCI than
those who do not. Chronic conditions, such as cervical spondylosis, spinal stenosis, arthritis, and scoliosis, are examples of conditions that increase the probability of injury.

A brief sampling of the multiple classification schemas available for the spine were described. The goal of any classification model should be to provide standard language as to the injury pattern, the severity of the injury, and the neurological status of the patient. Historically, classification schema described fracture patterns, striving to systematically derive the stable versus unstable spine. Emphasis and treatment decision making was placed on mechanism of injury. However, neurological status and prognosis were not thoroughly accounted for. In 2007, the Spinal Trauma Study Group developed a classification scheme that includes the following six elements: spinal level; injury morphology; bony injury description; discoligamentous complex status; neurological status; and confounding variables such as pre-existing stenosis, osteoporosis, previous surgery, and so on.²²

The goal of classification schema from a physician standpoint is to have a common language regarding the injury, severity, and prognosis—to help guide treatment decision making. From a neuroscience nursing perspective, while it is important to know there are various injury types, likely more important is to appreciate that the severity and neurological status of any one patient can be highly variable, dependent on their particular circumstances. An appreciation of neurological sequalae of the incurred trauma is the cornerstone of neuroscience nursing patient care.

Spinal Cord Injuries

Injury to the spinal cord is all too often devastating with resultant loss of function, and thus potential socioeconomic and self-purpose/self-esteem losses. The loss of function may be permanent or temporary as well as various degrees and intensities, depending on the level and type of injury. The several syndromes related to SCI are summarized in Chart 17-2. Injuries to the spinal cord are classified by type of injury and by the syndrome produced.

Classification by Cause

The spinal cord can be injured by concussion, contusion, compression, shear, laceration, and damage to the blood vessels that supply the cord.

Concussion: causes a transient paralysis and/or sensory changes that subside within 2 to 3 days.²³ No identifiable macro-neuropathological changes are noted on examination of the cord.
Contusion: results from direct, acute compression of the spinal cord from bone or disc depending on the severity and factors such as continued compression, which leads to the secondary injury described below. The complex cascade of secondary injury includes vascular dysfunction, edema, ischemia, excitotoxicity, inflammation, electrolyte imbalance and shifts, free radical production, and delayed apoptotic cell death. The events of secondary injury spread in all directions within the spinal cord.⁸
Compression: can occur from distortion of the normal curvatures, ligaments, disc herniation, or bone fragments putting direct pressure onto the spinal cord subsequent to SCI.
Shear: results from forces applied in a horizontal (anteroposterior) plane as with subluxation (one vertebral body moving forward on the one below it). It also occurs in sudden forceful hyperextension (an elderly person falling and hitting their chin). A “pincer-like” action of the spinal cord being pulled over a spondylotic spine can occur, creating shear (horizontal) stresses in the center of the cord.⁹
Laceration: an actual tear in the cord results in permanent injury to the cord; may be the result of penetration of an object, or overstretching of the spinal cord. Secondary injury accompanies a laceration.
Transection: a more severe form of laceration, severing of the cord can be complete or incomplete. Actual complete transection is rare. However, clinical presentations, which mimic complete transection, are frequently seen.
Injury to the blood vessels that supply the cord: interference with or injury to the vessels that supply the spinal cord, the anterior spinal artery, or the two posterior spinal arteries results in ischemia and secondary injury.

Syndrome of SCI Without Radiologic Abnormality (SCIWORA)

The syndrome of SCI without radiologic abnormality (SCIWORA) is traumatic myelopathy that is either transient or permanent, not associated with vertebral fracture or ligamentous injury demonstrated on plain radiographs or computed tomography (CT). It is more likely to occur in children although the incidence is rare. Currently, Magnetic resonance imaging (MRI) is of paramount importance to fully evaluate spinal trauma pediatric patients with neurological deficits.²⁴

Pathophysiology

SCI results from both the initial mechanical insult, or the primary injury, and the secondary injury, complex systemic and biochemical processes affecting cellular function following the primary insult. The primary injury is most commonly the result of a compressive-contusive type of impact from stretching, bony fragments, discs, or ligaments. There is additional potential if continued compression or stretching from distraction. The common mechanisms as previously stated include shear, stretching, laceration, or transection. The degree of injury depends on the magnitude and direction of the energy applied to the spinal cord.

Collectively called secondary injury, several concurrent and overlapping vascular, chemical, inflammatory, and neuropathological changes occur following primary injury. These are interdependent cascades of systemic and cellular events initiated by the primary mechanical damage.²⁵ These intrinsically initiated destructive processes occur immediately following injury, lasting in the chronic phase for months to years.²⁶ Within seconds of injury, a cascade of concurrent events including alterations in blood flow, edema, hemorrhage, electrolyte abnormalities, membrane injury, and the release of vasoactive agents, cellular enzymes, cytotoxic mediators, excitotoxic neurotransmitters, and inflammatory mediators occurs and contributes to cellular membrane injury and post-traumatic ischemia (Fig. 17-15).

This interruption of the cord microcirculation results in ischemic injury; it is caused by direct vascular injury, hypotension related to neurogenic shock, loss of autoregulation, vasospasm, and vasospasm-induced thrombosis. Ischemia, increased vascular permeability, and expansive edema result. The microcirculatory changes are noted initially at the point of injury, but then encompass a wider area above and below the segment of injury. Injury site edema spreads from the primary core site to ascending and descending spinal cord levels, further decreasing neurological function. Evidence suggests that ischemia- and reperfusion-induced

endothelial damage in vessels that were damaged all contribute to the deleterious secondary injury cascade. The release of proteolytic and lipolytic enzymes from the injured cells causes vasospasm, delayed swelling, and necrosis in the spinal cord.

CHART 17-2 Spinal Cord Injury Syndromes


(A) Central cord syndrome. (B) Brown-Séquard syndrome. (C) Anterior cord syndrome.
Several terms related to spinal cord injury are defined. Tetraplegia refers to a lesion involving one of the cervical segments of the spinal cord that results in dysfunction of both arms, both legs, bowel, and bladder. Paraplegia refers to a lesion involving the thoracic, lumbar, or sacral regions of the spinal cord that results in dysfunction of the lower extremities, bowel, or bladder. A complete lesion (e.g., complete tetraplegia or complete paraplegia) implies total loss of sensation and voluntary muscle control below the injury. An incomplete lesion implies preservation of the sensory or motor fibers, or both, below the lesion. Incomplete lesions are classified according to the area of damage: central, lateral, anterior, or peripheral.
Central Cord Syndrome Presentation: The most common incomplete SCI, motor deficits are more significant in the upper extremities, with the lower extremities classically not affected; sensory loss varies but is more pronounced in the upper extremities; may have severe dysesthetic burning pain in the upper extremities, especially the hands; bowel/bladder dysfunction is variable, or function may be completely preserved. Cause: Injury, edema, or hemorrhage of the cervical central cord caused by hyperextension injuries, particularly if spondylosis or central canal stenosis is present. Injury can result from low impact, such as falls from standing height. Occurs more frequently in older individuals. Result: Edema in the central cord exerts pressure on the anterior horn cells. The cervical fibers of the corticospinal tract are located in a more central or medial position in the cord than the sacral fibers, which are located in the periphery. As a result, motor deficits are disproportionately greater in the upper extremities. Treatment: Severe traumatic central cord syndrome patients may benefit from early surgery; patients with rapidly improving neurological examination, immobilization with a rigid collar, and delayed surgical intervention is generally the treatment of choice. The prognosis varies.
Anterior Cord Syndrome Presentation: Loss of motor function, pain, and temperature sensation below the level of the lesion; light touch, position, and vibration sensation remain intact. Cause: Potential causes include acute disc herniation or hyperflexion injuries. It also may occur as a result of injury to the anterior spinal artery, which supplies the anterior two-thirds of the spinal cord. Result: Injury to the anterior two-thirds of the spinal cord, which includes the lateral spinothalamic tracts (pain/temperature), corticospinal tracts (motor), and anterior gray horn motor neurons, is noted. Treatment: Emergent surgical decompression and stabilization has been shown to potentially improve functional outcomes. The prognosis varies.
Brown-Séquard Syndrome Presentation: Ipsilateral paralysis or paresis is noted, together with ipsilateral loss of pressure, proprioception, and vibration and contralateral loss of light touch, pain, and temperature. Cause: The uncommon syndrome may be caused by transverse hemisection of the cord, usually as a result impalement from a knife- or missile-type object, rarely from bony fracture. Result: With right-sided cord transection, for example, the following would occur: paralysis of all voluntary muscles below the level of injury on the right side of the body (lateral corticospinal tract); loss of perception of touch, vibration, and position on the right side of the body below the level of injury (posterior columns, which include the fasciculus gracilis and fasciculus cuneatus); and loss of pain and temperature perception on the left side of the body below the injury (lateral spinothalamic tracts). Fibers that carry pain and temperature cross to the opposite side of the cord immediately after entering the cord and then ascend. The other tracts mentioned do not cross until they reach the brainstem. Treatment: Surgery is dependent on the cause of the injury.
Conus Medullaris Syndrome Presentation: A lumbar enlargement of the spinal cord corresponds to the innervation for the lower extremities. The conus medullaris is the cone-shaped lower end of the spinal cord. At approximately the T-12-L-1 disc space, the spinal cord begins to taper, ending at approximately L-1-L-2. Exactly where the conus begins anatomically is only currently definable microscopically. A fine pial thread called the filum terminale travels from the end of the conus medullaris to the first coccygeal segment. The conus is located directly opposite vertebral bodies T-12 and L-1. In most people, the tip of the conus does not extend past the L-1-L-2 disc space. This anatomic area is a transition area of high stress from the rigid thoracic spine to the more mobile lumbar spine, which increases the risk of flexion-distraction and burst fractures.^* Lesions of the conus medullaris and cauda equina cause similar signs and symptoms and can be difficult to differentiate. With injury to the conus medullaris, a range of lower extremity dysfunction, usually with lower extremity weakness or flaccid paralysis, loss of bladder and anal sphincter function early, male sexual dysfunction, and loss of Achilles reflex, is seen.^* Sensory loss is variable, with saddle anesthesia possible and pain uncommon. Generally, symptoms are symmetrical (right/left). Causes: High-energy trauma is the most frequent cause. Other potential causes include, compression from spinal tumor or intervertebral disc herniation. Result: Compression of the conus medullaris will result in the signs and symptoms outlined above. Treatment: Trauma: Surgical decompression and stabilization. CT generally adequate after trauma. An MRI may or may not be indicated. For compressive lesions, an MRI is indicated to define pathology and guide treatment decisions.^*	Cauda Equina Syndrome Presentation: The spinal cord terminates at approximately L-1-L-2 with the cauda equina flowing below within the dural sac. The nerve roots from the lumbar, sacral, and coccygeal that extend distally from the conus medullaris are collectively called the “cauda equine”, Latin for “horse’s tail”. Although the cauda equina is not a true spinal cord injury, spinal fractures to the thoracolumbar and lumbar levels can cause injury to nerves within the cauda equina, and is nonetheless a serious problem considered within the context of spinal cord injury. Presentation is highly variable, depending on the level of injury, and precisely what nerves were involved. Patients generally present with asymmetric weakness or complete paralysis of lower extremities with at least partial preservation of sensation. Pain is often severe, asymmetric, and radicular. The patellar and Achilles reflexes are classically absent. Sphincter disturbance are variable from minor to complete loss of sphincter tone and sexual dysfunction. There should be no upper motor signs in pure cauda equina syndrome. However, if the injury is at the thoracolumbar junction, there may also be conus medullaris injury. With acute, large, central disc herniation perianal numbness, saddle dysesthesia or anesthesia and diminished loss of anal reflex/rectal tone. Difficulty with urination, retention or overflow incontinence, leg pain followed by sensory changes. Causes: Can be acute, such as trauma or acute large herniated disc. Can be from chronic causes also such as tumor, spinal stenosis, hemorrhage, iatrogenic. Result: The compression of the spinal nerves results in loss of neurological function that can be permanent if not relieved. Radiologic evaluation helps to determine treatment options. Treatment: Emergent surgery is indicated for cauda equina syndrome. The timing depends on the progression of motor deficits and pain, but is usually within 24 hrs. The outcome of surgery varies, but return of bladder function is best when cauda equina syndrome is diagnosed early and decompression is completed expeditiously.
Cross-sections of spinal cord in this chart are from Kitt, S., & Kaiser, J. (1990). Emergency nursing: A physiological and clinical perspective. Philadelphia: W. B. Saunders.

Figure 17-15 ▪ Diagram illustrating the zone of primary injury progressively expanding because of the events of secondary injury. Acute and chronic inflammatory cascades lead to secondary tissue damage, axonal loss, and demyelization. A cystic cavity surrounded by a rim of preserved white matter is the result. Scar tissue forms the periphery of the lesion—presenting a physical and chemical barrier to axonal regeneration.

Calcium disruption in relation to SCI is important. A basic role of calcium is its role in regulation of the movement of sodium and potassium across the intracellular and extracellular space and also release of neurotransmitters at the synaptic junctions. After initial injury, calcium balance changes from an increase of intracellular calcium to a decrease in extracellular calcium. The shift in intracellular calcium activates calcium-dependent proteases and impairs mitochondrial and other intracellular functions.

Concurrently, the inflammatory process that was stimulated immediately after injury continues for several weeks to months as a complex multifactorial response, which includes endothelial damage; the release of inflammatory mediators such as T cells, neutrophils, invading monocytes, microglia and astrocytes; changes in vascular permeability; development of cytotoxic edema; and migration of peripheral inflammatory cells.²⁵, ²⁶, ²⁷.

The function of highly specialized central nervous system cells is disrupted by ischemia and hypoxia within seconds of injury. Microhemorrhage and petechial hemorrhage progress to ischemia and possibly on to infarction and tissue necrosis. Irreversible nerve damage develops as a result of glial and neuronal tissue changes that replace normal neural elements with fibrotic scar tissue. As a result, neurological deficits currently become permanent.²⁸

ACUTE SPINAL CORD TRAUMA

Terminology

Incomplete Versus Complete Spinal Cord Injury

A complete SCI results in the absence of sensory and voluntary motor function below the level of injury, including the lowest sacral segments (S-4 and S-5). An incomplete SCI occurs when there is partial preservation of sensory (including position sense), motor (voluntary), or a combination of sensory-motor function including the lowest sacral segments. Sparing of the lowest sacral segments is called sacral sparing (sensation around the anus, voluntary rectal sphincter contraction). Types of incomplete spinal lesions include central cord syndrome, Brown-Séquard syndrome, anterior cord syndrome, and posterior cord syndrome (each discussed further in the chapter). Complete SCI is not determined until after the patient is out of spinal shock, generally 24 to 72 hours after injury.²⁹

Differentiating Spinal Shock and Neurogenic Shock

Spinal shock refers to the transient state of complete loss of all motor, sensory, and reflex activity below the level of the lesion. During spinal shock, no spinal cord function is present, including sacral sparing. Return of the sacral reflexes, such as the bulbocavernosus reflex or anal wink at generally 24 to 72 hours post injury, indicates the end of spinal shock.²⁹, ³⁰

Neurogenic shock refers to cardiovascular hypotension. Cardiovascular effects are a result of acute interruption of the sympathetic function, leaving parasympathetic function unopposed.³⁰ The autonomic dysfunction is characterized by systemic hypotension, warm skin, and bradycardia/bradyarrhythmias.

Under normal conditions, the preganglionic axons of the sympathetic nervous system, which have origins in the thoracolumbar region of the spinal cord, receive impulses for reflex control of blood pressure and heart rate through the cardiac accelerator and vasoconstriction reflexes. In patients with cervical or upper thoracic spinal cord injuries, hypotension and bradycardia caused by sympathetic failure and peripheral vascular vasodilation define the state of “neurogenic shock.” The loss of sympathetic input to the systemic vasculature and the heart and subsequent decreased peripheral vascular resistance result in decreased peripheral vascular tone below the level of injury.³¹ The bradycardia results from the suppression of the cardiac accelerator reflex. The unopposed vagal tone causes vasodilation and bradycardia. Treatment with crystalloid solutions or plasma expanders, a mainstay of treatment of hypovolemic shock, is used carefully in neurogenic shock, to prevent pulmonary edema from fluid overload. Conversely, vasopressors are utilized to maintain adequate mean arterial pressure in neurogenic shock. Current national SCI guidelines recommend maintaining a mean arterial pressure of 85 to 90 mm Hg for 7 days post injury to promote spinal cord perfusion.⁸, ³²

Clinical Pearl: Note the difference between neurogenic shock and hypovolemic shock, tension pneumothorax, or other causes of hypotension in the critically ill trauma patient. In neurogenic shock, the nurse will note, hypotension, bradycardia, and warm dry skin. The complete SCI patient can have secondary injuries leading to hypovolemic shock. In these complicated clinical picture, other causes for hypotension need to be ruled out. Thus, in the trauma patient, neurogenic shock is a diagnosis of exclusion once other life threatening possibilities have been ruled out.

Figure 17-16 ▪ ASIA motor and sensory scales. (Copyright, American Spinal Injury Association, from International standards for neurological and functional classification of spinal cord injury, revised 2011).

Clinically, it is difficult to ascertain a clear picture in the first few hours after SCI when there is a mixture of the temporary spinal shock with the permanent effects of SCI. In general, the loss of motor power and sensation that results from spinal shock resolves within 24 to 72 hours after injury. Any weakness or sensory loss remaining after the return of sacral reflexes, namely bulbocavernosus or anal wink, is likely permanent. Return of deep tendon reflexes generally occurs at approximately 2 weeks after injury, bladder reflexes at about 2 months, and hypotension from neurogenic shock at about 4 to 6 weeks.³⁰

Immediate Signs and Symptoms of Spinal Cord Trauma

When the spinal cord is suddenly injured, there is loss of motor and sensory function below the level of injury. See also the discussion of spinal shock above. If no motor or sensory function is present after spinal shock resolves, the injury is considered complete. The ASIA publishes the ASIA Impairment Scale often used by clinicians to determine the extent of SCI (Table 17-3 and Fig. 17-16). Specific functional losses, based on level of SCI, are also listed in Table 17-4. However, the ASIA Impairment Scale is not valid for the first 72 hours, until the patient is out of spinal shock.³³

TABLE 17-3 ASIA IMPAIRMENT (AIS) SCALE

ASIA Impairment (AIS) Scale

A = Complete. No sensory or motor function is preserved in the sacral segments S-4-S-5.
B = Sensory Incomplete. Sensory but not motor function is preserved below the neurological level and includes the sacral segments S-4-S-5 (light touch pin at S-4-S-5: or deep anal pressure [DAP]), 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 neurological level,^a and more than half of key muscle functions below the single neurological level of injury (NLI) have a muscle grade less than 3 (Grades 0-2).
D = Motor Incomplete. Motor function is preserved below the neurological level,^a and at least half (half or more) of key muscle functions below the NLI have a muscle grade ≥3.
E = Normal. If sensation and motor function as tested with the ISNCSCI are graded as normal in all segments, and the patient had prior deficits, then the AIS grade is E. Someone without an initial SCI does not receive an AIS grade.

^aFor an individual to receive a grade of C or D, that is motor incomplete status, they 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. The standards at this time allows even nonkey muscle function more than three levels below the motor level to be used in determining motor incomplete status (AIS B vs. C).

NOTE: When assessing the extent of motor sparing below the level for distinguishing between AIS B and C, the motor level on each side is used; whereas to differentiate between AIS C and D (based on proportion of key muscle functions with strength grade 3 or greater) the single neurological level is used.

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Jul 14, 2016 | Posted by drzezo in NURSING | Comments Off

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