11/25/2018 1/47 Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8eChapter 258: Spine Trauma Steven Go INTRODUCTION AND EPIDEMIOLOGY Trauma to the spine can cause a vertebral spinal column injury, a spinal cord injury, or both. A few studies have tried to estimate the annual incidence of spinal column injury in the general population with results ranging from 11.8 to 64 cases per 100,000, 1,2 but no current figures are available for the U.S. population. In contrast, the estimated annual incidence of spinal cord injury in the United States is 40 cases per million or 12,000 new cases per year, with 81% male victims, a mean age of 42.6 years, and a 67% Caucasian predominance. 3 Since 2010, the leading causes of spinal cord injury are vehicular (37%), falls (29%), and violence (14%). Lifetime costs for spinal cord injury victims vary according to age at time of injury, severity of injury, and socioeconomic status; however, estimates range in millions of dollars per patient. 3 FUNCTIONAL ANATOMY VERTEBRAL COLUMN The vertebral column is composed of 33 vertebrae: 7 cervical, 12 thoracic, 5 lumbar, 5 fused sacral, and 4 (usually fused) coccygeal. The axial vertebrae (C1 and C2) are anatomically unique in that they are designed for rotary motion. The odontoid (dens) of the axis (C2) is held against the atlas (C1) by the strong transverse ligament. The remaining vertebrae share some common anatomical features (Figure 258-1). A typical subaxial vertebra is composed of an anterior body and a posterior vertebral arch. The vertebral arch is comprised of two pedicles, two laminae, and seven processes (one spinous, two transverse, and four articular). These articulations enable the spine to engage in flexion, extension, lateral flexion, rotation, or circumduction (combination of all movements). The orientation of these articular facet joints changes at dierent levels of the spine and accounts for variations in motion of specific regions of the vertebral column. Due to its inherent flexibility, the cervical spine is the most commonly injured region of the spinal column, with most injuries occurring at the C2 level and from C5 to C7. 4 The second most common region of injury is in the thoracolumbar transition zone. FIGURE 258-1. Vertebral anatomy. Each vertebra consists of a vertebral body and posterior element. Vertebrae are stabilized by an anterior longitudinal ligament, posterior ligament, and interspinous ligament.
47
Embed
INTRODUCTION AND EPIDEMIOLOGY FUNCTIONAL ANATOMY · 2018-11-25 · INTRODUCTION AND EPIDEMIOLOGY Trauma to the spine can cause a vertebral spinal column injury, a spinal cord injury,
This document is posted to help you gain knowledge. Please leave a comment to let me know what you think about it! Share it to your friends and learn new things together.
Transcript
11/25/2018
1/47
Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e
Chapter 258: Spine Trauma Steven Go
INTRODUCTION AND EPIDEMIOLOGY
Trauma to the spine can cause a vertebral spinal column injury, a spinal cord injury, or both. A few studies have tried to estimate the annual
incidence of spinal column injury in the general population with results ranging from 11.8 to 64 cases per 100,000,1,2 but no current figuresare available for the U.S. population. In contrast, the estimated annual incidence of spinal cord injury in the United States is 40 cases per
million or 12,000 new cases per year, with 81% male victims, a mean age of 42.6 years, and a 67% Caucasian predominance.3 Since 2010, theleading causes of spinal cord injury are vehicular (37%), falls (29%), and violence (14%). Lifetime costs for spinal cord injury victims vary
according to age at time of injury, severity of injury, and socioeconomic status; however, estimates range in millions of dollars per patient.3
FUNCTIONAL ANATOMY
VERTEBRAL COLUMN
The vertebral column is composed of 33 vertebrae: 7 cervical, 12 thoracic, 5 lumbar, 5 fused sacral, and 4 (usually fused) coccygeal. The axialvertebrae (C1 and C2) are anatomically unique in that they are designed for rotary motion. The odontoid (dens) of the axis (C2) is held againstthe atlas (C1) by the strong transverse ligament. The remaining vertebrae share some common anatomical features (Figure 258-1). A typicalsubaxial vertebra is composed of an anterior body and a posterior vertebral arch. The vertebral arch is comprised of two pedicles, twolaminae, and seven processes (one spinous, two transverse, and four articular). These articulations enable the spine to engage in flexion,extension, lateral flexion, rotation, or circumduction (combination of all movements). The orientation of these articular facet joints changes atdi�erent levels of the spine and accounts for variations in motion of specific regions of the vertebral column. Due to its inherent flexibility, the
cervical spine is the most commonly injured region of the spinal column, with most injuries occurring at the C2 level and from C5 to C7.4 Thesecond most common region of injury is in the thoracolumbar transition zone.
FIGURE 258-1.
Vertebral anatomy. Each vertebra consists of a vertebral body and posterior element. Vertebrae are stabilized by an anterior longitudinalligament, posterior ligament, and interspinous ligament.
11/25/2018
2/47
A series of ligaments serves to maintain alignment of the spinal column. The anterior and posterior longitudinal ligaments run along thevertebral bodies. Surrounding the vertebral arch are the ligamentum flavum and the supraspinous, interspinous, intertransverse, andcapsular ligaments. Between adjacent vertebral bodies are the intervertebral disks, consisting of a peripheral annulus fibrosus and a centralnucleus pulposus. The intervertebral disks act as shock absorbers to distribute axial load. When compressive forces exceed the absorptivecapacity of the disk, the annulus fibrosus ruptures. This allows the nucleus pulposus to protrude into the vertebral canal, and this may resultin spinal nerve or spinal cord compression.
SPINAL CORD
The spinal cord is a cylindrical structure that begins at the foramen magnum, where it is continuous with the medulla oblongata of the brainand extends down the spinal canal to the first and second lumbar vertebrae. The spinal cord gives rise to 31 pairs of spinal nerves: 8 cervical,12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. Each spinal nerve emerges through the intervertebral foramen corresponding to theappropriate spinal cord level. The lower nerve roots form an array of nerves called the cauda equina.
PATHOPHYSIOLOGY
SPINAL COLUMN INJURIES
Given their multiple axes of motion, the bony vertebrae can be injured via several mechanisms and present with a number of di�erent injury
patterns (Table 258-1).5,6,7,8,9,10
11/25/2018
3/47
TABLE 258-1
Major Spinal Column Injuries
Mechanism
of InjuryInjury
Spinal
Column
Regions
Typically
A�ected
Image Notes
Flexion Anterior
subluxation
(hyperflexion
sprain) (usually
stable, but
depends on the
integrity of
posterior
ligaments)
Cervical
[Photo contributors: Mark Silverberg, MD/Steven Pulitzer, MD. Reproduced with
permission from Shah BR, Lucchesi M, Amodio J (eds): Atlas of Pediatric Emergency
[Reproduced with permission from Block J, Jordanov MI, Stack LB, Thurman RJ
(eds): The Atlas of Emergency Radiology. McGraw-Hill, Inc., 2013. Fig 8-24.]
Coccygeal
injuries are
usually
associated with
a direct fall onto
the buttocks,
with resultant
coccyx pain
exacerbated by
sitting or
straining.
Localized
tenderness can
be elicited with
coccyx
palpation
during a rectal
exam, but this is
not required for
diagnosis.
Imaging is not
needed to
diagnose
coccygeal
fractures.
Treatment is
symptomatic
with analgesics
and use of a
rubber
doughnut
pillow.
The variable anatomic qualities of the regions of the spinal column cause characteristic injury patterns in each region. The exposure andextreme mobility of the cervical spine (C1-C7) make it particularly vulnerable to injury, because it is the most flexible and mobile portion ofthe spinal column. The cervicothoracic junction (C7-T1) is one of the transitional zones of the spinal column, which are locations where thevertebral morphology changes. This designation is important because transitional zones sustain the greatest amount of stress during motionand are most vulnerable to injury. In contrast to the cervical spine, the thoracic spine (T1-T10) is a rigid segment, with its sti�ness enhancedby articulation with the rib cage. Therefore, not only is injury to the thoracic spine less common than in other regions, but this also meansthat the presence of a thoracic vertebral injury indicates the patient was subjected to severe traumatic forces and is at high risk forintrathoracic injuries. Moreover, the spinal canal in the thoracic region is also narrower than in other regions. This increases the risk of cordinjury, which is o�en complete when it occurs. The thoracolumbar junction (T11-L2) is a transitional zone between the highly fixed thoracic
11/25/2018
25/47
and relatively mobile lumbar spine. In addition to this change in bone anatomy, the thoracolumbar junction serves as the level of transitionfrom the end of the spinal cord (about L1) to the nerve roots of the cauda equina. Relative to the thoracic spine, the width of the spinal canalin the thoracolumbar region is greater. Therefore, despite a large number of vertebral injuries at the thoracolumbar junction, most do nothave neurologic deficits, or, if present, they are partial or incomplete. Relative to the thoracic and thoracolumbar regions, the lower lumbarspine (L3-L5) is more mobile. Because of the width of the spinal canal in the lumbar region and the ending of the spinal cord at the L1 level,isolated fractures of the lower lumbar spine rarely injure the spinal cord or result in neurologic injury. The sacrum and coccyx form the lowerportion of the spinal column. The vertebral foramina of the sacrum together form the sacral canal that contains the nerve roots of the lumbar,sacral, and coccygeal spinal nerves and the filum terminale. The coccyx, which articulates with the sacrum, consists of four vertebrae fusedtogether. When neurologic injuries occur, they are usually complete cauda equina lesions or isolated nerve root deficits. Sacral fractures thatinvolve the central sacral canal can produce bowel or bladder dysfunction.
FRACTURE STABILITY
Much has been written regarding determining whether or not a particular injury is "stable." Spinal stability is defined as the ability of thespine to limit patterns of displacement under physiologic loads so as not to damage or irritate the spinal cord or nerve roots. Severalparadigms have been created, including the Denis column system, which splits the spinal column into anterior, middle, and posterior
elements.11 A spine injury is considered unstable if at least two columns of a particular region are involved. Although this schema and other
instability scoring systems have been published,12,13,14 determining spinal stability a�er an acute injury in the ED is particularly di�icult. Thisis because these injuries o�en occur in the setting of polytrauma, altered mental status, and severe pain, which may result in suboptimalinitial imaging. In addition, many EDs lack quick access to emergent MRI to evaluate the spinal ligaments. Therefore, assume any spinefracture is unstable and maintain appropriate precautions until expert consultation can be obtained from a spine surgeon.
SPINAL CORD INJURIES
Damage to the spinal cord is the result of two types of injury. First is the primary injury from mechanical forces from traumatic impact. Thisinsult sets into motion a series of vascular and chemical processes that lead to secondary injury. The initial phase is characterized byhemorrhage into the cord and formation of edema at the injured site and surrounding region. Local spinal cord ischemia ensues secondary tovasospasm and thrombosis of the small arterioles within the gray and white matter. Extension of edema may further compromise blood flowand increase ischemia. A secondary tissue degeneration phase begins within hours of injury. This is associated with neural membrane
dysfunction, driven by a pathologic excitation of sodium ion channels, an influx of calcium ions, and the release of glutamine.15 Cell deathensues from a combination of mechanisms including electrolyte imbalances, cell edema, and the formation and release of oxidative
substances.15
SPINAL CORD LESIONS
The severity of spinal cord injury determines the prognosis for recovery of function, so it is important to distinguish between complete andincomplete spinal cord injuries. The American Spinal Injury Association defines a complete neurologic lesion as the absence of sensory andmotor function below the level of injury. This includes loss of function to the level of the lowest sacral segment. In contrast, a lesion isincomplete if sensory, motor, or both functions are partially present below the neurologic level of injury. This may consist only of sacralsensation at the anal mucocutaneous junction or voluntary contraction of the external anal sphincter upon digital examination. Completelesions have a minimal chance of functional motor recovery. Patients with incomplete lesions are expected to have at least some degree ofrecovery. The di�erentiation between complete and incomplete spinal cord damage may be complicated by the presence of spinal shock.Patients in spinal shock lose all reflex activities below the area of injury, and lesions cannot be deemed truly complete until spinal shock hasresolved.
A significant number of descending and ascending tracts have been identified in the spinal cord (Figure 258-2). The three most important ofthese in terms of neuroanatomic localization of cord lesions are the corticospinal tracts, spinothalamic tracts, and dorsal (posterior) columns.
FIGURE 258-2.
The anatomy of a cross section of cervical spinal cord. [Reproduced with permission from Simon RR, Sherman SC (eds): EmergencyOrthopedics, 6th ed. McGraw-Hill, Inc., 2011. Fig 9-5.]
11/25/2018
26/47
The corticospinal tract is a descending motor pathway. Its fibers originate from the cerebral cortex through the internal capsule and themiddle of the crus cerebri. The tract then breaks up into bundles in the pons and finally collects into a discrete bundle, forming the pyramid ofthe medulla. In the lower medulla, approximately 90% of the fibers cross to the side opposite that of their origin and descend through thespinal cord as the lateral corticospinal tract. These fibers synapse on lower motor neurons in the spinal cord. The 10% of corticospinal fibersthat do not cross in the medulla descend in the anterior funiculus of the cervical and upper thoracic cord levels as the ventral corticospinaltract. Damage to the corticospinal tract neurons (upper motor neurons) in the spinal cord results in ipsilateral clinical findings such as muscleweakness, spasticity, increased deep tendon reflexes, and a Babinski's sign.
The two major ascending pathways that transmit sensory information are the spinothalamic tracts and the dorsal columns. Thespinothalamic tract transmits pain and temperature sensation. As the axons of the first neurons enter the spinal cord, most ascend one or twolevels before entering the dorsal gray matter of the spinal cord, where they synapse with the second neuron of the spinothalamic tract. Thesecond neuron immediately crosses the midline in the anterior commissure of the spinal cord and ascends in the anterolateral funiculus asthe lateral spinothalamic tract. When the spinothalamic tract is damaged, the patient experiences loss of pain and temperature sensation inthe contralateral half of the body. The (pain and temperature) sensory loss begins one or two segments below the level of the damage.
The dorsal columns transmit vibration and proprioceptive information. Neurons enter the spinal cord proximal to pain and temperatureneurons. They di�er from pain and temperature neurons in that they do not immediately synapse in the spinal cord. Instead, these axonsenter the ipsilateral dorsal column and do not synapse until they reach the gracile or cuneate nuclei of the medulla. From these nuclei, fiberscross the midline and ascend in the medial lemniscus to the thalamus. Injury to one side of the dorsal columns will result in ipsilateral loss ofvibration and position sense. The sensory loss begins at the level of the lesion. Light touch is transmitted through both the spinothalamictracts and the dorsal columns. Therefore, light touch is not completely lost unless there is damage to both the spinothalamic tracts and thedorsal columns.
Each spinal nerve is named for its adjacent vertebral body (see Figure 258-3). In the cervical region, there is an additional pair of spinal nerveroots compared to the number of vertebral bodies. The first seven spinal nerves are named for the first seven cervical vertebrae, each exitingthrough the intervertebral foramen above its corresponding vertebral body. The spinal nerve exiting below C7, however, is referred to as theC8 spinal nerve, although no eighth cervical vertebra exists. All subsequent nerve roots, beginning with T1, exit below the vertebral body forwhich they are named.
FIGURE 258-3.
Spinal cord level. The spinal cord level of injury can be delineated by physical examination, including a detailed neurologic examination.
11/25/2018
27/47
During fetal development, the downward growth of the vertebral column is greater than that of the spinal cord. Because the adult spinal cordends as the conus medullaris at the level of the lower border of the first lumbar vertebra, the lumbar and sacral nerve roots must continueinferiorly below the termination of the spinal cord to exit from their respective intervertebral foramina. These nerve roots form the caudaequina. A potential consequence of this arrangement is that injury to a single lower vertebra can involve multiple nerve roots in the caudaequina. For example, an injury at the L3 vertebra can involve the L3 nerve root as well as the lower nerve roots that are progressing to a levelcaudal to the L3 vertebra.
PREHOSPITAL CARE
The prehospital treatment of patients with spinal injury involves recognition of patients at risk, appropriate immobilization, and triage to anappropriate facility (see chapters 1, "Emergency Medical Services" and 2, "Prehospital Equipment"). Presume that patients with anappropriate traumatic mechanism who have complaints of neck or back pain, tenderness on prehospital exam, neurologic complaints,significant injury above the clavicles, or altered sensorium that precludes accurate evaluation of the spine to have a spinal cord injury, andtake appropriate spinal precautions. Transport of the patient to a center that is capable of rapid diagnostics and therapeutics is important tooptimize outcome following spinal injury.
Prehospital care for spinal injuries traditionally involves immobilization of the entire spine at the scene with a rigid cervical collar (or similardevices) plus a long backboard. However, there is little evidence that cervical collars and/or long spine boards reduce neurologic injury,
spinal instability, or mortality.16,17 In contrast, cervical collars and long backboards can induce complications such as pressure sores,18,19
patient discomfort,20 and respiratory compromise.21 In light of these data, some experts have recommended retaining the cervical collar but
transporting the patient on a gurney with a scoop stretcher22 or other so�, padded devices23 to avoid the rigid spine board. Some authors
have even proposed abandoning the routine use of cervical collars.24 Nevertheless, in the absence of controlled data regarding the safety of
such measures, current neurosurgery guidelines25 still recommend usage of the rigid cervical collar and long spine board. In contrast, spinalimmobilization is no longer recommended for fully conscious, neurologically intact patients with isolated penetrating neck injury because
collars can delay resuscitation and obscure neck injuries.26,27
INITIAL ED STABILIZATION
AIRWAY
ED evaluation of the patient with potential spinal injury should not di�er substantially from that of any patient with multiple injuries, with thefirst priority being the airway. The higher the level of spinal injury, the more likely is the need for early airway intervention. For example,unstable spine lesions above C3 can cause immediate respiratory arrest, and lesions a�ecting C3-C5 can a�ect the phrenic nerve anddiaphragm function. For this reason, some experts recommend that any patient with an injury at C5 or above should have the airway securedby endotracheal intubation. Delayed respiratory compromise can occur if spinal cord edema from more caudal lesions progresses rostrally tocause phrenic nerve paralysis. Many patients can initially support ventilatory function using intercostal muscles or abdominal breathing, butthey eventually tire and subsequently develop respiratory failure. Therefore, be vigilant for respiratory compromise in patients with highcervical injuries. If safety allows, perform a brief focused neurologic assessment before sedation and intubation.
Maintain in-line spinal stabilization while intubating, because human cadaver studies demonstrate less cervical motion and glottisvisualization with in-line stabilization than with cervical collars in place, and movement of an unstable cervical spine can worsen or produce
spinal cord injury.28 Video-assisted intubation improves intubation success over direct laryngoscopy, but manual in-line stabilization is still
necessary to minimize cervical extension.28
HYPOTENSION
Hypotension in patients with spinal cord injuries may be due to neurogenic shock, blood loss, cardiac injury, tension pneumothorax, or otherinjuries. Although hypotension and relative bradycardia are classic signs of neurogenic shock, bradycardia can also be associated with
intraperitoneal bleeding or prior medication with calcium channel blockers or β-blockers. In one study,29 74% of hypotensive patients withpenetrating spinal cord injury had major blood loss causing hypotension. Therefore, presume blood loss as the cause of hypotension in spinalinjury patients until proven otherwise. Hypotension is initially treated with IV crystalloid.
SPINE IMMOBILIZATION
Long spine boards are associated with pressure sores, so remove them as soon as possible. Log rolling is the traditional method for boardremoval, because it requires only a few sta� and allows visualization of the patient's back and performance of a rectal examination. Some
experts recommend the "6+ li� and slide maneuver" because it produces less spine motion than log rolling.30 The 6+ maneuver consists firstof unstrapping the patient from the board. Next, one person maintains in-line stabilization at the head, while six others positioned at thechest, pelvis, and lower extremities levels li� the patient as a unit 10 to 20 cm above the board. Another person slides the board out fromunder the patient, and the patient is then lowered to the bed, maintaining spinal alignment. Disadvantages are the need for many sta�
members to perform this maneuver and inability to visualize the patient's back.31
Hard cervical collars are associated with patient discomfort and pressure sores of the neck.32 Therefore, promptly clear the cervical spine ifpossible (see "Clinical Decision Rules in Cervical Spine Imaging" and "Cervical Spine Imaging" below). Do not overtighten the cervical collar
on head-injured patients, because jugular venous compression can raise intracranial pressure,33 although Stifneck® and Miami J® collars may
be better than other rigid collars in this regard.34
CLINICAL FEATURES
HISTORY
If the patient is able to give a history, focus on key historical points as they pertain to spine injury. Specifically, seek the presence or absence
of the historical elements included in imaging decision rules (see Tables 4,35 5,36 and 637). Evaluate for symptoms of midline spine pain,painful distracting injury, paresthesias, loss of function, change in mental status (including loss of consciousness), or other neurologic
11/25/2018
29/47
symptoms (especially urinary or fecal incontinence or priapism). Pay particular attention to any symptoms indicating present or impendingrespiratory compromise, including dyspnea, palpitations, abdominal breathing, and anxiety, which may indicate a high cervical spine injury.
PHYSICAL EXAMINATION
Once the patient is stabilized and other life-threatening injuries have been excluded or treated, perform a detailed neurologic assessment. Anappropriately detailed initial neurologic examination is important to allow for comparison later should the patient deteriorate. Assess thepatient's mental status and note any clinical evidence of intoxication. Physical examination should focus on delineating the level of the spinalcord injury (Figure 258-3). Document the presence or absence of midline neck or back tenderness. Test motor function for muscle groups(Table 258-2). Determine the level of sensory loss (Figure 258-4), and investigate proprioception or vibratory function to examine posteriorcolumn function. Test for "saddle anesthesia," which is sensory deficit in the region of the buttocks, perineum, and inner aspect of the thighs.Test deep tendon reflexes along with anogenital reflexes because "sacral sparing" with preservation of anogenital reflexes denotes anincomplete spinal cord level, even if the patient has complete sensory and motor loss. To test the bulbocavernosus reflex, squeeze the penisto determine whether the anal sphincter simultaneously contracts. Assess rectal tone at the same time. Test the cremasteric reflex by strokingthe medial thigh with a blunt instrument. If the scrotum rises, some spinal cord integrity exists. Document rectal tone and sensation aroundthe anus. An "anal wink reflex" (contraction of the anal musculature when the perianal region is stimulated with a pin) indicates some sacralsparing. Conversely, priapism implies a complete spinal cord injury. In 2013, the American Spinal Injury Association published a revised
version of the International Standards for Neurological Classification of Spinal Cord Injury.38 This scoring system is used by spine surgeons to
document their initial examination and has prognostic value39; however, the scale is rather lengthy and is not practical for ED initialassessment.
TABLE 258-2
Motor Grading System
Grade Movement
0 No active contraction
1 Trace visible or palpable contraction
2 Movement with gravity eliminated
3 Movement against gravity
4 Movement against gravity plus resistance
5 Normal power
FIGURE 258-4.
Dermatomes for sensory examination.
11/25/2018
30/47
INCOMPLETE SPINAL CORD SYNDROMES
There are three major incomplete spinal cord syndromes identified by predictable physical examination findings, although overlap in findingsmay occur (Table 258-3).
11/25/2018
31/47
*Outcome improves when the e�ects of secondary injury are prevented or reversed.
TABLE 258-3
Four Major Incomplete Spinal Cord Syndromes
Syndrome Mechanisms SymptomsGeneral
Prognosis*
Anterior
cord
Direct anterior cord
compression
Complete paralysis below the lesion with loss of pain and temperature sensation Poor
Flexion of cervical
spine
Thrombosis of anterior
spinal artery
Preservation of proprioception and vibratory function
Central
cord
Hyperextension
injuries
Quadriparesis—greater in the upper extremities than the lower extremities. Some loss of
pain and temperature sensation, also greater in the upper extremities
Good
Disruption of blood
flow to the spinal cord
Cervical spinal stenosis
Brown-
Séquard
Transverse
hemisection of the
spinal cord
Ipsilateral spastic paresis, loss of proprioception and vibratory sensation, and contralateral
loss of pain and temperature sensation
Good
Unilateral cord
compression
ANTERIOR CORD SYNDROME
The anterior cord syndrome results from damage to the corticospinal and spinothalamic pathways, with preservation of posterior columnfunction. This is manifested by loss of motor function and pain and temperature sensation distal to the lesion. Only vibration, position, andtacticle sensation are preserved. This syndrome may occur following direct injury to the anterior spinal cord. Flexion of the cervical spine mayresult in cord contusion or bone injury with secondary cord injury. Alternatively, thrombosis of the anterior spinal artery can cause ischemicinjury to the anterior cord. Anterior cord injury can also be produced by an extrinsic mass that is amenable to surgical decompression. Theoverall prognosis for recovery of function is poor.
CENTRAL CORD SYNDROME
The central cord syndrome is usually seen in older patients with preexisting cervical spondylosis who sustain a hyperextension injury. Asnamed, this injury preferentially involves the central portion of the cord more than the peripheral. The centrally located fibers of thecorticospinal and spinothalamic tracts are a�ected. The neural tracts providing function to the upper extremities are most medial in positioncompared with the thoracic, lower extremity, and sacral fibers that have a more lateral distribution. Clinically, patients with a central cordsyndrome present with decreased strength and, to a lesser degree, decreased pain and temperature sensation, more in the upper than thelower extremities. Vibration and position sensation are usually preserved. Spastic paraparesis or spastic quadriparesis can also be seen. Themajority will have bowel and bladder control, although this may be impaired in the more severe cases.
BROWN-SÉQUARD SYNDROME
11/25/2018
32/47
The Brown-Séquard syndrome results from hemisection of the cord. It is manifested by ipsilateral loss of motor function, proprioception, andvibratory sensation, and contralateral loss of pain and temperature sensation. The most common cause of this syndrome is penetrating
injury.40 It can also be caused by lateral cord compression secondary to disk protrusion, hematomas, spine fractures, infections, infarctions,or tumors.
CAUDA EQUINA SYNDROME
Cauda equina syndrome is not a true spinal cord syndrome because the cauda equina is composed entirely of lumbar, sacral, and coccygealnerve roots; therefore, injuries to this region produce peripheral nerve injuries. Symptoms and signs may include bowel and/or bladderdysfunction, decreased rectal tone, "saddle anesthesia" (sensory deficit over the perineum, buttocks, and inner thighs), variable motor andsensory loss in the lower extremities, decreased lower extremity reflexes, and sciatica. Bowel or bladder incontinence is not a universal
finding, because rectal tone can be spared,41 and if the patient presents early, the patient's bladder may not yet be full enough to cause
overflow incontinence. Careful history and physical examination, including identification of saddle anesthesia,42 are helpful to suggest the
diagnosis, but no one symptom or sign has 100% predictive value for this entity.42 Therefore, perform an MRI of the lumbosacral spinal cord ifclinical suspicion warrants. See the section "Epidural Compression Syndrome" in chapter 279, "Neck and Back Pain," for further discussion ofcauda equina syndrome.
NEUROGENIC SHOCK
Neurogenic shock is a type of distributive shock that can occur with CNS or spinal cord injury that probably occurs in less than 20% of spinal
cord–injured patients.43 Loss of peripheral sympathetic innervation results in extreme vasodilatation secondary to loss of sympatheticarterial tone. This causes blood pooling in the distal circulation with resultant hypotension. If the T1 through T4 cord levels are compromised,loss of sympathetic innervation to the heart leaves unopposed vagal parasympathetic cardiac innervation. This results in bradycardia or anabsence of reflex tachycardia. In general, patients with neurogenic shock are warm, peripherally vasodilated, and hypotensive with a relativebradycardia. Patients tend to tolerate hypotension relatively well, because peripheral oxygen delivery is presumably normal. Loss ofsympathetic tone and subsequent inability to redirect blood from the periphery to the core may cause excessive heat loss and hypothermia.
The diagnosis of neurogenic shock is one of exclusion. Certain clues, such as bradycardia and warm, dry skin, may be evident, buthypotension in the trauma patient can never be presumed to be caused by neurogenic shock until other possible sources of hypotension are
excluded.29
SPINAL SHOCK
Spinal shock is not neurogenic shock; the two terms have very di�erent meanings and are not interchangeable. Spinal shock is the temporaryloss or depression of spinal reflex activity that occurs below a complete or incomplete spinal cord injury. The typical presentation involves
flaccidity, loss of reflexes, and loss of voluntary movement.44 The lower the level of the spinal cord injury, the more likely it is that all distalreflexes will be absent. Loss of neurologic function that occurs with spinal shock can cause an incomplete spinal cord injury to mimic acomplete cord injury. Therefore, cord lesions cannot be called complete until spinal shock has resolved. The delayed plantar and
bulbocavernosus reflexes are among the first to return as spinal shock resolves.45 The duration of spinal shock is variable; it generally lasts for
days to weeks but can persist for months.46
DIAGNOSIS
Although spinal column and spinal cord injuries can sometimes be diagnosed clinically, diagnostic imaging is necessary to confirm thediagnosis and direct definitive care. However, judicious use of imaging is desirable to avoid unnecessary costs and ionizing radiationexposure to patients. Therefore, the challenge is identifying the appropriate patients to image and selecting the appropriate imagingmodality.
CLINICAL DECISION RULES IN CERVICAL SPINE IMAGING
In some cases, it is obvious who needs cervical spine imaging. For example, patients with head or neck trauma who are not fully alert(Glasgow coma scale score of <15) should undergo imaging of their cervical spine because the frequency of cervical spine injury in association
*Defined as Glasgow coma scale score <15; disorientation to person, place, time, or events; inability to remember three objects at 5 minutes; delayed or
inappropriate response to external stimuli.
†Any injury thought "to have the potential to impair the patient's ability to appreciate other injuries."
with traumatic brain injury ranges from 1.7% to 8%.47 However, in less obvious cases, the decision to perform imaging is not quite so clearcut.
An unstructured clinical exam is not adequately sensitive for the detection of cervical spine injuries,48 so guidelines can assist clinicaljudgment in deciding whom to image. In alert, stable adult trauma patients who have no neurologic deficits (i.e., low-risk trauma patients),two major clinical decision rules have been defined to avoid unnecessary radiography.
The first decision rule was derived by the National Emergency X-Radiography Utilization Study (NEXUS), which determined that plain cervical
spine imaging is unnecessary in patients who lack any one of five clinical criteria (Table 258-4).35 In the study population of 34,069 patients,the NEXUS criteria were 99.6% sensitive (95% confidence interval [CI], 98.6% to 100%) for detecting prospectively defined clinically significantcervical spine injuries, but only 12.9% specific (95% CI, 12.8% to 13.0%), with a negative predictive value of 99.9% (95% CI, 99.8% to 100%).The original NEXUS trial excluded patients >60 years old, but the criteria were subsequently shown to be 100% sensitive (95% CI, 97.1% to
100%) and 14.7% specific (95% CI, 14.6% to 14.7%) for clinically significant injuries in 2943 patients ≥65 years of age.49 In a subsequentprospective trial (n = 2785) investigating NEXUS's performance in patients ≥65 years of age, NEXUS was only 65.9% sensitive (vs 84.2% in
younger patients) for cervical spine injuries detected on CT.50 However, this trial contained several sources of bias (use of conveniencesample, a very high incidence of cervical spine injuries in the elderly group [12.8% vs 4.6% in the previous trial], and every elderly patientincluded was a trauma team activation). This latter study did not clarify whether the fractures detected on CT were clinically significant or ifany intervention was required.
TABLE 258-4
NEXUS Criteria
Absence of midline cervical tenderness
Normal level of alertness and consciousness*
No evidence of intoxication
Absence of focal neurologic deficit
Absence of painful distracting injury†
The Canadian Cervical Spine Rule for Radiography (CCR) was developed for alert, stable trauma patients to reduce practice variation and
ine�iciency in the ED use of plain cervical spine radiography.36 The Canadian rule consists of three assessments, which are asked in
sequential order (Table 258-5).36 To proceed to the next assessment, the answer to the previous assessment must be "Yes." If the answer toany assessments is "No," then imaging is immediately performed. In the original study sample of 8924 patients, the CCR was 100% sensitive
(95% CI, 98% to 100%) and 42.5% specific (95% CI, 40% to 44%) for identifying patients with "clinically important" cervical spine injuries.36
The CCR has also been validated in both larger hospital-based studies51 and prehospital studies,52 but has been criticized for its complexity
relative to NEXUS.53
11/25/2018
34/47
*Defined as fall from a height of >3 feet; an axial loading injury; high-speed motor vehicle crash, rollover, or ejection; motorized recreational vehicle or
bicycle collision.
TABLE 258-5
Canadian Cervical Spine Rule for Radiography: Cervical Spine Imaging Unnecessary in Patients Meeting These Three Criteria
Assessment Definitions
Assessment #1:
There are no high-risk factors that mandate radiography.
High-risk factors include:
Age 65 years or older
A dangerous mechanism of injury*
The presence of paresthesias in the extremities
Assessment #2:
There are low-risk factors that allow a safe assessment of range of motion.
Low-risk factors include:
Simple rear-end motor vehicle crashes
Patient able to sit up in the ED
Patient ambulatory at any time
Delayed onset of neck pain
Absence of midline cervical tenderness
Assessment #3:
The patient is able to actively rotate his/her neck (regardless of pain).
Can rotate neck 45 degrees to the le� and to the right
There is one published direct prospective comparison of NEXUS and CCR (n = 8283) that reported that CCR was more accurate for detectingcervical spine injury compared to NEXUS, with superior sensitivity (99% vs 91%), specificity (45% vs 37%), positive likelihood ratio (1.81 vs
1.44), and negative likelihood ratio (0.01 vs 0.25).54 However, some have questioned the methodology of this comparison as being biased in
favor of CCR.55,56 A meta-analysis of 15 studies (79,526 patients) concluded that the CCR appeared to have better diagnostic accuracy than
NEXUS57; however, the quality of methods of the included studies were termed "modest," and further more rigorous studies were suggestedto be done. In both rules, the more subjective parts ("absence of painful distracting injury" and "no evidence of intoxication" for NEXUS;"dangerous mechanism of injury" and assessment of range of motion for CCR) are the most common misinterpretation of the rules, which
obviously a�ects their performance.57
Both NEXUS and CCR were developed in an era prior to the routine use of CT as a primary tool to evaluate the cervical spine in blunt traumapatients. Consequently, studies have been done to compare both decision rules using CT scan as the gold standard. In a 2011 study of 2606blunt trauma patients, NEXUS was found to only be 82.8% sensitive and 45.7% specific for spine injury. Of the 26 missed injuries, 19 patients
required further intervention, including 2 who went to the operating room and 1 needing a Halo.58 The same group compared CCR to CT scan
(3201 blunt trauma patients), finding excellent sensitivity of 100% but only 0.60% specificity.59 Nevertheless, the use of NEXUS has been
recommended for use in several national guidelines and trauma societies.60,61
In summary, many experts feel that because both NEXUS and CCR have been widely validated and have demonstrated adequate sensitivity,
either rule may be used to determine which low-risk patients should undergo plain or CT cervical spine imaging.57
CERVICAL SPINE IMAGING
Plain Radiography
Standard radiography for the identification of bony cervical injury includes three views of the cervical spine: lateral, anterior-posterior, and
odontoid. A single lateral cervical spine film will identify only about 90% of injuries to bone and ligaments.24 The anterior-posterior and open-mouth odontoid views will identify many of the remaining abnormalities. It is important to image all seven cervical vertebrae, along with the
11/25/2018
35/47
superior border of the first thoracic vertebra, given the propensity for injuries at the cervical-thoracic junction. Therefore, a "swimmers view"may be necessary to visualize this junction clearly, but this o�en requires an assistant to pull down the shoulders during the radiograph. Themain advantages of plain radiography are that it can be done at the bedside, exposes the patient to only small amounts of ionizing radiation,and has a relatively low cost. One of the main disadvantages of plain films is that they are poor for imaging C1 and C2. In addition,visualization of the entire cervical spine by plain films is o�en problematic in obese, elderly, or extremely muscular patients, especially with acervical collar in place.
Cervical Spine CT
The practice in many trauma centers is to obtain CT as the initial imaging modality to evaluate the cervical spine. Multidetector CT is more
sensitive and specific than plain radiography for evaluating the cervical spine in trauma patients and can be performed quickly.62,63 CT canbe used to visualize the entire cervical spine and is particularly useful at the craniocervical and cervicothoracic regions, where the sensitivityof plain films is most limited. In addition, a 3-year retrospective review found that plain radiography did not add any clinically useful
information to a cervical spine CT.64 Furthermore, a cost analysis showed CT to be cost-e�ective to screen for cervical spine injuries in
moderate- to high-risk patients.65 The Eastern Association for the Surgery of Trauma recommends CT as the primary diagnostic tool for
suspected cervical spine injury.60 In addition, if plain radiography is chosen as the primary imaging modality, a CT should be ordered if aninjury is detected or suspected or if the initial plain radiograph is inadequate.
Imaging for Cervical Ligamentous Injury
In patients with pure ligamentous injuries, the ligaments are disrupted, but the spine spontaneously reduces to a normal position. Theresulting instability risks subsequent neurologic injury if the spine moves. Signs and symptoms include persistent neck pain/midlinetenderness, extremity paresthesias, or focal neurologic findings despite normal plain radiographs and/or CT.
Although flexion and extension radiographs have been traditionally used to try to detect ligamentous instability, numerous studies havedemonstrated their lack of sensitivity and ine�iciency (30% to 80% of flexion and extension radiographs are inadequate), and they provide no
further information beyond a CT.66,67,68,69,70 Therefore, flexion and extension radiographs should not be ordered when more advancedimaging is available.
MRI is the imaging modality of choice if a ligamentous injury is strongly suspected because MRI has excellent sensitivity for so� tissue
injuries.71,72 However, there are practical limitations on its use, including the requirement for the patient to be stable, availability, cost, andpatient tolerance for the procedure. If emergent MRI is not feasible, reliable patients with persistent pain but normal CT can be discharged ina firm foam collar with outpatient follow-up in 3 to 5 days. Most patients' symptoms will resolve over a few days. A patient with persistentpain at follow-up will likely require additional imaging. Unreliable patients with severe persistent pain and normal CT images should beconsidered for an MRI study, although this is rarely indicated as part of the initial investigation. In fact, some data have suggested that newer-
generation CTs are su�icient to detect significant injuries without MRI even in obtunded patients.73,74 However, the results of these studiescannot currently be externally generalized to awake, symptomatic patients.
Thoracic and Lumbar Spine Imaging
As of this writing, there are no well-validated clinical decision rules for imaging in possible thoracolumbar spine injuries. However, Table 258-
6 provides practice guidelines for imaging in blunt trauma victims who are suspected of having thoracolumbar injuries.37,75
Eastern Association for the Surgery of Trauma Guidelines for Thoracic and Lumbar Imaging a�er Trauma
Level I (convincingly
justifiable based on
scientific evidence)
When imaging is deemed necessary, CT scans with axial collimation should be used to screen for and diagnose injury,
because CT scans are superior to plain films in identifying thoracolumbar spine fractures.
Level II (reasonably
justifiable based on
scientific evidence and
expert opinion)
Patients with back pain, thoracolumbar spine tenderness on examination, neurologic deficits referable to the
thoracolumbar spine, altered mental status, intoxication, distracting injuries, or known or suspected high-energy
mechanisms should be screened for thoracolumbar spine injury with CT scan.
In blunt trauma patients with a known or suspected injury to the cervical spine, or any other region of the spine,
thorough evaluation of the entire spine by CT scan should be strongly considered due to a high incidence of spinal
injury at multiple levels within this population.
Patients without complaints of thoracolumbar spine pain who have normal mental status, as well as normal neurologic
and physical examinations, may be excluded from thoracolumbar spine injury by clinical examination alone, without
radiographic imaging, provided that there is no suspicion of high-energy mechanism or intoxication with alcohol or
drugs.
Level III (supported by
available data, but
scientific evidence
lacking)
MRI should be considered in consultation with the spine service for CT findings suggestive of neurologic involvement
and of gross neurologic deficits.
As with the cervical spine, CT has largely supplanted plain radiography in the imaging of thoracic and lumbar injuries with significant blunttrauma. CT scanning is indicated in almost all patients with proven bony spinal injury, subluxations, neurologic deficits (but no apparentabnormalities on plain films), or severe neck or back pain (with normal plain films) and when the thoracic and lumbar spine should beexamined to define the anatomy of a fracture and the extent of impingement on the spinal canal. Rather than obtaining separate plainradiographs or dedicated CT images, the thoracic and abdominal CT scans obtained to evaluate the multiple trauma patient can be used toreconstruct images of the thoracic and lumbar spine, although some authors have suggested that spinal image reconstruction is not
necessary because the spine can be seen on the visceral CT scans.76,77 CT can reveal the anatomy of an osseous injury, grade the extent ofspinal canal impingement by bone fragments, and assess the stability of an injury. If an associated spinal cord or nerve root injury issuspected, MRI is the imaging study of choice.
It is less clear how to screen for thoracolumbar injuries in patients who have less severe mechanisms of injuries. Although it has been shown
repeatedly that CT is more sensitive for thoracolumbar injuries in severely injured patients,37 there has been no prospective controlledcomparison between plain radiography and CT in more mildly injured patients. Nevertheless, some published guidelines suggest CT should
be considered the standard screening modality for thoracolumbar injuries.37
Spinal Cord and Neural Tissue Imaging
MRI is not as sensitive as CT for detecting or delineating bone injuries but is superb at defining neural, muscular, and so� tissue injury. MRI isthe diagnostic test of choice for describing the anatomy of nerve injury. Entities such as herniated disks or spinal cord contusions can also bedelineated on MRI. MRI is indicated in patients with neurologic findings with no clear explanation a�er plain films and/or CT scanning. If thepatient is stable and MRI is unavailable, transfer to a tertiary care facility with MRI capabilities is appropriate.
The determination of a spinal column injury at one level should prompt imaging of the entire remainder of the spine with CT because
approximately 20% of patients with a spine fracture in one segment will have a noncontiguous second fracture at another segment.78,79
Spine Imaging in Obtunded Patients
While experts recommend that all obtunded patients with significant blunt trauma should have their entire spine imaged, consensus doesnot yet exist on what imaging is necessary to clear the spine in obtunded patients. Specifically, it is controversial whether a negative CT of the
spine is adequate or if a subsequent MRI needs to be done,80 although at this writing, the trend in the literature suggests that a negative CT is
su�icient.73,74 In the absence of definitive data, maintain spinal precautions in the obtunded trauma patient in the ED, and defer any spineclearance to local expert consultants.
TREATMENT AND DISPOSITION OF SPINAL COLUMN INJURIES
The goals of treatment are to prevent secondary injury, alleviate cord compression, and establish spinal stability. Maintain spinalimmobilization and keep movement to a minimum. Obtain emergent consultation with a spine surgeon (neurosurgeon or orthopedic surgeondepending on the particular facility) on all spinal column fractures or ligamentous injuries, regardless of neurologic compromise.
CERVICAL SPINE FRACTURES
The majority of cervical spinal fractures will require admission for definitive treatment or for the care of associated injuries. Until transfer ofcare to a surgeon, spine precautions should be maintained, associated injuries stabilized, and the patient carefully monitored for respiratoryor neurologic deterioration.
THORACIC AND LUMBAR SPINE FRACTURES
Thoracolumbar fractures are also high risk for associated spinal cord or other traumatic injuries, such as aortic, intrathoracic, or intra-abdominal visceral injuries. Although many of these injuries will require admission, there are two types of thoracolumbar factures that maybe amenable to outpatient therapy.
Compression fractures, also known as "wedge" or "anterior" compression fractures, comprised approximately 52% of thoracolumbar
fractures in one published series.81 These fractures occur as a result of a hyperflexion during an axial load that crushes the anterior portion ofthe vertebra. If the percentage of loss of vertebral height is <40%, the patient may be a candidate for outpatient therapy, and this should bediscussed on a case-by-case basis by the spine surgeon. However, if the loss of vertebral height is ≥50% or if the angle between the damagedvertebra and the rest of the spinal column is >25% to 30%, the compression fracture is generally considered unstable.
In addition, make certain that an apparent compression fracture seen on plain radiographs is not a burst fracture, which is a compression-type fracture that involves the posterior half of the vertebrae. Burst fractures may result in retropulsed fragments that can impinge on thespinal canal and cause neurologic injury. In two studies, the incidence of misdiagnosis of burst fractures on plain radiographs ranged from
20% to 23%.82,83 Another fracture that is sometimes misdiagnosed as a wedge compression fracture on plain radiograph is the Chancefracture. This fracture occurs via a flexion-distraction mechanism and involves minor anterior vertebral compression and significantdistraction of the middle and posterior ligamentous structures. Typical radiographic findings reveal a transverse fracture lucency in thevertebral body, an increased height of the posterior vertebral body, fracture of the posterior wall of the vertebral body, and posterior openingof the disk space. Finally, minor to moderate trauma can cause pathologic fractures secondary to preexisting neoplastic, infectious, orosteoporotic processes in the spine. Because the above mentioned fractures can be easily misdiagnosed with plain radiography alone, some
experts recommend that compression fractures of the thoracolumbar spine on plain radiographs be further evaluated with CT.84
If, a�er a thorough evaluation, a stable wedge compression fracture with no neurologic compromise is diagnosed, the patient may be treatedas an outpatient with analgesia, heat, massage, rest, and appropriate follow-up for consideration of physical therapy.
SACRUM AND COCCYX FRACTURES
Injuries of the sacral spine and nerve roots are very unusual. When they occur, they are frequently associated with fractures of the pelvis. Ingeneral, transverse fractures through the body are most significant in that they cause injury to part or all of the cauda equina. Longitudinalfractures may cause radiculopathy. Sacral fractures that involve the central sacral canal can produce bowel or bladder dysfunction.
11/25/2018
38/47
One notable exception to the need for emergent consultation is an isolated coccyx fracture. Coccygeal injuries are usually associated with adirect fall onto the buttocks, with resultant coccyx pain exacerbated by sitting or straining. Imaging is not needed to diagnose coccygealfractures. Treatment is symptomatic with analgesics and use of a rubber doughnut pillow.
SPECIAL CONSIDERATIONS
CORTICOSTEROIDS
High-dose methylprednisolone remains a controversial treatment in acute blunt spinal cord injury and should not be given routinely. Themajor neuroprotective mechanism by which high-dose methylprednisolone is believed to work is in its inhibition of free radical–induced lipidperoxidation. Other proposed beneficial actions include its ability to increase levels of spinal cord blood flow, increase extracellular calcium,and prevent loss of potassium from injured cord tissue. Methylprednisolone is advocated in preference to other steroids because it crossescell membranes more rapidly and completely.
In the 1990s, the National Acute Spinal Cord Injury Study (NASCIS) group published three prospective, double-blind studies to evaluate the
e�icacy of methylprednisolone in blunt spinal cord injury: NASCIS I, II, and III.85,86,87 NASCIS I compared high-dose methylprednisolone and alower-dose methylprednisolone regimen (n = 330). NASCIS I showed no evidence in recovery of function between the groups. NASCIS IIcompared a higher dose of methylprednisolone (Table 258-7), naloxone, and placebo (n = 427). This trial was also negative, but based on posthoc subgroup analysis, NASCIS II showed modest improvements in motor function when steroids were administered within 8 hours of injury.NASCIS III compared high-dose methylprednisolone for 24 hours, high-dose methylprednisolone for 48 hours, and tirilazad mesylate for 24hours (n = 499). NASCIS III was also a negative trial, but post hoc analysis found that patients who received the 48-hour methylprednisoloneregimen within 3 to 8 hours of their injury showed motor improvement. In all three trials, patients who received high-dosemethylprednisolone and longer duration protocols were more likely to develop complications such as severe sepsis, severe pneumonia,wound infection and delayed healing, pulmonary embolism and deep vein thrombosis, GI bleeding, and death. A recent Cochrane systematicreview (written by the lead author of the NASCIS trials) essentially confirmed the conclusions of NASCIS II and III that high-dosemethylprednisolone was beneficial when administered within 8 hours of injury, but these patients were also more likely to develop
complications.88 The systematic review also recommended that more randomized trials be done urgently.
TABLE 258-7
The National Acute Spinal Cord Injury Study II High-Dose Methylprednisolone Protocol
Indications Blunt trauma
Neurologic deficit referable to the spinal cord
Treatment must be started within 8 h of injury
Treatment Methylprednisolone, 30 milligrams/kg IV bolus over 15 min
Followed by a 45-min pause
Methylprednisolone, 5.4 milligrams/kg/h IV is then infused for 23 h
The results of the NASCIS clinical trials have been criticized as not providing su�icient clinical evidence to support the use of steroids in acutespinal cord injury. Examples of bias cited include the use of post hoc subgroup analysis, the artificiality of the 3- and 8-hour time limits, and adi�erence in the severity of injury in particular treatment groups. Reassessment, meta-analysis, and studies by other authors have
questioned the validity of the NASCIS trials and the e�ectiveness of high-dose steroid therapy in these patients.89,90,91 Consequently, the2013 updated guidelines for the management of acute spinal cord injuries endorsed by the American Association of Neurological Surgeonsand the Congress of Neurological Surgeons stated that "there is no consistent or compelling medical evidence of any class to justify theadministration of methylprednisolone for acute spinal cord injury," and that "methylprednisolone should not be routinely used in the
treatment of patients with acute spinal cord injury."92 Moreover, the U.S. Food and Drug Administration has not approved corticosteroids for
acute spinal cord injury.93
Nevertheless, the use of methylprednisolone persists in some centers. Therefore, given the continued controversy over its use,94,95 thedecision to start corticosteroids should only be made in conjunction with the surgeon who will ultimately be caring for the patient, and not
It is important to realize that the NASCIS trial protocol was evaluated only in patients with blunt spinal cord injury, while penetrating injurieswere excluded from these studies. In fact, high-dose methylprednisolone therapy has not been found to be e�icacious in penetrating spinal
cord injury.96 In addition, because corticosteroids worsen outcomes in brain-injured patients, they should be avoided in this population as
well.97
CARDIOVASCULAR COMPLICATIONS
If neurogenic shock is present, initiate an infusion of IV crystalloid to correct this relative hypovolemia. If IV fluids are not adequate tomaintain organ perfusion, positive inotropic pressor agents may be beneficial adjuncts to improve cardiac output and raise perfusionpressure. In terms of target systolic blood pressure and mean arterial pressure, the evidence in the literature is limited at best. However, it hasbeen recommended that systolic blood pressure should be kept greater than 90 mm Hg, with the mean arterial pressure kept at 85 to 90 mm
Hg.98 The aggressive use of fluids in neurogenic shock should be performed with careful monitoring, because there is danger of excessivefluid replacement, resulting in heart failure and pulmonary edema. There is no definitive evidence that any particular vasopressor is superior
to another for this indication.99
Bradycardia, when present, usually occurs within the first few hours or days a�er spinal cord injury because of a predominance of vagal toneto the heart. In cases of hemodynamically significant bradycardia, atropine may be needed. Rare occurrences of atrioventricular conductionblock with significant bradycardia require a pacemaker.
PENETRATING INJURY
Penetrating injuries to the neck are discussed in chapter 260, "Trauma to the Neck." For spinal gunshot wounds with a transabdominal ortransintestinal trajectory, administer prophylactic broad-spectrum IV antibiotics in the ED. Corticosteroids are contraindicated in patientswith any type of penetrating spinal injuries, and emergent consultation with a spine surgeon is indicated.
Acknowledgments: The author gratefully acknowledges the prior contributions of Bonny J. Baron, Kevin J. McSherry, James L. Larson, Jr.,and Thomas M. Scalea, the authors of this chapter in the previous edition. The author would also like to thank Lawrence R. Ricci, DO, for hisinvaluable assistance with locating images.
REFERENCES
Fredo HL, Rizvi SA, Lied B, Ronning P, Helseth E: The epidemiology of traumatic cervical spine fractures: a prospective population studyfrom Norway. Scand J Trauma Resusc Emerg Med 20: 85, 2012.
[PubMed: 23259662]
Hu R, Mustard CA, Burns C" Epidemiology of incident spinal fracture in a complete population. Spine 21: 492, 1996. [PubMed: 8658254]
https://www.nscisc.uab.edu/PublicDocuments/fact_figures_docs/Facts%202013.pdf (National Spinal Cord Injury Statistical Center: Spinalcord injury facts and figures at a glance, 2013.) Accessed June 18, 2014.
Greenbaum J, Walters N, Levy PD: An evidenced-based approach to radiographic assessment of cervical spine injuries in the emergencydepartment. J Emerg Med 36: 64, 2009.
[PubMed: 18783909]
Holmes JF, Miller PQ, Panacek EA, Lin S, Horne NS, Mower WR: Epidemiology of thoracolumbar spine injury in blunt trauma. Acad EmergMed 8: 866, 2001.
Amorosa LF, Vaccaro AR: Current concepts in cervical spine trauma. Instr Course Lect 63: 255, 2014. [PubMed: 24720311]
Dickman CA, Hadley MN, Pappas CT, Sonntag VK, Geisler FH: Cruciate paralysis: a clinical and radiographic analysis of injuries to thecervicomedullary junction. J Neurosurg 73: 850, 1990.
[PubMed: 2230968]
Harris JH Jr, Carson GC, Wagner LK: Radiologic diagnosis of traumatic occipitovertebral dissociation: 1. Normal occipitovertebralrelationships on lateral radiographs of supine subjects. AJR Am J Roentgenol 162: 881, 1994.
[PubMed: 8141012]
Denis F: The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine 8: 817, 1983. [PubMed: 6670016]
Lewkonia P, Paolucci EO, Thomas K: Reliability of the thoracolumbar injury classification and severity score and comparison with thedenis classification for injury to the thoracic and lumbar spine. Spine 37: 2161, 2012.
Grossman RG, Fehlings MG, Frankowski RF et al.: A prospective, multicenter, phase I matched-comparison group trial of safety,pharmacokinetics, and preliminary e�icacy of riluzole in patients with traumatic spinal cord injury. J Neurotrauma 31: 239, 2014.
[PubMed: 23859435]
Horodyski M, DiPaola CP, Conrad BP, Rechtine GR 2nd: Cervical collars are insu�icient for immobilizing an unstable cervical spine injury.J Emerg Med 41: 513, 2011.
[PubMed: 21397431]
Kwan I, Bunn F, Roberts I: Spinal immobilisation for trauma patients. Cochrane Database Syst Rev 2: CD002803, 2001. [PubMed: 11406043]
Tescher AN, Rindflesch AB, Youdas JW et al.: Range-of-motion restriction and craniofacial tissue-interface pressure from four cervicalcollars. J Trauma 63: 1120, 2007.
[PubMed: 17993960]
Linares HA, Mawson AR, Suarez E, Biundo JJ: Association between pressure sores and immobilization in the immediate post-injuryperiod. Orthopedics 10: 571, 1987.
[PubMed: 3575181]
Luscombe MD, Williams JL: Comparison of a long spinal board and vacuum mattress for spinal immobilisation. Emerg Med J 20: 476,2003.
[PubMed: 12954698]
Totten VY, Sugarman DB: Respiratory e�ects of spinal immobilization. Prehosp Emerg Care 3: 347, 1999. [PubMed: 10534038]
Del Rossi G, Rechtine GR, Conrad BP, Horodyski M: Are scoop stretchers suitable for use on spine-injured patients? Am J Emerg Med 28:751, 2010.
[PubMed: 20837250]
Hemmes B, Poeze M, Brink PR: Reduced tissue-interface pressure and increased comfort on a newly developed so�-layered longspineboard. J Trauma 68: 593, 2010.
[PubMed: 19918198]
Sundstrom T, Asbjornsen H, Habiba S, Sunde GA, Wester K: Prehospital use of cervical collars in trauma patients: a critical review. JNeurotrauma 31: 531, 2014.
[PubMed: 23962031]
Theodore N, Hadley MN, Aarabi B et al.: Prehospital cervical spinal immobilization a�er trauma. Neurosurgery 72 (Suppl 2): 22, 2013. [PubMed: 23417176]
Connell RA, Graham CA, Munro PT: Is spinal immobilisation necessary for all patients sustaining isolated penetrating trauma? Injury 34:912, 2003.
[PubMed: 14636733]
Haut ER, Kalish BT, Efron DT et al.: Spine immobilization in penetrating trauma: more harm than good? J Trauma 68: 115, 2010. [PubMed: 20065766]
Azia M: Use of video-assisted intubation devices in the management of patients with trauma. Anesthesiol Clin 31: 157, 2013. [PubMed: 23351541]
Horodyski M, Conrad BP, Del Rossi G, DiPaola CP, Rechtine GR 2nd: Removing a patient from the spine board: is the li� and slide saferthan the log roll? J Trauma 70: 1282, 2011.
[PubMed: 21610441]
Conrad BP, Rossi GD, Horodyski MB, Prasarn ML, Alemi Y, Rechtine GR: Eliminating log rolling as a spine trauma order. Surg Neurol Int 3(Suppl 3): S188, 2012.
[PubMed: 22905325]
Powers J, Daniels D, McGuire C, Hilbish C: The incidence of skin breakdown associated with use of cervical collars. J Trauma Nurs 13:198, 2006.
[PubMed: 17263104]
Ho AM, Fung KY, Joynt GM, Karmakar MK, Peng Z: Rigid cervical collar and intracranial pressure of patients with severe head injury. JTrauma 53: 1185, 2002.
[PubMed: 12478051]
Karason S, Reynisson K, Sigvaldason K, Sigurdsson GH: Evaluation of clinical e�icacy and safety of cervical trauma collars: di�erences inimmobilization, e�ect on jugular venous pressure and patient comfort. Scand J Trauma Resusc Emerg Med 22: 37, 2014.
[PubMed: 24906207]
Ho�man JR, Mower WR, Wolfson AB, Todd KH, Zucker MI: Validity of a set of clinical criteria to rule out injury to the cervical spine inpatients with blunt trauma: National Emergency X-Radiography Utilization Study Group. N Engl J Med 343: 94, 2000.
[PubMed: 10891516]
Stiell IG, Wells GA, Vandemheen KL et al.: The Canadian C-spine rule for radiography in alert and stable trauma patients. JAMA 286: 1841,2001.
Sixta S, Moore FO, Ditillo MF et al.: Screening for thoracolumbar spinal injuries in blunt trauma: an Eastern Association for the Surgery ofTrauma practice management guideline. J Trauma Acute Care Surg 73 (5 Suppl 4): S326, 2012. [PubMed: 23114489]
http://www.asia-spinalinjury.org/elearning/ISNCSCI.php (American Spinal Injury Association: ASIA Learning Center Materials:International Standards for Neurological Classification of Spinal Cord Injury Exam Worksheet. 2014.) Accessed August 22, 2014.
Scivoletto G, Tamburella F, Laurenza L, Torre M, Molinari M: Who is going to walk? A review of the factors influencing walking recoverya�er spinal cord injury. Front Hum Neurosci 8: 141, 2014.
[PubMed: 24659962]
Amendola L, Corghi A, Cappuccio M, De Iure F: Two cases of Brown-Sequard syndrome in penetrating spinal cord injuries. Eur Rev MedPharmacol Sci 18 (1 Suppl): 2, 2014.
[PubMed: 24825034]
Gooding BW, Higgins MA, Calthorpe DA: Does rectal examination have any value in the clinical diagnosis of cauda equina syndrome? Br JNeurosurg 27: 156, 2013.
Guly HR, Bouamra O, Lecky FE: The incidence of neurogenic shock in patients with isolated spinal cord injury in the emergencydepartment. Resuscitation 76: 57, 2008.
[PubMed: 17688997]
Ditunno JF, Little JW, Tessler A, Burns AS: Spinal shock revisited: a four-phase model. Spinal Cord 42: 383, 2004. [PubMed: 15037862]
Ko HY, Ditunno JF Jr, Graziani V, Little JW: The pattern of reflex recovery during spinal shock. Spinal Cord 37: 402, 1999. [PubMed: 10432259]
D'Amico JM, Condli�e EG, Martins KJ, Bennett DJ, Gorassini MA: Recovery of neuronal and network excitability a�er spinal cord injuryand implications for spasticity. Front Integr Neurosci 8: 36, 2014.
[PubMed: 24860447]
Fujii T, Faul M, Sasser S: Risk factors for cervical spine injury among patients with traumatic brain injury. J Emerg Trauma Shock 6: 252,2013.
[PubMed: 24339657]
Bandiera G, Stiell IG, Wells GA et al.: The Canadian C-spine rule performs better than unstructured physician judgment. Ann Emerg Med42: 395, 2003.
[PubMed: 12944893]
Touger M, Gennis P, Nathanson N et al.: Validity of a decision rule to reduce cervical spine radiography in elderly patients with blunttrauma. Ann Emerg Med 40: 287, 2002.
[PubMed: 12192352]
Goode T, Young A, Wilson SP, Katzen J, Wolfe LG, Duane TM: Evaluation of cervical spine fracture in the elderly: can we trust our physicalexamination? Am Surg 80: 182, 2014.
Stiell IG, Clement CM, Grimshaw J et al.: Implementation of the Canadian C-Spine Rule: prospective 12 centre cluster randomised trial.BMJ 339: b4146, 2009.
[PubMed: 19875425]
Vaillancourt C, Stiell IG, Beaudoin T et al.: The out-of-hospital validation of the Canadian C-Spine Rule by paramedics. Ann Emerg Med54: 663, 2009.
[PubMed: 19394111]
Mower WR, Ho�man JL: Comparison of the Canadian C-Spine rule and NEXUS decision instrument in evaluating blunt trauma patientsfor cervical spine injury. Ann Emerg Med 43: 515, 2004.
[PubMed: 15039696]
Stiell IG, Clement CM, McKnight RD et al.: The Canadian C-spine rule versus the NEXUS low-risk criteria in patients with trauma. N Engl JMed 349: 2510, 2003.
[PubMed: 14695411]
Yealy DM, Auble TE: Choosing between clinical prediction rules. N Engl J Med 349: 2553, 2003. [PubMed: 14695417]
Mower WR, Wolfson AB, Ho�man JR, Todd KH: The Canadian C-spine rule. N Engl J Med 350: 1467, 2004. [PubMed: 15070802]
Michale� ZA, Maher CG, Verhagen AP, Rebbeck T, Lin CW: Accuracy of the Canadian C-spine rule and NEXUS to screen for clinicallyimportant cervical spine injury in patients following blunt trauma: a systematic review. CMAJ 184: E867, 2012.
[PubMed: 23048086]
Duane TM, Mayglothling J, Wilson SP et al.: National Emergency X-Radiography Utilization Study criteria is inadequate to rule outfracture a�er significant blunt trauma compared with computed tomography. J Trauma 70: 829, 2011.
[PubMed: 21610391]
Duane TM, Wilson SP, Mayglothling J et al.: Canadian Cervical Spine rule compared with computed tomography: a prospective analysis.J Trauma 71: 352, 2011.
[PubMed: 21825938]
Como JJ, Diaz JJ, Dunham CM et al.: Practice management guidelines for identification of cervical spine injuries following trauma:update from the eastern association for the surgery of trauma practice management guidelines committee. J Trauma 67: 651, 2009.
[PubMed: 19741415]
Ryken TC, Hadley MN, Walters BC et al.: Radiographic assessment. Neurosurgery 72 (Suppl 2): 54, 2013. [PubMed: 23417179]
Bailitz J, Starr F, Beecro� M et al.: CT should replace three-view radiographs as the initial screening test in patients at high, moderate,and low risk for blunt cervical spine injury: a prospective comparison. J Trauma 66: 1605, 2009.
[PubMed: 19509621]
Gale SC, Gracias VH, Reilly PM, Schwab CW: The ine�iciency of plain radiography to evaluate the cervical spine a�er blunt trauma. JTrauma 59: 1121, 2005.
[PubMed: 16385289]
Hashem R, Evans CC, Farrokhyar F, Kahnamoui K: Plain radiography does not add any clinically significant advantage to multidetectorrow computed tomography in diagnosing cervical spine injuries in blunt trauma patients. J Trauma 66: 423, 2009.
Grogan EL, Morris JA Jr, Dittus RS et al.: Cervical spine evaluation in urban trauma centers: lowering institutional costs andcomplications through helical CT scan. J Am Coll Surg 200: 160, 2005.
[PubMed: 15664088]
Insko EK, Gracias VH, Gupta R, Goettler CE, Gaieski DF, Dalinka MK: Utility of flexion and extension radiographs of the cervical spine inthe acute evaluation of blunt trauma. J Trauma 53: 426, 2002.
[PubMed: 12352475]
Khan SN, Erickson G, Sena MJ, Gupta MC: Use of flexion and extension radiographs of the cervical spine to rule out acute instability inpatients with negative computed tomography scans. J Orthop Trauma 25: 51, 2011.
[PubMed: 21085024]
McCracken B, Klineberg E, Pickard B, Wisner DH: Flexion and extension radiographic evaluation for the clearance of potential cervicalspine injures in trauma patients. Eur Spine J 22: 1467, 2013.
[PubMed: 23404352]
Goodnight TJ, Helmer SD, Dort JM, Nold RJ, Smith RS: A comparison of flexion and extension radiographs with computed tomographyof the cervical spine in blunt trauma. Am Surg 74: 855, 2008.
[PubMed: 18807677]
Tran B, Saxe JM, Ekeh AP: Are flexion extension films necessary for cervical spine clearance in patients with neck pain a�er negativecervical CT scan? J Surg Res 184: 411, 2013.
Mnaker J, Stein DM, Philp AS, Scalea TM: 40-slice multidetector CT: is MRI still necessar American Spinal Injury Association AmericanSpinal Injury Association y for cervical spine clearance a�er blunt trauma? Am Surg 76: 157, 2010.
[PubMed: 20336892]
Khanna P, Chau C, Dublin A, Kim K, Wisner D: The value of cervical magnetic resonance imaging in the evaluation of the obtunded orcomatose patient with cervical trauma, no other abnormal neurological findings, and a normal cervical computed tomography. J TraumaAcute Care Surg 72: 699, 2012.
[PubMed: 22491556]
Satahoo SS, Davis JS, Garcia GD et al.: Sticking our neck out: is magnetic resonance imaging needed to clear an obtunded patient'scervical spine? J Surg Res 187: 225, 2014.
[PubMed: 24157265]
O'Connor E, Walsham J: Review article: indications for thoracolumbar imaging in blunt trauma patients: a review of current literature.Emerg Med Australas 21: 94, 2009.
[PubMed: 19422405]
Mancini DJ, Burchard KW, Pekala JS: Optimal thoracic and lumbar spine imaging for trauma: are thoracic and lumbar spine reformatsalways indicated? J Trauma 69: 119, 2010.
[PubMed: 20622586]
Gross EA: Computed tomographic screening for thoracic and lumbar fractures: is spine reformatting necessary? Am J Emerg Med 28: 73,2010.
Sharma OP, Oswanski MF, Yazdi JS, Jindal S, Taylor M: Assessment for additional spinal trauma in patients with cervical spine injury. AmSurg 73: 70, 2007.
[PubMed: 17249461]
Miller CP, Brubacher JW, Biswas D, Lawrence BD, Whang PG, Grauer JN: The incidence of noncontiguous spinal fractures and othertraumatic injuries associated with cervical spine fractures: a 10-year experience at an academic medical center. Spine 36: 1532, 2011.
[PubMed: 21242872]
Schoenfeld AJ, Bono CM, McGuire KJ, Warholic N, Harris MB: Computed tomography alone versus computed tomography and magneticresonance imaging in the identification of occult injuries to the cervical spine: a meta-analysis. J Trauma 68: 109, 2010.
[PubMed: 20065765]
Holmes JF, Miller PQ, Panacek EA, Lin S, Horne NS, Mower WR: Epidemiology of thoracolumbar spine injury in blunt trauma. AcadEmerg Med 8: 866, 2001.
[PubMed: 11535478]
Dai LY: Imaging diagnosis of thoracolumbar burst fractures. Chin Med Sci J 19: 142, 2004. [PubMed: 15250254]
Ballock RT, Mackersie R, Abitbol JJ, Cervilla V, Resnick D, Garfin SR: Can burst fractures be predicted from plain radiographs? J BoneJoint Surg Br 74: 147, 1992.
[PubMed: 1732246]
Dai LY, Wang XY, Jiang LS et al.: Plain radiography versus computed tomography scans in the diagnosis and management ofthoracolumbar burst fractures. Spine 33: E548, 2008.
[PubMed: 18628696]
Bracken MB, Collins WF, Freeman DF et al.: E�icacy of methylprednisolone in acute spinal cord injury. JAMA 251: 45, 1984. [PubMed: 6361287]
Bracken MB, Shepard MJ, Collins WF et al.: A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acutespinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med 322: 1405, 1990.
[PubMed: 2278545]
Bracken MB, Shepard MJ, Holford TR et al.: Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours inthe treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury randomized controlled trial. National AcuteSpinal Cord Injury Study. JAMA 277: 1597, 1997.
Sayer FT, Kronvall E, Nilsson OG: Methylprednisolone treatment in acute spinal cord injury: the myth challenged through a structuredanalysis of published literature. Spine J 6: 335, 2006.
[PubMed: 16651231]
Ito Y, Sugimoto Y, Tomioka M, Kai N, Tanaka M: Does high dose methylprednisolone sodium succinate really improve neurological statusin patient with acute cervical cord injury? A prospective study about neurological recovery and early complications. Spine 34: 2121, 2009.
[PubMed: 19713878]
Suberviola B, Gonzalez-Castro A, Llorca J, Ortiz-Melon F, Minambres E: Early complications of high-dose methylprednisolone in acutespinal cord injury patients. Injury 39: 748, 2008.
Hurlbert RJ: Methylprednisolone for the treatment of acute spinal cord injury: point. Neurosurgery 61 (Suppl 1): 32, 2014. [PubMed: 25032528]
Fehlings MG, Wilson JR, Cho N: Methylprednisolone for the treatment of acute spinal cord injury: counterpoint. Neurosurgery 61 (Suppl1): 36, 2014.
[PubMed: 25032529]
Levy ML, Gans W, Wijesinghe HS, SooHoo WE, Adkins RH, Stillerman CB: Use of methylprednisolone as an adjunct in the managementof patients with penetrating spinal cord injury: outcome analysis. Neurosurgery 39: 1141, 1996.
[PubMed: 8938768]
Alderson P, Roberts I: Corticosteroids for acute traumatic brain injury. Cochrane Database Syst Rev 1: CD000196, 2005. [PubMed: 15674869]
Ryken TC, Hurlbert RJ, Hadley MN et al.: The acute cardiopulmonary management of patients with cervical spinal cord injuries.Neurosurgery 72 (Suppl 2): 84, 2013.
[PubMed: 23417181]
Ploumis A, Yadlapalli N, Fehlings MG, Kwon BK, Vaccaro AR: A systematic review of the evidence supporting a role for vasopressorsupport in acute SCI. Spinal Cord 48: 356, 2010.
[PubMed: 19935758]
PRACTICE GUIDELINES AND USEFUL WEB RESOURCES
2013 American Association of Neurological Surgeons/Congress of Neurological Surgeons Guidelines for the Management of Acute CervicalSpine and Spinal Cord Injuries. (These are the current practice guidelines from the American Association of Neurological Surgeons/Congressof Neurological Surgeons Joint Guidelines Committee. The chapters regarding prehospital care, initial clinical assessment, and radiographicassessment are particularly relevant to the emergency physician. Online and full-text access is free.)—http://neurosurgerycns.wordpress.com/2013/02/20/guidelines-for-the-management-of-acute-cervical-spine-and-spinal-cord-injury/
Eastern Association for the Surgery of Trauma Practice Management Guidelines (This site contains relevant practice guidelines for cervicaland thoracolumbar spinal injuries.)—http://www.east.org/resources/treatment-guidelines
National Spinal Cord Injury Statistics Center (This webpage contains a link to both a two-page summary and a more detailed report of themost current epidemiologic data regarding spinal cord injuries in the United States in PDF FORM.)—https://www.nscisc.uab.edu/
National Spinal Cord Injury Association—http://www.spinalcord.org; and National Institute of Neurological Disorders and Stroke—http://www.ninds.nih.gov/disorders/sci/sci.htm (These sites have patient information regarding spinal cord injury. The National Institute ofNeurological Disorders and Stroke site includes links to current trials regarding spinal cord injury.)