Strange and Schafermeyer's Pediatric Emergency Medicine, Fourth Edition (Strange, Pediatric Emergency Medicine), 4th Ed.

CHAPTER 24. Cervical Spine Injury

Julie Catherine Leonard

Jeffrey Russell Leonard

HIGH-YIELD FACTS

• Suspect cervical spine injury in any child who has suffered traumatic respiratory arrest and perform rapid sequence orotracheal intubation with in-line cervical spine stabilization.

• Because of differences in anatomy and physiology, children sustain proportionally more upper cervical spine and spinal cord injury without radiographic abnormality (SCIWORA) injuries compared with adults.

• CT scan is more sensitive for bony injury, and MRI for soft-tissue injury.

• Although spine immobilization is indicated when cervical spine injury is suspected, complications can occur. Decisions to immobilize should target those at greatest risk for cervical spine injury.

Cervical spine injuries are serious, but rare events in children.13 Emergency physicians are often the first to evaluate pediatric trauma patients with cervical spine injury and must quickly triage children with the potential for worsening neurologic deficits from those with either no cervical spine injury or cervical sprain. Occasionally, these decisions are made in the absence of adequate cervical spine imaging when dealing with a child’s unstable airway or other life-threatening injuries. These challenges raise some specific questions. Are there specific subsets of children at the highest risk for cervical spine injuries? Which children should be immobilized and how is this best achieved? How is the cervical spine “cleared”?

EPIDEMIOLOGY

Cervical spine injury represents a small subset of injured children. Cervical spine injury affects less than 1% of children undergoing trauma evaluation and only 1.5% of children enrolled in the National Pediatric Trauma Registry.35It is estimated that there is an overall 17% mortality associated with cervical spine injury in children; however, this rate may be as high as 60% in children 8 years.3,5 This increased risk of mortality is likely associated with proportionately higher rates of upper cervical spine injuries in young children.3,5

Motor vehicle collisions are the most common cause of cervical spine injuries.3,6,7 However, the mechanisms vary by age. Neonates may suffer cervical spine injuries from birth trauma, particularly in the case of breech or forceps deliveries.8,9 The incidence of nonaccidental trauma is likely underestimated in the pediatric population.10 Sports-related injuries, pedestrians hit by motor vehicles, and falls are common mechanisms of cervical spine injury in older children and adolescents; whereas violent injuries, including assault and gunshot wounds, occur in the late teenage years.6,7

ANATOMY AND PHYSIOLOGY

Although the development of the subaxial vertebrae is relatively consistent, the components of the craniocervical junction and upper cervical spine (occiput, atlas, and axis) have distinctive developmental patterns. Recognition of this is critical in differentiating fracture from normal developmental anatomy, as they may appear nearly identical radiographically.

The atlas (C1) has three primary ossification centers: one anterior arch and two neural arches. There are open cartilaginous synchondroses between the anterior arch and either neural arch as well as posteriorly between the two neural arches. By age of 3 years, the neural arches are typically fused to form the solid posterior ring of C1. The neurocentral synchondrosis fuses by age of 7 years.11 Four identifiable ossification centers are present in the developing axis (C2).11,12 The neural arches of C2 fuse posteriorly by age of 3 years. The body of C2 fuses with the neural arches and the dens between ages 3 and 6 years. However, the subdental synchondrosis may be seen until ages 10 to 11. Any lucency at the base of the dens beyond this age is abnormal and should be considered a fracture.13 Each vertebrae of the subaxial cervical spine (C3 to C7) follows the same developmental pattern. Three primary ossification centers occur at each level: a centrum for the body and two neural arches. In the subaxial spine, the neural arches fuse by age 3 years, whereas the body fuses with the neural arches by ages 3 to 6 years.11 Secondary ossification centers in the transverse and spinous processes are present by puberty and fuse completely by the third decade.11

A relatively large head size in comparison with the remainder of the body, immature neck and paraspinal musculature, underdeveloped ligaments, incompletely ossified bone, anterior wedging of vertebral bodies, absent uncinate processes, and shallow, horizontally oriented facets all contribute to hypermobility in the pediatric cervical spine.1418 As a result, the fulcrum of motion in the pediatric cervical spine is at C2 to C3, rendering the upper cervical spine more prone to injury. With maturation of the spine and supporting soft tissues, the fulcrum migrates to C5 to C6 by age 14 years, making the biomechanics of the cervical spine and the injuries sustained similar to those observed in adults.16,19

EVALUATION AND MANAGEMENT

All trauma evaluations begin with attention to the ABCs: airway, breathing, and circulation. Airway obstruction is common in the unconscious or severely injured child and should be treated rapidly. The unconscious child may be unable to cough or clear mucus, vomitus, blood, or other debris. Be cognizant of the potential for a cervical spine injury, which could be worsened by excessive motion of the spine (Fig. 24-1), and stabilize the cervical spine.

image

FIGURE 24-1. Algorithm for cervical spine clearance in blunt trauma injury.

The spine-injured patient may become hypopneic because of diminished diaphragmatic activity or intercostal muscle paralysis. Provide oxygen, assist ventilations. Although the bag-mask technique will permit ventilation, its prolonged use increases the likelihood of aspiration of gastric contents. Cervical spine immobilization with an orthotic device makes direct laryngoscopy three times more difficult compared with manual immobilization during intubation.20 Manual in-line cervical stabilization, rapid sequence induction, and oral endotracheal intubation are the preferred techniques to achieve airway stabilization in children with suspected cervical spine injury (Fig. 24-2). In children, blind nasotracheal intubation is unreliable because it can be technically difficult. The emergency physician must ensure an adequate airway and should not delay doing so while waiting for the cervical spine to be cleared.

image

FIGURE 24-2. In-line stabilization for endotracheal intubation: (A) above and (B) below.

Hypotension in the injured child may be secondary to either hypovolemia or spinal shock. A clue to differentiating these is the pulse, which is slow in spinal shock and rapid in hypovolemic shock. Adequate fluid (crystalloid, colloid, and blood) is administered to combat hypovolemia. In the case of spinal shock, vasopressors, such as dopamine, may be needed. The patient with spinal shock may be more sensitive to temperature variations than other patients and may require warming or cooling if subjected to extreme environmental temperatures either at the scene or during transport. Protect areas of the body that may have lost sensation from hard, protruding objects, as they may cause skin necrosis, especially on long transports.

Once the patient’s cardiopulmonary status is stabilized, a thorough physical assessment and neurologic examination is performed carefully. Sensation should be checked, both light touch and pressure. Evaluate for weakness by having the child handle an item or hold each extremity off of the stretcher for a count of 5 if the child is conscious and old enough to follow commands. More ingenuity is needed for the infant and toddler. A useful diagnostic mnemonic is to evaluate the “six P’s”: pain, position, paralysis, paresthesia, ptosis, and priapism. Conscious children old enough to talk may complain of pain localized to the involved vertebra. Head injury with diminished level of consciousness or intoxication may make the localization of cervical pain unreliable. The patient’s head and neck positioning may indicate a spine injury. A head tilt may be associated with a rotary subluxation of C1 on C2 or a high cervical injury. The prayer position (arms folded across the chest) may signify a fracture in the C4 to C6 area. Paresis or paralysis of the arms or legs should always suggest spine injury. Paresthesia, a “pins and needles” sensation or numbness or burning, may be related to peripheral nerve injury; however, these symptoms when occurring bilaterally can be taken as indicators of potential spine injury. Some patients complain of a transient shock-like or electrical sensation transmitted down the spine during neck flexion and/or rotation (Lhermitte’s sign). Horner’s syndrome (ptosis and a miotic pupil) suggests a cervical cord injury. Priapism is present only in approximately 3% to 5% of spine-injured patients, but indicates that the sympathetic nervous system is involved. Absence of the bulbocavernosus reflex in the presence of flaccid paralysis carries a grave prognosis. To elicit the bulbocavernosus reflex, a finger is inserted into the rectum, and then the glans of the penis or the head of the clitoris is squeezed. A normal response is a reflex contraction of the anal sphincter.

There are also characteristic cord syndromes (Table 24-1). In spinal shock, there is flaccid paralysis below the level of the lesion, absent reflexes, decreased sympathetic tone, and autonomic dysfunction. Sensation may be preserved, but if it is absent, the prognosis for recovery is poor. Central cord syndrome is often associated with extension injuries, which can cause circumferential pinching of the spinal cord by the ligamentum flavum. The anterior cord syndrome is associated with severe flexion injuries, especially teardrop fractures, in which a fragment of the fractured vertebral body is driven posteriorly into the anterior portion of the spinal cord.

TABLE 24-1

Syndromes Associated with Spinal Cord Injury

Image

Upper extremity position and function may provide clues not only to the presence of a cervical cord injury but also to the level of injury. With injuries at C5, patients can flex at the elbows, but are unable to extend them; with injuries at C6 to C7, they can flex and extend at the elbows; and injuries at the T1 level allow finger and wrist flexion.

During trauma evaluation, determine whether the child is at risk for cervical spine injury and warrants cervical spine immobilization and radiographic evaluation. Clinical criteria for “clearing” the cervical spine have been established in adults. The National Emergency X-ray Utilization Study (NEXUS) collaboration identified five clinical screening criteria (posterior midline cervical tenderness, altered alertness, distracting injury, intoxication, and focal neurologic findings), which have nearly 100% sensitivity for cervical spine injury and had good interrater agreement among emergency physicians.2124Alternatively, the Canadian C-spine Rule has been reported to have nearly 100% sensitivity for cervical spine injury in alert and stable adult trauma patients. The Canadian C-spine Rule was based on clinical, epidemiologic, and mechanism of injury variables.25,26 Neither of these studies focused on children. Recently, a large, multicentered study of 540 cervical-spine–injured children was completed and eight variables were identified that predicted who was at risk for cervical spine injury (Table 24-2).27 When one or more of these factors were present, the model was 98% sensitive and 26% specific for detection of cervical spine injury.27 Although this eight-variable model requires prospective refinement, the consistency of the model with smaller pediatric studies and large adult trials allows the clinician to utilize these findings until further evidence is developed.27

TABLE 24-2

Factors Associated with Cervical Spine Injury in Children

Image

All trauma victims should be unstrapped and removed from the rigid long board, which is used for extrication and patient transfers in the out-of-hospital setting. This aspect of “full spine immobilization” is known to be associated with adverse effects. Ventilation of trauma victims may be encumbered by full spinal immobilization. Studies in healthy adults and children who were fully immobilized demonstrated a mean reduction in forced vital capacity (FVC) to 80% of their unrestrained supine FVC.28,29 Full spinal immobilization has been reported to cause substantial pain, which may last well beyond the immediate period of immobilization.3034 Furthermore, pain caused by spinal immobilization may be confused with pain caused by injury leading to unnecessary diagnostic evaluations.30 In spine-injured patients, prolonged immobilization on a rigid long board is associated with an increased risk of developing pressure sores during the immediate postinjury period.35,36 The cervical collar can be discontinued once it has been determined either clinically or radiographically that the victim is free of cervical spine injury.

If a child may be at risk for cervical spine injury, take steps to maintain neutral cervical spine positioning. In this position, the cervical spine is in lordosis, and there is maximal spinal canal diameter. Achieving this position in children can be difficult. Studies evaluating spine positioning during immobilization indicate that patients, depending on habitus, are often immobilized in nonphysiologic positions. In children younger than 8 years, supine positioning without shoulder padding results in cervical kyphosis due to a relatively large head (Fig. 24-3).37,38 In adults, however, supine positioning causes relative cervical lordosis.39,40 The normal variation in the ratio of head to body among children results in a range of cervical spine positioning of up to 27-degree flexion or extension from neutral during immobilization for trauma transport.41 Thus, as a child grows, padding may be required in either the shoulder or occipital regions to provide neutral positioning.

image

FIGURE 24-3. Backboard modifications for children. A. Young child on a modified backboard that has a cutout to recess the occiput, obtaining a safe supine cervical positioning. B. Young child on a modified backboard that has a double-mattress pad to raise the chest, obtaining a safe supine cervical positioning.

Children attended to in the prehospital setting often arrive at the emergency department with immobilization of the cervical spine. Rigid collars are available for infants and children; however, the availability of these devices is limited in the prehospital setting. Cloth tape or straps across the forehead and external orthoses, including a rigid backboard, are usually employed to complete the immobilization. The decision regarding the type of orthosis needed depends on the age of the patient, the affected levels, and the restriction of movement needed (flexion, extension, rotation, etc.). Studies have demonstrated that the commonly available rigid cervical collars, such as Aspen, Miami J, and Philadelphia, all provide significant restriction in neck movement but have subtle variations and the final choice of cervical collar is often based on availability and the recommendations of a spine surgeon.42

Corticosteroid use in the management of confirmed spinal cord injury in children remains controversial. The investigators of the second National Acute Spinal Cord Injury Study reported that high-dose methylprednisolone (30 mg/kg) followed by 5.4 mg/kg/h for 23 hours, if given within 8 hours of acute spinal cord injury, improved the neurologic recovery as compared with placebo or naloxone.43,44Children younger than 13 years were excluded from the study. The putative mechanism of action is the ability of the steroid at these doses to inhibit oxygen free radical–induced lipid peroxidation. Lipid peroxidation is thought to mediate cell membrane degeneration and to explain other documented tissue-protective effects of steroids: support of energy metabolism, prevention of posttraumatic ischemia, reversal of intracellular calcium accumulation, prevention of neurofilament degradation, inhibition of vasoactive prostaglandin F2 and thromboxane generation, and retardation of axonal degeneration. Still, there are no clinical trials confirming the efficacy of this regimen in children, but it remains an acceptable option.45 Follow your local or regional trauma center recommendations.

ANALYSIS OF RADIOGRAPHS

The standard screening series for adults consists of three views: cross-table lateral view (CTLV), anteroposterior view (AP), and open-mouth view (OM). The OM view is used to visualize C1, C2, and the atlantoaxial and atlantooccipital articulations. Because the OM view is difficult to obtain in younger children, the value of requiring the OM view has been questioned. The Waters view can be substituted to allow visualization of the odontoid projected through the foramen magnum. The steps in evaluating the CTLV are presented in Table 24-3. On the AP view, symmetry of longitudinal alignment of vertebral bodies, facets, pillars, and spinous processes is assessed. Evidence of linear or compression fractures as well as more subtle indicators such as stepoffs, subluxations, and malalignments are sought. On the OM view, the alignment of the atlantooccipital and atlantoaxial joints, alignment of the margins of the lateral arches of C1 with C2, and the position of the odontoid between the lateral arches of C1 are evaluated. These bony structures are also examined for fractures.

TABLE 24-3

Criteria for Clearing the Lateral Spine

Image

In a large multicentered prospective observational study, the sensitivity for cervical spine injury of a three-view standard plain radiograph series was 89.4% (95% CI, 86.9%–91.4%).46 Within this cohort, the negative predictive value of normal screening films for any injury was 99.9% (95% CI, 99.9%–100.0%). The majority of missed patients had initial radiographs interpreted as nondiagnostic or inadequate (436 injuries in 237 patients) and further imaging was pursued.46 A large multicentered retrospective study of 206 cervical-spine–injured children showed that adequate cervical spine radiography was 90% (95% CI, 85%–94%) sensitive which is consistent with other smaller retrospective series of spine-injured children.47

Other imaging modalities are available when clinical suspicion of a cervical spine injury is high despite a negative screening series or when the standard views fail to delineate the cervical anatomy adequately, which is frequently the case in the patient with altered mental status. These options include the swimmer’s view to delineate the lower cervical spine, flexion and extension views, supine oblique views, thin-section tomography, computed tomography (CT), and magnetic resonance imaging (MRI). Some of these techniques, especially flexion and extension (stress) views, require positioning the head and neck out of neutral position and must be performed under careful medical supervision. One should not perform stress imaging of the cervical spine in patients who have altered mental status or who are otherwise incapable of clear communication about the effect of such manipulation. Flexion and extension views are indicated in neurologically intact children who have normal three-view screening films and complain of persistent midline, neck pain.48 In a child with altered mental status, inadequate or abnormal plain three-view series, or focal neurologic findings indicative of a cervical spine injury, thin-section CT scan should be obtained.49 MRI is the modality of choice for assessing the supportive soft tissues of the spine and the spinal cord itself. Therefore, MRI can evaluate the extent of injury and offer prognostic information in situations in which cord damage is present, including spinal cord injury without radiographic abnormality (SCIWORA). In addition, MRI can be used to complete cervical spine injury clearance in the hemodynamically stable child with persistent altered mental status.50,51 However, a recent large study suggested that in the presence of a normal CT in a comatose patient, MRI findings were ligamentous and soft tissue only and none of these injuries were unstable or required surgical intervention.52

INJURY PATTERNS

image ATLANTOOCCIPITAL DISLOCATION

Injuries involving the craniocervical junction are severe and frequently fatal (Fig. 24-4).53 High mortality rates associated with these injuries make estimation of true incidence difficult.54 Children are at increased risk for craniocervical injury, particularly atlantooccipital dislocation (AOD), because of biomechanics of the pediatric cervical spine. Reported data suggest that the incidence of this injury is more than double of that observed in adults (15% vs. 6%).55 Mechanisms which produce AOD include motor vehicle collisions or other high-impact trauma and results from excessive motion of the head relative to the upper cervical spine.56

image

FIGURE 24-4. Ten-year-old unrestrained passenger in a high-speed motor vehicle collision with respiratory arrest at the scene. A. The AP view shows a normal relationship between the lateral masses of C1 and C2. Superior to the lateral mass of C1, a lucency exists suggesting AOD. B. The lateral view shows the posterior dislocation of C1 relative to the occipital condyle (arrow). This illustrates the difficulty in detecting AOD on plain x-rays. The practioner should carefully examine all views paying, close attention to the craniocervical junction.

image ATLAS FRACTURE

Trauma with axial loading may result in a compressive force significant enough to cause a burst fracture of the atlas, otherwise known as a Jefferson fracture (Fig. 24-5). Neurologic injury is uncommon with Jefferson fractures because of the large canal diameter at this level and the propensity for burst fragments to project outward from the ring of C1.57 True Jefferson fractures have four separate fracture lines involving both the anterior and posterior aspects of the C1 ring bilaterally. “Jefferson fracture” is also loosely applied to two- or three-point fractures of the atlas. Atlas fractures are stable unless there are severe compressive forces causing a combined C1 to C2 fracture complex or disruption of the transverse ligament with concomitant instability.58 C1 injuries are initially evaluated with plain cervical spine x-rays. The atlanto-dens interval (ADI) noted on lateral C-spine x-rays may be as much as 5 mm in pediatric patients.59 ADI values in excess of 5 mm indicate transverse ligament disruption and resulting cervical instability (Fig. 24-6). The OM view is useful for assessing transverse ligament stability. According to the Rule of Spence, a lateral mass overhang of C1 over C2 greater than 6.9 mm indicates transverse ligament disruption.60

image

FIGURE 24-5. (A) Eleven-month-old infant (male) with an axial CT scan showing the normal anatomy of C1 with open synchondroses (three arrows) compared with (B) axial CT scan of C1 showing a Jefferson fracture in a 17-year-old suffered after landing on her head (four arrows).

image

FIGURE 24-6. A normal atlantodental interval is defined as the distance between the dens and anterior arch of C1. A lateral x-ray taken of a 4-year-old after a fall shows a normal ADI (arrow).

image ATLANTOAXIAL DISLOCATION

The atlantoaxial articulation provides significant rotation and to a lesser extent flexion–extension movement of the cervical spine.61 Although the atlantoaxial articulation is effective in providing cervical rotatory motion, its structural design predisposes it to a subset of traumatic injury patterns. High-energy mechanisms, such as motor vehicle–pedestrian collisions, may result in translational atlantoaxial subluxation (AAS).62 Estimation of the true incidence of traumatic AAS is difficult because it carries a high mortality rate.63 Some survivors will present with severe head injury, while others present with the complaint of neck pain or subtle signs of myelopathy or C2 sensory changes.62Traumatic AAS is most commonly characterized by anterior translation of C1 on C2 and rupture of the transverse ligament of the atlas.64 Severe hyperextension injuries with fracture of the anterior arch of C1 or the odontoid process define posterior AAS.

image ATLANTOAXIAL ROTATORY INJURY

Atlantoaxial rotatory subluxation (AARS) can follow head and neck surgery or in the setting of pharyngeal, upper respiratory tract or cervical infection (Grisel’s syndrome), and after any trauma.65,66 On physical examination, patients have a painful “Cock-Robin” torticollis characterized by chin rotation to the contralateral side and flexion of the neck. Patients with AARS are usually neurologically intact. A C2 radiculopathy or myelopathy are rarely present. Ligamentous laxity, inherent in the pediatric spine, predisposes children to rotatory subluxation of C1 on C2. In some cases, atlantoaxial rotatory fixation (AARF) can occur. In this situation, the neck remains locked in rotation. C1 to C2 facet dislocation and trapping of robust synovium in the articular surfaces may all contribute to AARF.67 Severe neck pain may also prevent reduction of this position. Evaluation and diagnosis of AARS/AARF involve CT scan in addition to plain C-spine x-rays. Often, the AP x-ray is suggestive of the injury, which is then confirmed with CT. If the diagnosis is in question (physiologic C1 to C2 rotation is often present and is due to noncompliance of the pediatric patient with positioning) or if AARF is suspected, dynamic CT scan may be performed (Fig. 24-7). With light sedation, the examiner can perform a CT scan in three positions: at rest, in neutral position, and rotated to the opposite side. This determines whether the AARS/AARF results from a true bony lock or from soft-tissue blockage of rotation.68 AARS/AARF frequently resolves when patients are managed in a rigid cervical collar and provided analgesia, thus dynamic CT should be reserved for those patients whose symptoms do not resolve after 1 to 2 weeks.

image

FIGURE 24-7. Seven-year-old presents after wrestling with no neurologic deficits and a Cock-Robin deformity. Axial computed tomography (A and B) shows rotation of C1 about the dens (arrow) with dislocation of the C1–2 joint resulting in anterior subluxation of C1 on C2 (dotted line).

image AXIS FRACTURES

In children <7 years of age, the weakest point in the C2 body–dens complex is the cartilaginous subdental epiphysis ensuring that odontoid fractures nearly always involve this region.69,70 Although uncommon, significant displacement of the fractured dens can result in neurologic deficit.57,71 Without displacement of the fracture, it may be difficult to distinguish injury from normal anatomy; however, anterior angulation of the dens is common and may aid in identifying epiphysiolysis (Fig. 24-8).70 These are thought to be caused by the combination of a relatively large head and an incompletely ossified synchondrosisof C2. The synchondrosis typically ossifies by age 7 years but can, rarely, remain open into adolescence. True fractures of the odontoid process are seen in older children and adolescents. The most common mechanism of injury is flexion with substantial force (e.g., motor vehicle collision). These fractures are classified by their location.72 Type I odontoid fractures involve the superior portion of the dens and are caused by avulsion of the alar ligament. Type I fractures are rare, but are most often discovered in the setting of unstable craniocervical junction injuries.73 Type II odontoid fractures involve the base of the neck of the dens and are considered unstable.74,75 Type III odontoid fractures extend into the body of C2 such that the fracture fragment incorporates the entire odontoid process and a portion of the body of C2 (Fig. 24-9).76 Bilateral pars interarticularis fractures of C2 or the “hangman’s fracture” result from hyperextension with axial loading. A critical distinction must be made between pathologic C2 to C3 subluxation and C2 to C3 pseudosubluxation—a common physiologic finding on pediatric C-spine x-rays (Fig. 24-10).

image

FIGURE 24-8. Sagittally (A) and coronally (B) reconstructed CT of the cervical spine from a 4-year-old after a fall showing a diastasis at the level of the synchondrosis of C2 (arrows).

image

FIGURE 24-9. Sagittally reformatted CT scan of a 17-year-old presenting with a type III odontoid fracture through the body of C2 (arrow).

image

FIGURE 24-10. Eight-year-old presents status postmotor vehicle accident with the diagnosis of pseudosubluxation. There is mild subluxation of C2–3; however, the spinolaminar line is well aligned (dotted line).

Os odontoideum is a term used to describe a bony fragment with smooth cortical margins located cranially to the body of the axis, independent from a small or hypoplastic dens (Fig. 24-11).77 It may appear to be an old, healed type I or type II dens fracture (Fig. 24-12). Historically thought to be a congenital anomaly related to nonunion of the dens to the C2 body, recent evidence favors fracture as the cause.7880Congenital ligamentous or bony dysplasias (e.g., Morquio’s syndrome and Down’s syndrome) and upper respiratory infections may also contribute to the development of os odontoideum.81 Clinical significance of os odontoideum is determined by flexion–extension x-rays, which are used to evaluate the stability of the cruciate ligaments.

image

FIGURE 24-11. A. A 17-year-old presents with progressive neck pain. Sagittally reformatted CT scan shows os odontoideum, which is subluxed with the arch of C1 relative to the body of C2 (arrow). B. A 14-year-old presents after a motor vehicle accident. This sagittally reformatted CT scan shows a normally aligned cervical spine with a normal atlantodental interval (arrow).

image

FIGURE 24-12. Sagittally reformatted CT scan of a 13-month-old presenting with a severely dysmorphic atlas. Bony corticated fragments anterior to C2 may represent old fracture of dens (arrow).

image SUBAXIAL CERVICAL SPINE INJURIES

The structure and biomechanics of the levels of the subaxial cervical spine (C3–C7) are similar, allowing for grouping of injuries. Prior to 8 years of age, injury in the region is uncommon.3,5 Mechanisms producing vertical axial loading (e.g., motor vehicle collisions, sports-related injuries, falls from height, and diving into shallow water) cause compression or burst fractures of the vertebral body.15,82Compression fractures are generally considered stable and usually heal without surgical intervention. Burst fractures, however, can be unstable and involve retropulsion of bony fragments into the spinal canal (Fig. 24-13).

image

FIGURE 24-13. Sagittally reconstructed CT scan of the cervical spine of a 15-year-old who suffered a C5 burst fracture while playing football. There is more than 50% loss of height and retropulsion of bony fragments into the spinal canal.

Flexion injury results in an avulsion fracture, which is identified by a small “teardrop” of bone observed at the anteroinferior margin of the vertebral body. A true teardrop fracture involves disruption of the facet joints, the anterior and posterior longitudinal ligaments, and the disk, and is thus considered unstable.83 Flexion–extension x-rays and MRI may reveal subluxation or ligamentous damage, allowing the clinician to distinguish between a simple avulsion and a true unstable teardrop fracture. Hyperflexion with or without distraction may result in facet dislocation. Hyperflexion with rotation can cause unilateral facet dislocation, whereas hyperflexion alone may result in bilateral facet injuries. Various terms used to describe facet dislocation of varying degrees include perched, jumped, sprung, or locked (Fig. 24-14).

image

FIGURE 24-14. A 15-year-old restrained passenger who suffered subluxation at C5–6. Lateral plain x-rays show a unilateral perched facet (arrow).

Flexion-distraction injuries can cause ligamentous disruption without fracture, potentially resulting in occult cervical instability with normal plain radiographic findings. Subluxation may be apparent on neutral lateral cervical spine x-rays; however, flexion–extension views can reveal movement that would have otherwise been missed on neutral films. Posterior ligamentous disruption may present with increased interspinous distance on lateral x-ray or sagittal CT scan reconstructions. Hyperflexion or direct impact to the spinous process produces avulsion of a subaxial spinous process, often C7, and is referred to as a “clay shoveler’s fracture.” Lateral mass, transverse process, or uncinate fractures occur with lateral hyperflexion. Alternatively, spinous process, laminar, and pedicle fractures are produced with hyperextension. Milder hyperextension followed by flexion is associated with classic “whiplash.”

There is one more important type of fracture that is seen only in the pediatric population. Separation of the vertebral body from the end plate through the epiphysis is termed a physeal fracture.84 Diagnosis is critical because certain subtypes of physeal fractures, specifically the Salter–Harris type I observed in young children, are unstable and require operative stabilization.84

image SPINAL CORD INJURY WITHOUT RADIOGRAPHIC ABNORMALITY

SCIWORA was originally used to describe traumatic myelopathy in individuals with no radiographic evidence of vertebral injury on plain x-rays (including flexion–extension views), myelogram, or CT scan. The reported incidence of SCIWORA ranges from 4% to 66% among all children with spinal cord injuries.69 Most patients experience transient symptoms at the time of injury, ranging from Lhermitte’s sign to paresthesias, weakness, or paralysis. Over time, the neurologic course is variable.69 Several studies suggest that the neurologic examination on initial presentation is predictive of long-term outcome in SCIWORA. Children with mild deficits at presentation regain full function; however, the more severely injured children tend to make a limited recovery.23 SCIWORA occurs because the inherent hypermobility of the pediatric spine allows for transient deformation of the spinal column without fracture or ligamentous disruption at the expense of the spinal cord.2 SCIWORA remains a diagnosis of exclusion, and clinicians must be vigilant to rule out persistent ligamentous incompetence that may place the patient at risk for further injury. With more widespread use of MRI in traumatically injured patients, the definition and epidemiology of SCIWORA continues to evolve.

REFERENCES

1. U.S. Department of Health and Human Services. Healthy people 2010. http//www.healthypeople.gov. Accessed March 11, 2009.

2. Center for Disease Control and Prevention, National Center for Injury Prevention and Control. Center for Disease Control Injury Research AgendaAtlanta, GA; 2002.

3. Mohseni S, Talving P, Branco PC, et al. Effect of age on cervical spine injury in pediatric population: a National Trauma Data Bank review. J Pediatr Surg. 2011;46:1771.

4. Viccellio P, Simon H, Pressman BD, et al. A prospective multicenter study of cervical spine injury in children. Pediatrics. 2001;108:e20.

5. Patel JC, Tepas DL III, Mollitt DL, et al. Pediatric cervical spine injuries: defining the disease. J Pediatr Surg. 2001;36:373.

6. Brown RL, Brunn MA, Garcia VF. Cervical spine injuries in children: a review of 103 patients treated consecutively at a level I pediatric trauma center. J Pediatr Surg. 2001;36:1107.

7. Cirak B, Ziegfeld S, Knight VM, et al. Spinal injuries in children. J Pediatr Surg. 2004;39:607.

8. Abroms IF, Bresnan MJ, Zuckerman JE, Fischer EG, Strand R. Cervical cord injuries secondary to hyperextension of the head in breech presentation. Obstet Gynecol. 1973;41:369.

9. Mills JF, Dargaville PA, Coleman LT, Rosenfeld JV, Ekert PG. Upper cervical spinal cord injury in neonates: the use of magnetic resonance imaging. J Pediatr. 2001;138:105.

10. Ghatan S, Ellenbogen RG. Pediatric spine and spinal cord injury after inflicted trauma. Neurosurg Clin North Am. 2002;13:227.

11. Pang D. Special problems of spinal stabilization in children. In: Cooper P, ed. Management of Posttraumatic Spinal Instability. Park Ridge, IL: American Association of Neurological Surgeons; 1990:181.

12. Ogden JA. Radiology of postnatal skeletal development-XI: the first cervical vertebra, XII: the second cervical vertebra. Skeletal Radio. 1984;12:12.

13. Harris JH Jr, Mirvis SE. The radiology of acute cervical spine trauma. In: Mitchell C, ed. The Normal Cervical Spine. 3rd ed. Baltimore, MD: Williams & Wilkins; 1996:1.

14. Koloska ER, Keller MS, Rallo MC, Weber TR. Characteristics of pediatric cervical spine injuries. J Pediatr Surg. 2001;36:100.

15. Roche C, Carty H. Spinal trauma in children. Pediatr Radiol. 2001;31:677.

16. McGrory BJ, Klassen RA, Chao EY, Staeheli JW, Weaver AL. Acute fractures and dislocations of the cervical spine in children and adolescents. J Bone Joint Surg Am. 1993;75:988.

17. Herman MJ, Pizzutillo PD. Cervical spine disorders in children. Orthop Clin North Am. 1999;30:457.

18. Pang D, Li V. Atlantoaxial rotatory fixation: 1. Biomechanics of normal rotation of the atlantoaxial joint in children. Neurosurgery. 2004;55:614.

19. Hadley MN, Bishop RC. Injuries of the craniocervical junction and upper cervical spine. In: Tindall GT, Cooper PR, Barrow DL, eds. The Practice of Neurosurgery. Baltimore, MD: Williams & Wilkins; 1996:1687.

20. Heath KJ. The effect on laryngoscopy of different cervical spine immobilization techniques. Anaesthesia. 1994;49:843.

21. Hoffman JR, Schriger DL, Mower W, Luo JS, Zucker M. Low-risk criteria for cervical-spine radiography in blunt trauma: a prospective study. Ann Emerg Med. 1992;21:1454.

22. Hoffman JR, Mower WR, Wolfson AB, Todd KH, Zucker MI. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. NEJM. 2000;343:94.

23. Touger M, Gennis P, Nathanson N, et al. Validity of a decision rule to reduce cervical spine radiography in elderly patients with blunt trauma. Ann Emerg Med. 2002;40(3):287.

24. Mahadevan S, Mower W, Hoffman JR, Peeples N, Goldberg W, Sonner R. Interrater reliability of cervical spine injury criteria in patients with blunt trauma. Ann Emerg Med. 1998;31(2):197.

25. Stiell IG, Wells GA, Vandemheen K, et al. The Canadian C-Spine Rule for radiography in alert and stable trauma patients. J Am Med Assoc. 2001;286:1841.

26. Stiell IG, Clement CM, McKnight RD, et al. The Canadian C-spine rule versus the NEXUS low-risk criteria in patients with trauma. NEJM. 2003;349:2510.

27. Leonard JC, Kuppermann N, Olsen C, et al. Factors associated with cervical spine injury in children after blunt trauma. Ann Emerg Med. 2011;58:145–155.

28. Schafermeyer RW, Ribbeck BM, Gaskins J, Thomason S, Harlan M, Attkisson A. Respiratory effects of spinal immobilization in children. Ann Emerg Med. 1991;20(9):1017.

29. Bauer D, Kowalski R. Effect of spinal immobilization devices on pulmonary function in the healthy nonsmoking man. Ann Emerg Med. 1988;17(9):915.

30. Leonard JC, Mao J, Jaffe DM. Potential adverse effects of spinal immobilization in children. Prehospital Emergency Care. 2012;16(4):513.

31. Chan D, Goldberg RM, Mason J, Chan L. Backboard versus mattress splint immobilization: a comparison of symptoms generated. J Emerg Med. 1996;14(3):293.

32. Chan D, Goldberg R, Tascone A, Harmon S, Chan L. The effect of spinal immobilization on healthy volunteers. Emerg Med Serv. 1994;23(1):48.

33. Cordell WH, Hollingsworth JC, Olinger ML, et al. Pain and tissue interface pressures during spine board immobilization. Ann Emerg Med. 1995;26:13.

34. Lerner EB, Billittier AJ, Moscati R. Effects of neutral positioning with and without padding on spinal immobilization. Prehosp Emerg Care. 1998;2:112.

35. Linares H, Mawson A, Suarez E, Biundo J. Association between pressure sores and immobilization in the immediate post-injury period. Orthopedics. 1987;10(4):571.

36. Mawson AR, Biundo JJ, Neville P, Linares HH, Winchester Y, Lopez A. Risk factors for early occurring pressure ulcers following spinal cord injury. Am J Phys Med Rehabil. 1988;67(3):123.

37. Herzenberg JE, Hensinger RN, Dedrick DK, Phillips WA. Emergency transport and positioning of young children who have an injury of the cervical spine. The standard backboard may be hazardous. J Bone Joint Surg. 1989;71A(1):15.

38. Nypaver M, Treloar D. Neutral cervical spine positioning in children. Ann Emerg Med. 1994;23(2):208.

39. Schriger DL, Larmon B, LeGassick T, Blinman T. Spinal immobilization on a flat backboard: does it result in neutral position of the cervical spine? Ann Emerg Med. 1991;20(8):878.

40. DeLorenzo RA, Olson JE, Boska M, et al. Optimal positioning for cervical immobilization. Ann Emerg Med. 1996;28(3):301.

41. Curran C, Dietrich AM, Bowman MJ, Ginn-Pease ME, King DR, Kosnik E. Pediatric cervical-spine immobilization: achieving neutral position? J Trauma. 1995;39(4):729.

42. Tescher AN, Rindflesch AB, Youdas JW. Range-of-motion restriction and craniofacial tissue interface pressure from four cervical collars. J Trauma. 2007;63:1120.

43. Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. N Engl J Med. 1990;322:1405.

44. Bracken MB, Shepard MJ, Holford TR, et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. JAMA. 1997;277:1597.

45. Bracken MB. Steroids for acute spinal cord injury. Cochrane Database Syst Rev 2012;1:CD001046.

46. Mower WR, Hoffman JR, Pollack CV, et al. Use of plain radiography to screen for cervical spine injuries. Ann Emerg Med. 2001;38(1):1.

47. Nigrovic LE, Rogers AJ, Adelgais KM, et al. Utility of plain radiographs in detecting traumatic injuries of the cervical spine in children. Pediatr Emerg Care. 2012;28(5):426.

48. Pollack CV Jr, Hendey GW, Martin DR, Hoffman JR, Mower MR. Use of flexion-extension radiographs of the cervical spine in blunt trauma. Ann Emerg Med. 2001;38(1):8.

49. Rozycki GS, Tremblay L, Feliciano DV, et al. Prospective comparison of admission CT scan and plain film of the upper cervical spine in trauma patients with altered LOC. J Trauma. 2001;51(4):663.

50. Flynn JM, Closkey RF, Soroosh M, Dormans JP. Role of magnetic imaging in the assessment of pediatric cervical spine injuries. J Pediatr Orthop. 2002;22(5):573.

51. Frank JB, Lim CK, Flynn JM, Dormans JP. The efficacy of magnetic resonance imaging in pediatric cervical spine clearance. Spine. 2002;27(11):1176.

52. Khanna P, Chau C, Dublin A, et al. The value of cervical magnetic resonance imaging in the evaluation of the obtunded or comatose patient with cervical spine trauma, no other abnormal neurological findings, and a normal cervical computed tomography. J Trauma Acute Care Surg. 2012;72(3):699.

53. Montane I, Eismont FJ, Green BA. Traumatic occipitoatlantal dislocation. Spine. 1991;16:112.

54. Menezes A. Management of occipito-cervical instability. In: Cooper P, ed. Management of Posttraumatic Spinal Instability. Park Ridge, IL: American Association of Neurologic Surgeons; 1990:65.

55. Bucholz RW, Burkhead WZ. The pathological anatomy of fatal atlan-to-occipital dislocations. J Bone Joint Surg Am. 1979;61:248.

56. Bucholz RW, Burkhead WZ, Graham W, Petty C. Occult cervical spine injuries in fatal traffic accidents. J Trauma. 1979;19:768.

57. Ogden J. Skeletal Injury in the Child. Philadelphia, PA: W.B. Saunders; 1990.

58. Hadley MN, Dickman CA, Browner CM, Sonntag VKH. Acute traumatic atlas fractures: management and long-term outcome. Neurosurgery. 1988;23:31.

59. Locke GR, Gardner JI, Van Epps EF. Atlas-dens interval (ADI) in children: a survey based on 200 normal cervical spines. Am J Roentgenol Radium Ther Nucl Med. 1966;97:135.

60. Spence KF Jr, Decker S, Sell KW. Bursting atlantal fracture associated with rupture of the transverse ligament. J Bone Joint Surg. 1970;52:543.

61. Phillips WA, Hensinger RN. The management of rotatory atlanto-axial subluxation in children. J Bone Joint Surg Am. 1989;71:664.

62. DeBeer JD, Thomas M, Walters J, Anderson P. Traumatic atlantoaxial subluxation. J Bone Joint Surg Br. 1988;70:652.

63. Adams VI. Atlantoaxial dislocation—a pathological study of 14 traffic fatalities. J Forensic Sci. 1992;37:565.

64. Fielding JW, Cochran GB, Lawsing JF, Hohl M. Tears of the transverse ligament of the atlas. J Bone Joint Surg Am. 1974;56:1683.

65. Fielding JW, Hawkins RJ, Hensinger RN, Francis WR. Atlanto-axial rotatory deformities. Orthop Clin North Am. 1978;9A:955.

66. Grisel P. Enucleation des atlas et torticollis nasopharyngien. Presse Med. 1930;38:50.

67. Kawabe N, Hirotani H, Tanaka O. Pathomechanism of atlantoaxial rotatory fixation. J Pediatr Orthop. 1989;9:569.

68. Cowan IA, Inglis GS. Atlanto-axial rotatory fixation: improved demonstration using spiral CT. Australas Radiol. 1996;40:119.

69. Roche C, Carty H. Spinal trauma in children. Pediatr Radiol. 2001;31:677.

70. Lebwohl NH, Eismont FJ. Cervical spine injuries in children. In: Weinstein S, ed. The Pediatric Spine: Principles and Practice. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001:553.

71. Sherk HH, Nicholson JT, Chung SMK. Fractures of the odontoid process in young children. J Bone Joint Surg Am. 1978;60:921.

72. Anderson LK, D’Alonzo RT. Fractures of the odontoid process of the axis. J Bone Joint Surg Am. 1974;56(8):1663.

73. Dickman CA, Hadley MN, Browner C, Sonntag VK. Neurosurgical management of acute atlas–axis combination fractures: a review of 25 cases. J Neurosurg. 1989;70:45.

74. Wang J, Vokshoor A, Kim S, Elton S, Kosnik E, Bartkowski H. Pediatric atlantoaxial instability: management with screw fixation. Pediatr Neurosurg. 1999;30:70.

75. Hadley MN, Browner CM, Liu SS, Sontag VK. New subtype of acute odontoid fractures (Type IIA). Neurosurgery. 1988;22:67.

76. Sonntag VK. Nonoperative management of cervical spine injuries. Clin Neurosurg. 1988;34:630.

77. Fielding JW, Hensinger RN, Hawkins RL. Os odontoideum. J Bone Joint Surg Am. 1980;62:376.

78. Wollin DG. The os odontoideum: separate odontoid process. J Bone Joint Surg Am. 1963;45:1459.

79. Dai L, Yuan W, Ni B, Jia L. Os odontoideum: etiology, diagnosis and management. Surg Neurol. 2000;53:106.

80. Ricciardi JEKH, Louis DS. Acquired os odontoideum following acute ligament injury. J Bone Joint Surg Am. 1976;58:410.

81. Menezes A. Os odontoideum: pathogenesis, dynamics and management. In: Marlin A, ed. Concepts in Pediatric Neuro-surgery. Basel, Switzerland: Karger; 1988.

82. Osenbach RK, Menezes AH. Pediatric spinal cord and vertebral column injury. Neurosurgery. 1992;30:385.

83. Harris JH Jr, Edeiken-Monroe B, Kopanik DR. A practical classification of acute cervical spine injuries. Orthop Clin North Am. 1986;17:15.

84. Lawson JP, Ogden JA, Bucholz RW, Hughes SA. Physeal injuries of the cervical spine. J Pediatr Orthop. 1987;7:428.