Vertebrae and Spinal Cord
Injuries to the spine are common in trauma patients. The morbidity associated with these injuries can be significant and life-changing, and some injuries can be life-threatening. Because polytrauma patients are initially seen in urgent circumstances, many fractures may be overlooked. In addition, the diversity of injury patterns and the potential for neurologic compromise make the evaluation and treatment of spinal trauma complex. Failure to recognize these injuries or to properly manage known injuries can have catastrophic consequences. In this chapter, the epidemiology of injuries to the spinal column, the anatomy, biomechanics, and physiology of the spine and spinal cord, the acute management and evaluation of trauma patients with suspected spinal injury, and the management of specific injuries and situations will be reviewed.
To date, the bulk of the literature on the epidemiology of spinal injury in North America has focused on patients sustaining spinal cord injury (SCI), while the epidemiology concerning patients with spinal column injuries without SCI has been less studied. There is currently only one population-based study that has been conducted on spinal column injuries.1 This 1996 study by Hu et al.1 reviewed spinal injuries within the Canadian province of Manitoba in the early 1980s. More recent studies that have attempted to define the epidemiology of spinal injury have relied on the review of patients with blunt trauma presenting to emergency rooms.2,3 While these are perhaps a less accurate reflection of the true incidence, they provide a useful estimation of the scope of the problem.
In the United States, the incidence of spinal fractures has been estimated to be greater than 50,000 injuries per year. Hu et al.1 reported an annual incidence rate of spinal fractures to be 64 per 100,000 in Manitoba. In the United States, with a population of just over 300 million, this would translate to over 192,000 injuries per year. In patients with blunt trauma, the reported incidence of spinal injury is between 3% and 4% in the cervical spine and approximately 6% in the thoracolumbar spine.2,3 Demographically, young men and elderly women are most commonly involved. Although the incidence of females sustaining spinal injury has increased in recent years, males continue to account for the majority of all patients with injury to the spine (52–70%). The most common mechanism of injury is motor vehicle crashes, followed by falls, acts of violence (gunshots, stab wounds), and sports. In certain urban regions, assaults and gunshot wounds (GSWs) may surpass falls as the principal mechanism of spinal injury (Fig. 23-1).
FIGURE 23-1 Causes of SCI since 2005. (Reproduced with permission from National Spinal Injury Statistical Center (NSCISC).)
Data regarding the epidemiology of SCI are much more robust as a result of the vast amount of time, effort, and research that has been undertaken to improve outcomes with these devastating injuries. The National Spinal Cord Injury Statistical Center (NSCISC), established at the University of Alabama in Birmingham, supervises and directs the collection, management, and analysis of data from a network of 16 federally sponsored regional centers for SCI throughout the United States. Over the past 30 years in North America, the incidence of SCI has remained relatively stable and is currently estimated to be approximately 40 cases per million population (excluding lethal cases).4,5 In the United States, this translates to over 12,000 new disabled patients each year. Currently, approximately 260,000 Americans live with an SCI. The average age at injury is 40.2 years and has been increasing over the past three decades as a result of the increasing proportion of elderly individuals affected. The mode age (i.e., the most common age at injury), however, has remained relatively consistent at 19 years. Males account for 80% of patients with SCI, blacks are at higher risk than whites, and the percentage of cases occurring among blacks has been increasing in recent years. Median hospitalization days in the acute setting has declined from 24 days from 1973 to 1979 to 12 days from 2005 to 2009.5
The etiologies of SCIs are not significantly different from the etiologies of injuries to the spinal column. Motor vehicle crashes are the most common cause of SCIs, comprising approximately 41% of all injuries with rollovers accounting for 70% of these.5 Ejections occurred in 39% of those injured, and only 25% reported using seatbelts. The next most common etiology is falls (27%), followed by violence (15%), sports/recreation (8%), and other causes (9%) (Fig. 23-1).
A complex interplay of social issues and advances in regulatory oversight have influenced trends in spinal injury. Improvements in emergency medical services systems, the development of safer automobiles, legislation requiring safety measures such as seatbelts, more occupational safety standards, and better regulation of contact sports have resulted in more individuals with SCI surviving the prehospitalization phase of injury and having better outcomes in survivors. As evidence of this, 38% of individuals with SCIs in 1970 died before hospitalization. In 2000, this figure had decreased to 15.8%.6
The proportion of injuries that are due to violent acts has varied over time as well, reflecting variation in national crime rates. Violent acts caused 13% of SCIs prior to 1980 and then peaked at 25% from 1990 to 1999 before declining to only 15% from 2005 to 2009.4,5 In Canada, violent acts are less common and caused only approximately 4% of all cases of SCI between 1997 and 2001.6
Falls are responsible for an increasing proportion of injuries due to the aging of the population and continue to be a major public health concern.7 Prevention and appropriate medical treatment of osteoporosis may help mitigate this trend. The assessment of comorbidities is integral to outcome following traumatic injury to the spine in these patients.
The implementation of injury prevention programs developed through an understanding of injury mechanisms in national injury tracking registries and other observational studies has caused a decrease in sport-related SCIs. Previously, diving accounted for a large majority of sport-related SCIs, but the incidence of dive-related injuries has steadily decreased as a result of prevention programs. The majority of these now occur in unsupervised recreational settings.4 American football still accounts for a significant number of catastrophic spinal injuries in the United States, but the incidence of these has also decreased as a result of rule changes banning spear tackling (tackling maneuver using the crown of the head to “spear” an opposing player).8 Extreme sports such as snowboarding and mountain biking now account for an increasing percentage of SCIs.
Incomplete quadriplegia is the most frequent neurologic category of SCI (38%), followed by complete paraplegia (23%), incomplete paraplegia (22%), and complete quadriplegia (17%). Over the past 15 years, the proportion of persons with incomplete paraplegia has increased with a concomitant decrease in the proportion of persons with complete paraplegia and quadriplegia. Improved survival after occipitocervical and upper cervical injuries as a result of improvements in EMS and direct medical care has likely contributed to an increase in ventilator-dependent discharges in the last 30 years (2.3–6.8%).4
The overall impact of an SCI on the individual patient, family, and society remains staggering. Few conditions aside from SCI result so abruptly in such a degree of permanent disability. The young and highly functional individuals that SCI so typically affects (recall the mode age of 19 years) face the severe challenge of reintegrating into society after injury. The patient has suffered a devastating transformation in quality of life and loss of independence, and the injury will have a profound impact on his or her lifestyle, personal goals, economic security, and interpersonal relationships. Data from the NSCISC have shown that only one third of persons with paraplegia and about one fourth of those with quadriplegia were employed at postinjury year 8.5 Among those who were married at the time of injury, as well as those who marry after injury, the likelihood of their marriage remaining intact is much lower when compared to the general population.5 Also, less than 5% of patients with SCI will marry following their injury.
In addition, the economic burden of all persons living with SCIs in the United States has been estimated to approach $10 billion per year.5 The lifetime costs for health care and living expenses vary depending on severity of injury and age at the time of injury. Estimates for these lifetime costs (in 2009 dollars) range from $750,000 for a 50-year-old patient with paraplegia to $3.3 million for a 25-year-old individual with high quadriplegia (C1–C4). Note that these are the direct costs and do not account for the indirect costs associated with lost wages and productivity.
ANATOMY AND BIOMECHANICS OF THE SPINAL COLUMN
The spine functions to allow spinal motion while protecting the enclosed neural elements from injury. The spinal column is composed of 7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 4–5 coccygeal vertebral segments and forms the foundation of the axial skeleton of the body, extending from the base of the skull to the pelvis with articulations to the rib cage. Each vertebra has an opening that contributes to the anatomy of the spinal central canal as well as multiple processes that serve as lever arms for the ligamentous and muscular attachments (e.g., spinous process, transverse process). The normal spine in the uninjured state positions the head directly over the pelvis in the coronal and sagittal planes (i.e., coronal and sagittal balance). In the coronal plane the spine is straight, while, in the sagittal plane, the cervical and lumbar spines are lordotic and the thoracic spine is kyphotic. These sagittal curvatures in conjunction with the intervertebral discs provide resiliency to applied loads.
The unique, highly specialized anatomy of the upper cervical spine allows weight transfer between the head and neck, facilitates neck motion, and protects the neurovascular elements from injury (Fig. 23-2). The occiput articulates with the atlas through paired synovial joints formed between the convex occipital condyles located at the lateral margins of the foramen magnum and the concave facets of the atlantal lateral masses. The occipitoatlantal articulation is responsible for 50% of the normal flexion–extension arc. The atlas itself is composed of two lateral masses connected by anterior and posterior arches that serve as attachment points for controlling and stabilizing ligamentous and muscular insertions. Grooves on the superior surface of the posterior arch accept the paired vertebral arteries after they pass through the paired transverse foramina. The odontoid process, or dens, extends rostrally from the body of the axis to articulate with the posterior aspect of the anterior arch of the atlas. Embryologically, the odontoid is the former centrum of the atlas that separates during gestation and fuses with the centrum of the axis. These three atlantoaxial synovial articulations allow rotational motion to occur and are responsible for 50% of the normal rotational range of motion (ROM). The spinous process of the axis is generally large and bifid due to the multiple insertions it accommodates.
FIGURE 23-2 (A) Midsagittal section of the upper cervical spine. Note the tectorial membrane as the cranial continuation of the posterior longitudinal ligament (PLL). (B) Posterior view of the cruciate ligament composed of a transverse atlantal ligament (TR) with superior and inferior longitudinal bands. The strong transverse atlantal ligament (TR) is important for preventing atlantoaxial subluxation. Note the apical (AP) and alar (AL) ligaments just anterior to the cruciate ligament. (C) Anterior view of the apical and alar ligamentous attachments. (Reproduced with permission from Jackson RS, Banit DM, Rhyne AL, Darden B V. Upper cervical spine injuries. J Am Acad Orthop Surg. 2002;10:271. Copyright 2002 by the American Academy of Orthopaedic Surgeons.)
The motion afforded to the upper cervical spine by this complex osseous anatomy requires stabilizing ligamentous restraints to prevent damage to the enclosed neural elements. This reliance on ligamentous structures for stability is important, and proper evaluation of the stability of the upper cervical spine requires an assessment of the integrity of these ligamentous structures (i.e., dynamic radiography, magnetic resonance imaging, etc.).
Multiple ligaments stabilize the upper cervical articulations, and these can be divided into intrinsic and extrinsic ligaments. The intrinsic ligaments, located within the spinal canal, are the most important contributors to stability of the upper cervical articulations. They form three layers anterior to the dura and include, from dorsal to ventral, the tectorial membrane, the cruciate ligament, and the odontoid ligaments. The tectorial membrane is the cranial continuation of the posterior longitudinal ligament connecting the posterior body of the axis with the anterior margin of the foramen magnum. The cruciate ligaments lie just ventral to the tectorial membrane where they stabilize the odontoid articulation with the anterior arch of the atlas. The transverse atlantal ligament (TAL) is the strongest component of the cruciate ligament. Injury to it can result in instability of the atlantoaxial articulation. The odontoid ligaments are the furthest ventral and include the apical and paired alar ligaments. The smaller and less structurally important apical ligament connects the tip of the odontoid process with the anterior margin of the foramen magnum. The much stronger paired alar ligaments connect the odontoid to the occipital condyles. Extrinsic stability is provided by the ligamentum nuchae, which extends from the external occipital protuberance to the posterior arch of the atlas and the tips of the cervical spinous processes as well as the paired occipitoatlantal and atlantoaxial joint capsules.
In the upper cervical spine, flexion is limited by the bony anatomy, while extension is limited by the tectorial membrane. Rotation and lateral bending are restricted by the contralateral alar ligaments. The cruciate ligaments restrict potentially dangerous anterior translation during flexion, while still allowing torsion around the dens. Distraction >2 mm is prevented by the tectorial membrane and alar ligaments. Translation is limited by the facet joints when the tectorial membrane and alar ligaments are intact. The apical ligament has a negligible effect on restricting motion between the occiput and C2.
The remaining vertebrae of the subaxial cervical spine (C3–C7) more closely resemble the vertebrae of the thoracic and lumbar spines (Fig. 23-3). Vertebral bodies are separated by intervertebral disks. The posterior elements are composed of paired pedicles, lateral masses, facet joints, laminae, transverse processes, and a single spinous process. The transverse process contains the transverse foramen, through which the vertebral artery (the first major branch of the subclavian artery) passes. The motion segments are stabilized by three structures as follows: (1) the anterior longitudinal ligament running on the ventral aspect of the vertebral bodies from the foramen magnum to the sacrum; (2) the posterior longitudinal ligament running on the dorsal aspect of the vertebral bodies from the foramen magnum to the sacrum (its cranial extent between C2 and the occiput is referred to as the tectorial membrane); (3) and the posterior ligamentous complex (PLC). The anatomical structures of the PLC include the supraspinous ligament, interspinous ligament, ligamentum flavum, and facet joint capsules (Fig. 23-4). The PLC plays a critical role in protecting the spine and spinal cord against excessive flexion, rotation, translation, and distraction. Some have likened it to a posterior tension band that restricts excessive motion. Once disrupted, the ligamentous structures demonstrate poor healing and the need for adjunctive surgical stabilization of the involved vertebrae to prevent progressive kyphotic collapse. The PLC plays an important role in spinal stability in the thoracic and lumbar spines, as well.
FIGURE 23-3 Cervical vertebrae. Front, back, side, and axial views.
FIGURE 23-4 Midsagittal section of the lumbar spine detailing the components of the posterior ligamentous complex (PLC). This important posterior tension band is composed of the facet capsules, ligamentum flavum, and the interspinous and supraspinous ligaments.
Thoracic vertebrae are similar in structure to the cervical, but they are larger, lack transverse foramina, and have larger transverse and spinous processes. There is much more inherent stability of the thoracic spine compared with the cervical and lumbar regions due to the stabilizing effects of the rib cage and sternum. The thoracolumbar junction is a transition zone between the relatively rigid thoracic spine and the more flexible lumbar segments.
The lumbar vertebrae are the most stout as they must carry more body weight than their cervical and thoracic counterparts (Fig. 23-5). An important stabilizing ligament is the iliolumbar ligament, between the L5 transverse process and the ilium, which can be injured with spinal or pelvic trauma. The sacrum forms the base of the spinal column and also functions as the keystone of the pelvic ring. There are no true intervertebral disks within the sacrum though occasionally a rudimentary disk may be noted in the presence of transitional lumbosacral anomalies. These anomalies are important to recognize because they affect the numbering of vertebrae. In these situations, numbering from the sacrum up may not match up with the numbering when counting down from the last thoracic rib. This can result in confusion between caregivers and has been shown to contribute to wrong-level surgery. The sacral nerve roots lie within intraosseous sacral foramina. The S1 and S2 nerve roots are larger and take up more room within their foramina in contrast to the S3 and S4 nerve roots and are more susceptible to injury.
FIGURE 23-5 Lumbar vertebrae. Front, back, side, and axial views.
ANATOMY AND PHYSIOLOGY OF THE SPINAL CORD
The spinal cord represents the caudal continuation of the brain and brainstem, extending from the brainstem at the level of the foramen magnum through the spinal canal to T12–L1 where it terminates as the conus medullaris. A collection of lumbosacral nerve roots continues from the conus medullaris forming the cauda equina. At each intervertebral space, the ventral and dorsal roots join to form a nerve root that exits the spinal canal through the neural foramen. The central nervous system is invested by three layers of meninges from superficial to deep including the dura, arachnoid, and pia mater. The spinal cord and intraspinous portions of the nerve roots are contained within dura mater, the thickest of the meningeal layers. Between the arachnoid and the pia mater lies the subarachnoid space. Cerebrospinal fluid within the subarachnoid space surrounds the spinal cord providing a mechanical buffer to injury (i.e., shock absorber) and also allows for homeostatic regulation of the distribution of neuroendocrine factors.
The neural elements within the spinal cord itself are arranged geographically. The long neural tracts extending to and from the brain are arranged peripherally and are composed primarily of white matter. The more central gray matter contains the cell bodies of the lower motor neurons.
The main descending motor pathway is the lateral corticospinal tract. The upper motor neuron originates in the contralateral cerebral cortex, decussates in the midbrain, and descends on the ipsilateral periphery of the spinal cord. The upper motor neuron then synapses with its corresponding lower motor neurons in the anterior horn of the gray matter. The lateral corticospinal tract has traditionally been thought to be arranged with the tracts subserving function of the upper extremity more centrally located and the tracts subserving function of the lower extremity and sacral roots more peripherally located. This has been proposed as the reason for the disproportionately greater motor impairment in upper compared to lower extremities in patients with central cord syndrome; however, whether this lamination truly exists is controversial.
The major ascending sensory pathways include the posterior column tracts (fasciculus gracilis, fasciculus cuneatus) and the more ventrally located lateral spinothalamic tracts. Sensory input from the periphery synapses at the neuronal cell bodies located in the dorsal root ganglion and then enters the posterior horn of the gray matter. Pain and temperature input cross immediately to the opposite side of the spinal cord and ascend in the contralateral lateral spinothalamic tract. Proprioception and vibratory sensation ascend ipsilaterally in the posterior column of the spinal cord and decussate at the level of the brainstem. Similar to the lateral corticospinal tract, the dorsal columns are arranged such that tracts subserving function of the upper extremity are more centrally located and tracts subserving function of the lower extremity and sacral roots are more peripheral.
The major vessels (i.e., aorta and vena cava) lie anterior to the thoracic and lumbar vertebral bodies. Segmental branches arising from the aorta and iliac arteries course around the lateral edge of the vertebral bodies where they enter the vertebral foramina to form the anterior and paired posterior spinal arteries, the main blood supply to the spinal cord (Fig. 23-6).
FIGURE 23-6 Blood supply of the spinal cord. (Reproduced, with permission, from Prasad P, Price RS, Kranick SM, Woo JH, Hurst RW, Galetta S. Clinical reasoning: a 59-year-old woman with acute paraplegia. Neurology. 2007;69:E41–E47.)
Location of SCI
The cervical region and thoracolumbar junction are the most frequent sites of injury in patients with SCI. Cervical spine injuries can occasionally be lethal, especially when the upper cervical cord is involved because it is critical for respiratory drive. Fracture–dislocations and subluxations of the cervical spine are most common at the level of the C5–C6 vertebrae. Thoracic fractures are less common than cervical, and most of these involve the vertebrae of the thoracolumbar junction (T10–12). These injuries are typically caused by crushing or extreme flexion of the spine in motor vehicle crashes or falls. Injuries involving the lumbar spine can damage the conus or the cauda equina depending on the level of injury.
Primary and Secondary Spinal Cord Injury
Primary SCI results from direct mechanical forces such as shear, laceration, distraction, and compression that cause structural disruption of neural and vascular structures with abrupt and indiscriminate cell death. Persistent pressure on the cord by space occupying bone, ligaments, or a disc can potentiate mechanical damage to the cord after the primary injury.
As a response to the initial mechanical insult, hemorrhage, edema, and ischemia rapidly follow, extending to contiguous areas of neural tissue. A subsequent biochemical cascade of events that involves a variety of complex chemical pathways leads to delayed or secondary cell death that evolves over a period of days to weeks. These “secondary injury” mechanisms result in the death of a population of neural cells that otherwise would have survived the initial insult. Thus, except for petechial hemorrhage, the human spinal cord may show no significant macroscopic or histopathologic changes until 6–24 hours after trauma.9 Although the exact mechanism of secondary spinal cord damage is not well understood, various functional hypotheses are proposed.
After the initial hemorrhage, inflammation proceeds in the central gray matter. On a systemic level, hypotension, either from hypovolemia or from autonomic dysfunction with neurogenic shock, contributes to impaired perfusion of the spinal cord and ischemia. Experimental studies in animal models of SCI have shown an increase in products of anoxic metabolism in neural tissue. Multiple other theoretical mechanisms could potentially contribute to the pathophysiology of secondary injury; however, a synergistic effect of several of these mechanisms is most likely responsible.
In the inflammatory theory, increased activity of cyclooxygenase and lipoxygenase results in accumulation of inflammatory mediators (i.e., prostaglandins, leukotrienes, platelet-activating factor, serotonin) that produce secondary neuronal damage.10 The effect of inflammatory mediators seems to be potentiated in anoxic conditions with diminished tissue perfusion.11 The neurotransmitter theory posits that increased levels of excitatory amino acid neurotransmitters such as glutamate and aspartate are released as a result of primary SCI and may cause secondary neuronal injury.12 Evidence to support this theory includes the experimentally induced neurologic dysfunction that occurs when the cord is exposed to excitatory amino acids, as well as the reduction in the extent of functional deficits with pretreatment using amino acid antagonists.13 The free-radical theory suggests that free radicals accumulate in the injured neural tissue and damage nucleic acids within the cell as well as lipids and proteins that comprise the cell membrane. Inability to maintain the integrity of the cell membrane results in neuronal death due to uncontrolled influx of ions and unbalanced osmotic pressure. The calcium ion theory implicates the influx of extracellular calcium ions into nerve cells as the cause of secondary injury since intracellular accumulation of calcium with efflux of potassium has been observed in experimental SCI.14 An excess of calcium ions activates phospholipases, proteases, and phosphatases that in turn lead to interruption of mitochondrial activity and disruption of the cell membrane. Initial neuronal swelling is related to sodium influx, whereas subsequent neuronal disintegration results from calcium influx. Both competitive and noncompetitive calcium channel blockers have been demonstrated experimentally to reduce secondary neurologic injury.15 Another theory postulates the involvement of endogenous opioids such as peptides, dynorphin, endorphin, and enkephalins, because time-dependent injuries can be related to dynorphin. Also, application of opiate antagonists such as naloxone has improved neurologic recovery in experimental models.15
All spinal cord lesions can be classified as neurologically complete or incomplete using the American Spinal Injury Association (ASIA) Scale16 (Fig. 23-7). This distinction is important prognostically since incomplete injuries have a chance at neurologic recovery, whereas motor recovery is achieved in only 3% of patients with complete injury during the first 24 hours and never after 24–48 hours.17,18
FIGURE 23-7 The ASIA classification of neurologic deficit following spine injury. (This form may be copied freely but should not be altered without permission from the American Spinal Injury Association.)
Patients with complete cord injury have no motor or sensory function caudal to the level of the injury. Although the ASIA classification requires a patient to have sacral sparing in order to be classified as incomplete, any sensory or motor function caudal to the level of injury is sufficient to designate a patient as incomplete because this signifies at least partial continuity of the long white-matter tracts (i.e., corticospinal and spinothalamic) from the cerebral cortex to the conus medullaris. During the initial evaluation of a patient with SCI, sacral root sparing may be the only neurologic function present to differentiate incomplete from complete SCI. Evaluation for sacral sparing consists of perianal sensation to light touch and pinprick, rectal tone, and voluntary contraction of the external anal sphincter. Spinal shock can complicate this assessment. It is a temporary state of spinal cord dysfunction associated with complete areflexia that usually resolves 24–48 hours after the time of injury. Until spinal shock has resolved, the completeness of the neurologic injury cannot be determined. Return of the bulbocavernosus reflex heralds the end of spinal shock. This clinical test assesses the integrity of the local S3–S4 reflex arc and is performed by squeezing the glans penis, placing pressure on the clitoris, or tugging on a Foley catheter while performing a rectal exam. An intact reflex will result in contraction of the anal sphincter. If there continues to be no distal sensory or motor recovery at the point the bulbocavernosus reflex has returned, the injury is designated as complete and no further significant neurologic improvement can be expected.
Anterior Cord Syndrome
This incomplete SCI results classically from vascular injury, resulting in anterior spinal artery insufficiency and ischemic injury to the anterior two thirds of the cord, but can also occur after blunt trauma to the anterior spinal cord (Fig. 23-8). Clinically, patients present with loss of motor function and pain and temperature sensation below the level of injury from involvement of the ventrally located lateral corticospinal and spinothalamic tracts. They do, however, retain proprioception and the ability to sense vibration and deep pressure from preservation of the posterior columns. Because ischemic neural tissue has a poor prognosis for recovery, the chance of meaningful clinical recovery in anterior cord syndromes is poor.
FIGURE 23-8 The most common patterns of incomplete spinal cord injury.
Central Cord Syndrome
Classically, central cord syndrome results from a hyperextension injury in an older patient with preexisting cervical spondylosis. It can, however, arise from a variety of different mechanisms. Clinically, the upper extremities are more involved than the lower extremities, due to the more central location of the upper extremity axons within the spinal cord tracts. Patients typically regain the ability to walk, but have more limited return of upper extremity function.
This incomplete cord syndrome can result from hemitransection of the spinal cord with unilateral damage to the corticospinal tract, spinothalamic tract, and dorsal columns. Patients present with loss of ipsilateral light touch sensation, proprioception, and motor function and contralateral loss of pain and temperature sensation. The prognosis is generally good.
Posterior Cord Syndrome
This syndrome is rare and results from involvement of the dorsal columns with subsequent loss of proprioception and vibration and preserved motor function. The prognosis is variable with many patients experiencing difficulty walking due to the deficit in proprioceptive sensation.
Cervical Root Syndrome
This represents an isolated nerve root injury that causes a deficit in sensation and motor function. This injury can be associated with an acute disc herniation or facet fracture, subluxation, or dislocation.
The conus medullaris is typically located at the level of the L1–L2 intervertebral space. Injury can produce mixed upper and lower motor neuron findings. Isolated injury to the conus may result in loss of bowel and bladder control (no sacral sparing), and the prognosis for recovery is poor.
Cauda Equina Syndrome
The cauda equina extends distal to the conus and is composed of the lumbar and sacral nerve roots. Injury results in lower motor neuron findings with sensory loss and motor dysfunction. Involvement of the lower sacral roots can result in bladder and bowel dysfunction. Urgent decompression (within 72 hours) optimizes outcomes, and the prognosis for motor recovery is moderate.
Advances in prehospital screening and transport have helped reduce the chance of missing a significant spinal injury.19 Field evaluation of patients with suspected spinal injury begins with the primary and secondary surveys as detailed by the American College of Surgeons Advanced Trauma Life Support (ATLS) course. The primary survey begins with evaluation of the airway, breathing, and circulation, followed by assessment of disability and exposure (ABCDE).
All patients are considered to have a spinal injury until proven otherwise. If lack of significant spinal injury cannot be ruled out at presentation, then immediate institution of spinal precautions is necessary. The cervical spine can be immobilized with a rigid cervical collar, but this is not a substitute for careful handling of the patient. With complete ligamentous disruption, the collar provides minimal stabilization. Manual stabilization of the spine is much more important and effective in restricting motion during patient transfers than any external orthosis.20 The thoracic and lumbar spines can be immobilized with a backboard at the time of injury. Recently, considerable attention has been directed toward the role of immobilization at the scene of injury since uniform application of spinal immobilization to all trauma patients may be unnecessary (e.g., patient with GSW to torso).21
If it becomes necessary to secure an airway, care is required during intubation to prevent hyperextension of the neck that might cause an iatrogenic injury to the cervical spine or spinal cord. Therefore, intubation should be performed with in-line cervical traction, a cervical collar in place, or fiber-optic assistance. Maintenance of oxygenation and hemodynamic stability with supplemental oxygen, blood pressure support, and early use of blood products may minimize the potential for secondary ischemic injury in patients with a suspected SCI. Patients who present with hypotension and shock usually have hypovolemia from hemorrhage and should be aggressively treated with fluid resuscitation and blood products. In patients with an injury to the spinal cord, however, hypotension may result from neurogenic shock, which is due to disruption of sympathetic output to the heart and peripheral vasculature. Neurogenic shock is distinguished by bradycardia, instead of tachycardia, in the presence of hypotension. These patients typically require the use of inotropic and chronotropic support to maintain adequate systolic blood pressures. Aggressive fluid resuscitation in patients with neurogenic shock risks fluid overload, pulmonary edema, and heart failure. The secondary survey consists of a thorough head to toe evaluation of the patient, and a complete neurologic exam should be obtained.
Details of the injury and the past medical history of the patient should be obtained from the patient, family members, and bystanders and relayed to the treating team. Knowledge of the mechanism of injury is important for the caregivers because associated injuries can then be predicted. Any transient neurologic symptoms noted after the traumatic event should be reported to the trauma team in the emergency department because such findings after trauma, even transient ones, suggest spinal instability. Disease states that may predispose patients to spinal injury should be asked about, as well. Included would be diseases that affect the structural integrity of the vertebrae (e.g., osteoporosis, metastatic disease), those that may be associated with instability (e.g., rheumatoid arthritis, trisomy 13, skeletal dysplasias), and those that result in a stiff spinal column (e.g., ankylosing spondylitis [AS], diffuse idiopathic skeletal hyperostosis [DISH], Klippel–Feil syndrome). Also, preexisting stenosis of the spinal canal may predispose to acute SCI.
Urgent transport to centers with the appropriate resources should follow initial stabilization in the field. Ideally, patients with SCI should be transferred directly to a facility experienced in the care of these patients (i.e., regional SCI center). If immediate transport is not possible, provisions should be made for early transfer once the patient is stabilized.
EVALUATION IN THE EMERGENCY ROOM
On arrival in the emergency room, the primary and secondary surveys are repeated. In obvious cases of cervical SCI, the need for ventilatory assistance should be determined in patients with paradoxical abdominal movement with respirations. A patient with an SCI above C5 and complete neurologic lesion is more likely to require intubation. As oxygenation and hemodynamic parameters are maintained, the patient should be examined for signs of injury and a repeat neurologic examination should be performed.
During inspection of the face and trunk, it is important to keep in mind that certain injuries can be associated with significant visceral and axial skeletal injuries. Facial trauma should alert the examining physician to the possibility of an injury to the cervical spine. An abrasion under the strap of a restraint can be associated with significant injuries to the cervical spine and cervicothoracic junction. Lap belt contusions should heighten suspicion for flexion–distraction injuries to the thoracolumbar spine. These can be associated with visceral injury, as well. Calcaneal fractures from significant decelerations (e.g., falls, motor vehicle crashes) are associated with fractures of the thoracolumbar and lumbar spines.
The unstable spine is at risk for injury from careless manipulation. Therefore, strict logrolling is the preferred method for evaluation of the back of the patient with a suspected spinal injury. The paraspinal soft tissues should be inspected for evidence of swelling, malalignment, or bruising. Systematic palpation of the spinous processes of the entire spinal column can help to identify and localize a spinal injury as significant gapping between processes can occur from flexion–distraction and fracture–dislocation mechanisms.
Following a systematic inspection, a complete neurologic examination that includes assessment of light touch and pinprick, graded motor examination, and reflexes is performed. In the appropriate settings, examination of sacral root function can be critically important though spinal shock can complicate this assessment. In patients with SCI, the ASIA Impariment Scale is useful for the characterization of residual function below the level of the SCI.
The goal of the secondary assessment is to identify and provide initial treatment of potentially unstable spinal fractures from both a mechanical and a neurologic basis. All clinical examinations of the spine should follow a consistent and repeated pattern. This pattern allows for comparison of neurologic status on a longitudinal basis, thus avoiding potential confusion about a progressive neurologic deficit.
Clinicians should have a low threshold for obtaining appropriate x-rays in the polytrauma patient because missed spinal injuries complicated by a progressive neurologic deficit most commonly result from insufficient imaging studies. Two factors associated with missed injuries in at least one study were traumatic brain injuries and AS.22
Plain x-rays are useful screening tools and are good for assessing overall alignment, though they have largely been replaced by computed tomographic (CT) imaging when evaluating the cervical spine. This is because a cervical CT is quicker to perform, more accurate, and cost-effective. The major difficulty with plain x-rays is obtaining technically adequate studies that are orthogonal and visualize the cervicothoracic junction. The lateral view of the cervical spine is still commonly obtained in the setting of an unstable polytrauma victim, however, because it can provide sufficient information to the surgical team to allow the patient to proceed to the operating room (Fig. 23-9). While plain radiographs of the thoracic and lumbar spines are useful for screening, it is difficult to obtain technically adequate films, especially in bedridden patients.
FIGURE 23-9 Analyzing a lateral cervical spine x-ray. The anterior vertebral line, posterior vertebral line, and the spinolaminar line should be smooth, collinear curves. An adequate study should visualize the entire cervical spine to the C7–T1 junction. The retropharyngeal soft tissue shadow can suggest the presence of injury when its thickness exceeds 6 mm at C2 and 2 cm (i.e., 20 mm) at C6 (“6 at 2 and 2 at 6”).
CT allows for better visualization of bony detail and is especially useful for visualizing the occipitocervical and cervicothoracic junctions. During preoperative planning, it can assist the surgeon in appreciating fracture planes and the degree of compromise of the spinal canal. Subtle translations evident on CT may suggest soft tissue disruptions that can be further evaluated with MRI. In cases with known spinal injury, it is a rapid means of screening for noncontiguous injury that can be present in 15–20% of patients.23 It bears repeating that, in patients with an identified spinal injury, an aggressive search for noncontiguous injury should be undertaken as this is a common cause for iatrogenic morbidity.
Magnetic resonance imaging allows for a detailed assessment of the soft tissues and is especially helpful for identifying pathology of the neural elements, intervertebral disks, and ligaments. It is not routinely used in the evaluation of the polytrauma patient because of the time required to perform a technically adequate scan. MRI is useful in the following patients: (1) when radiographic imaging is inconsistent with a patient’s neurologic presentation; (2) in the determination of ligamentous disruption when evaluating for spinal instability; and (3) prior to reduction maneuvers to exclude the presence of extruded intervertebral disks that could potentially be displaced dorsally into the thecal sac.
Patients with AS or other conditions that result in long fused spinal segments (e.g., DISH, extensive degenerative disease) deserve special mention in terms of their evaluation. These patients are particularly susceptible to fracture, even with low-energy mechanisms, because their spine functions as a long bone with no intervertebral motion to absorb energy. Patients with AS may present with relatively benign complaints. During their evaluation, careful attention should be paid to the position of their cervical spine. Because these patients typically have significant thoracic kyphosis, allowing their head to rest on the bed may result in excessive hyperextension, potentially through an unstable fracture (Fig. 23-10). Their head should be propped up so that the cervical spine assumes its normal configuration with the thorax. It is imperative that the entire spine is thoroughly imaged as noncontiguous injuries are common. Also, these patients have an increased incidence of epidural hematoma, so close serial neurologic examinations are mandatory.
Clearing the Cervical Spine
Historically, nearly one third of patients with injuries to the cervical spine had a delay in diagnosis or treatment due to inappropriate assessment.17 Of these patients with “missed injuries,” up to 5% may experience neurologic deterioration. Thus, early recognition of these injuries may prevent or limit neurologic compromise. While making sure injuries are not missed is essential, equally important is timely clearance in the absence of significant injury. This is because protracted evaluations may prolong immobilization, inhibit or restrict the thorough assessment of other organ systems, and complicate or delay recovery. Unfortunately, issues surrounding access and cost containment do not allow for the indiscriminant use of medical imaging on every trauma patient. For these reasons algorithms have been developed to identify patients who would benefit most from selected imaging studies. Within the context of these algorithms, imaging of the cervical spine in patients with minor trauma and in obtunded patients generates the most controversy. As noted above, CT of the cervical spine is the current imaging of choice.24,25
Anderson et al.26 have described a useful algorithm for clearance of the cervical spine whereby patients are classified into four groups as follows: asymptomatic, temporarily nonassessable secondary to distracting injuries or intoxication, symptomatic, and obtunded. Asymptomatic patients can be cleared on clinical grounds without imaging. Current ATLS recommendations advocate immediate removal of a cervical collar in the awake, alert, sober, and neurologically normal patient who has no tenderness to palpation in the cervical spine and who exhibits full, pain-free ROM. Two relevant algorithms include the NEXUS Low-Risk Criteria and the Canadian C-Spine Rules (Figs. 23-10 and 23-11), and the latter has better sensitivity and specificity.27 Temporarily nonassessable patients can be reassessed within 24–48 hours after return of mentation or following treatment of painful injuries. In urgent situations, the evaluation is the same as that of the obtunded patient. Symptomatic patients require advanced imaging studies including adequate cervical x-rays and CT. The clearance of obtunded patients is controversial and, unfortunately, no clear standard has emerged despite extensive recent research. These patients should be evaluated in an expeditious manner to minimize the restrictions and sequelae of continued immobilization. Some major trauma centers have started clearing the cervical spine in obtunded patients if there is a normal CT scan. Advocates of the use of CT as a single modality argue that MRI may detect additional abnormalities (20–30%), but most of these are false positives and require no further treatment.28,29 Another option is to obtain an MRI if the CT is normal. Studies in favor of the use of MRI after a normal CT point to the high incidence of new abnormalities and an occasional unstable injury detected.30,31 Currently, both options can be supported in the literature.
FIGURE 23-10 NEXUS Low-Risk Criteria for clearance of the cervical spine. (Reproduced with permission from 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 J Med. 2003;349:2510. Copyright © 2003 Massachusetts Medical Society. All rights reserved.)
FIGURE 23-11 Canadian Cervical Spine Rules for clearance of the cervical spine. (Reproduced with permission from Anderson PA, Gugala Z, Lindsey RW, et al. Clearing the cervical spine in the blunt trauma patient. J Am Acad Orthop Surg. 2010;18:149. © 2010 by the American Academy of Orthopaedic Surgeons.)
Prophylaxis against deep vein thrombosis (DVT) and venous thromboembolism (VTE) is an important consideration in patients with trauma to the spine. The incidence of VTE in trauma patients (with and without spinal trauma) varies from 0.36% to 30% within the literature.32,33 In patients with spinal trauma with no or a minimal neurologic deficit, studies suggest that the rate is low (0–2.1%).34 In contrast, one clinical study of patients with SCI using venography showed rates of DVT in the calf approaching 80% when no prophylaxis was used.35 Symptomatic VTE has been reported to occur in 4–10% of patients with SCI.36 Risk factors for DVT and VTE in trauma patients include the following: ventilator dependency >3 days, age >40 years, fracture in the lower extremity, major traumatic brain injury, venous injury, major surgical procedure, blood transfusion, and SCI.33 General patient risk factors include the following: older age, male patients, tobacco usage, diabetes mellitus, cancer, and obesity. Specific risk factors associated with spine surgery include the following: prolonged procedures, prone positioning, and anterior exposures to the lumbar spine (because of retraction of the great vessels).
All patients sustaining spinal trauma, especially those with an associated SCI, should have mechanical prophylaxis instituted as soon as possible with graduated compression stockings, sequential compression devices, or both. Pharmacologic prophylaxis (e.g., unfractionated heparin [UH] or low-molecular-weight heparin [LMWH]) is an additional consideration, but the benefit obtained in terms of reduction of DVT and VTE must be weighed against the risk of bleeding complications (e.g., spinal epidural hematoma). LMWH appears to be more effective for the prevention of DVT with fewer bleeding complications than UH.37