Chapter 43: Principles of Spine Trauma Care

Adewale O. Adeniran, Adam M. Pearson, Sohail K. Mirza

Chapter Outline

Introduction

Failure to properly diagnose or manage spine injuries can result in neurologic deficits that permanently impair a patient’s function and quality of life and in some cases, may lead to death. In addition, the legal context of working in emergency rooms makes the difficult work of evaluating trauma patients for a potential spine injury even more stressful for training and practicing physicians. Making this work a little less stressful is the goal of this chapter. 
Archeological records from more than 4,500 years ago are noted to forewarn that paralysis is incurable128 and this remains sadly true today. This fact does not mean that that nothing can be done for patients who sustain severe neurologic deficits. Patients with spinal cord injury today regain mobility, improve their quality of life, and achieve prolonged survival.19 Research at the cellular and genetic level continues to improve our understanding of the fundamental processes,206 and clinical research methods to study spinal cord injury in real patient populations have improved, renewing optimism for novel spinal cord injury treatments.259 This chapter focuses on general principles of spinal injury care. Subsequent chapters in this section discuss specific injury patterns in greater detail. 

Mechanisms of Vertebral Column Injury

Spinal Cord Injury Mechanisms

Terminology of Spinal Cord Injury

Terms used to describe spinal cord injury vary in meaning, depending on the context of the discussion.169 Although precise definitions for many of these terms are lacking, broad interpretations are nevertheless useful for conveying a general meaning when discussing related processes. 
Neural tissue injuries are divided into two broad etiology-based categories: primary injury refers to physical tissue disruption caused by mechanical forces and secondary injury refers to additional neural tissue damage resulting from the biologic response initiated by the physical tissue disruption. The extent of structural damage to neural tissue is indicated by other descriptive terms. Concussion refers to physiologic disruption without anatomic injury. Contusion refers to physical neural tissue disruption leading to hemorrhage and swelling (the most common type of spinal cord injury). Laceration refers to loss of structural continuity of the neural tissue (rare in blunt trauma). The clinical response to injury is typically described in temporal terms: acute refers to the first few hours after injury; subacute refers to several hours to days following injury, and chronic refers to intervals of weeks to months after the injury. The functional consequences of spinal cord injury are usually described by terms that refer to the severity and pattern of neurologic dysfunction. Complete spinal cord injury, incomplete injury, or transient spinal cord dysfunction describe different grades of severity of neurologic injury. Names for different types of spinal cord injury syndromes, such as anterior cord syndromes, central cord syndrome, and Brown-Séquard syndrome, refer to patterns of neurologic dysfunction observed during clinical evaluation.273 

Mechanics of Neural Injury

Structural failure of the spinal column may displace bone and ligament structures into the neural space, the spinal canal, and neural frame. These displaced and disrupted structures apply forces on the neural tissue that result in either functional or anatomic disruption.26 Most spinal cord injuries are crushing injuries resulting in acute neural tissue contusion from applied physical forces. Laceration or transection of the spinal cord is rare, even in markedly displaced fracture dislocations.142 
Experimental models of spinal cord injury have identified several characteristics of the injury force that determine the extent of neural tissue damage. These include the rate of force application, the degree of neural tissue compression, and the duration of neural tissue compression.141 The severity of neural tissue disruption is proportional to the energy absorbed from the injury mechanism.10 For direct impact on neural tissue, contact velocity and maximum cord compression are better predictors of injury severity than either force or acceleration. 
The viscoelastic properties of soft tissues provide the principal resistance to deformation in the early stages of impact during compression injures.26,268 Spinal cord tolerance for compression decreases as the velocity of compression increases (Fig. 43-1).141 Minimum compression of the cord at high-contact velocity may produce severe anatomic injury and limited functional recovery.141 At about 50% cord compression, functional recovery is minimal regardless of the contact velocity.141 Although this threshold effect denotes an upper limit of compression in the acute injury model, it is not apparent in the extremely slow onset of cord compression seen in chronic degenerative conditions, such as cervical spondylotic myelopathy. Cord compression that develops over years of progressive arthritic changes can be quite severe but manifests minimal clinical symptoms. 
Figure 43-1
Effect of rate and severity of cord compression on potential for neurologic recovery.
 
The threshold varies inversely with the magnitude of compression and the velocity of compression of the spinal cord.
The threshold varies inversely with the magnitude of compression and the velocity of compression of the spinal cord.
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Figure 43-1
Effect of rate and severity of cord compression on potential for neurologic recovery.
The threshold varies inversely with the magnitude of compression and the velocity of compression of the spinal cord.
The threshold varies inversely with the magnitude of compression and the velocity of compression of the spinal cord.
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The spinal cord can withstand considerable axial displacement without sustaining structural or neurologic deficit. Contrary to the relationship between nerve roots and neural foramina during physiologic movement, the spinal cord does not slide up and down in the spinal canal during spinal flexion and extension. Rather, the cord appears to deform like an accordion.213 Physiologic movements can stretch the cord an average of 10%, and maximum change can be as much as 18% of the longitudinal length of the spinal cord.213 Maximum stretching occurs between C2 and T1. Cord deformations may be more severe in patients with spondylosis and, in these patients, may contribute to cord injury even in the absence of vertebral column disruption. 
The size of the spinal canal may be an important determinant of the presence and severity of neurologic damage and cervical spine trauma.76,261 The preinjury spinal canal diameter, as measured on lateral radiographs or sagittal magnetic resonance images, and the cross-sectional spinal canal area are important in determining the severity of cord injury.168,261 A narrow spinal canal is associated with a greater likelihood of neurologic injury and a higher probability of complete cord injury. Cervical spondylosis, by decreasing the size of the spinal canal, further predisposes the patient to neurologic injury. 
The physical energy of the injuring mechanism causes immediate depolarization of axonal membranes in the neural tissue. This results in a functional neurologic deficit that exceeds the actual tissue disruption. This condition is referred to as “spinal shock.”139 Although the mechanism of spinal shock is not established, it may relate to immediate depolarization of the entire cord.70 The clinical examination more accurately reflects the neural injury when spinal shock resolves and uninjured neural tissues and neural structures repolarize. 
Blunt trauma to the spinal cord causes contusion of the neural tissue.209 As physical displacement of the spinal cord damages neural tissue, the innermost regions of the spinal cord sustain the most severe injury.43,210 In less severe injuries, this compressive force may lead to demyelination and an acute central cord syndrome. The primary neural injury also causes Wallerian degeneration in ascending dorsal columns and descending motor tracks, independent of any secondary injury or vascular insult. These changes may result in a gap at the injury site, which is largely devoid of neural parenchymal matrix. 
Neural tissue disruption causes hemorrhage through macerated tissue and broken blood vessels at the injury site (Table 43-1). Hematomyelia, hemorrhage within the cord parenchyma, further displaces cells and axons away from the primary injury point. Within the first few hours following injury, tissue breakdown leads to expansion of the zone of injury. The size of the neural injury zone is fairly well defined by 1 week after injury. 
 
Table 43-1
Physiologic Response to Spinal Cord Injury
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Table 43-1
Physiologic Response to Spinal Cord Injury
Time from Injury Biologic Changes at Spinal Cord Injury Site
First few minutes Hemorrhage in the central gray matter and anterior horns
Petechial hemorrhages
Distended postcapillary venules
Red blood cells in perivascular spaces
1 h Endothelial cell disruption
Separation of endothelial junctions
Vacuolation and swelling of endothelial cells
Craters in capillary endothelium
1–6 h Necrotic changes in gray matter
Cytoplasmic eosinophilia in gray matter neurons
Ghost cells
Shrunken neurons, loss of Nissl bodies, irregular shape
Eosinophilic changes in perikarya
Apoptosis
4–8 h Radial expansion of hemorrhage
Hemorrhage in lateral columns
Aneurysmal dilatation and rupture of arterioles
Microthrombi in capillaries
Granulated platelets
Necrotic changes in white matter
Granular appearance, swelling
Separation of axon from its myelin sheath
Accumulation of organelles in axons
Retraction bulbs
4 h to 1 wk Edema formation
Vasogenic edema
Filtration edema
6 h to 1 wk Inflammatory cell infiltration
Neutrophil infiltration
Monocyte infiltration
2 d to 2 wk Central nervous system reactivity
Activation of microglia
Increased number of processes (pseudopods)
Upregulation of surface antigens
Phagocytic vacuoles
1 wk to 4 wk Activation of astrocytes
Hypertrophy
Proliferation
Accumulation at margins of lesion
Apoptosis in white matter
After 2 wk Cavity and scar formation (gliosis)
Demyelination
Inflammatory angiogenesis
Formation of network of astrocyte processes
Wallerian degeneration
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As inflammation at the injury zone progresses, macrophages remove damaged tissue and form a fluid-filled cavity. This cavity can expand to fill the entire area of neural tissue disruption and form cysts at the injury site. This process reaches a steady state if the surface of the cord remains intact and the spinal cord membranes, the pia-arachnoid, and dura, do not form adhesions. This can result in stable, nonexpanding cysts that show cavitation with loose borders and no astrocyte boundary at the periphery. If the layers of the pia scar to the dura and the cysts develop a border of astrocytes, the process can lead to expansile cysts or syrinx formation. Scarring between the pia and the dura can also lead to an apparent expansion of the cord or progressive noncystic myelomalacia. These mechanisms may contribute to delayed neurologic worsening following spinal cord injury, and they also form the basis for treatments for late neural deterioration, such as duraplasty and untethering of the scarred spinal cord. 

Biologic Response in the Injured Spinal Cord

Biologic response to spinal cord injury has been studied in various in vivo and in vitro models that attempt to mimic the processes in human spinal cord injury. The variability in the experimental designs and differences across species of tested animals has led to varied characterizations of the injury response. An optimal experimental model of spinal cord injury has not been established. Experimental constraints in the injury models somewhat limit the generalizability of the findings to clinical conditions. 
The physiologic response to spinal cord injury is rapid and complex.231 The initial mechanical tissue disruption triggers a cascade of interrelated processes (see Table 43-1). Local tissue elements undergo structural and chemical changes that elicit systemic responses. Hemorrhage at the injury site occurs within minutes of the injury in the gray matter and radially expands to involve the white matter in lateral columns. Endothelial cell disruption increases fluid extravasation and local swelling in the neural tissue. Extensive neural cell death occurs within the first few hours of injury.231 
Reactive cellular changes in the gray matter are evident within the first hour of injury. White matter necrosis begins within 4 hours of injury. Neural tissue loss in spinal cord injury is not purely a result of physical forces and cytotoxic processes but also includes programmed cell death (apoptosis).158 Apoptosis depends on active protein synthesis and begins to occur as early as 4 hours after injury. Apoptosis peaks initially at 24 hours following injury and then reoccurs in a second peak at approximately 7 days following injury. 
Secondary axonal injury is a gradual process.207 Cytoskeletal protein disruption in the axon membranes causes separation of axons and necrosis ascending from the injury site (Wallerian degeneration).207 Axons die back at approximately 1 mm per month.222 Above the lesion, sterile end bulbs form at failed regeneration attempts in descending tracks. Below the lesion, abortive sprouting of dorsal root ganglion cells results in proliferation of Schwann cells (schwannosis).207 
Changes in local blood flow, tissue edema, metabolite concentrations, and concentrations of chemical mediators lead to propagation of interdependent reactions. This pathophysiologic response, referred to as secondary injury, can propagate tissue destruction and functional loss. Ischemia and inflammation are prominent mechanisms in the secondary responses.47,49 Ischemia also contributes to delayed secondary injury.85,257 Severity of neurologic injury is also proportional to the duration of spinal cord deformation.194 In the injury zone, a reversible injury may become irreversible from local ischemia and inflammation. Irreversible axonal injury can also lead to cell death, extending beyond the primary injury site.189 Inflammatory response consists of polymorphonuclear cell infiltration within 6 hours of injury and macrophage infiltration beginning at 24 hours following injury (Fig. 43-2). 
Figure 43-2
The inflammatory response begins within 4 hours of injury.
 
Neutrophil infiltration precedes macrophage accumulation.
Neutrophil infiltration precedes macrophage accumulation.
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Figure 43-2
The inflammatory response begins within 4 hours of injury.
Neutrophil infiltration precedes macrophage accumulation.
Neutrophil infiltration precedes macrophage accumulation.
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The mechanism of cellular injury differs between white matter and gray matter.212 In the gray matter, disruption of the electrolyte balance may lead to anoxic cell injury.251 Intercellular sodium and calcium influx are key events in the pathogenesis of hypoxic-ischemic injury to neurons.82,99 Influx of these ions disrupts mitochondria and uncouples oxidative phosphorylation.136 Some injury models have shown reversal of the normal sodium calcium exchange processes in anoxic cell injury.250 Incomplete conversion of oxygen to carbon dioxide in water results in free radical formation, lipid poor oxidation, and membrane breakdown.113,290 
Sodium and calcium exchange processes in injured neurons and axons have received a great deal of attention in spinal cord injury research. Sodium-calcium exchange mechanisms have been noted to operate in reverse following an acute injury.250 Agents that block sodium-calcium exchange, such as choline, ketamine, and mk-801, decrease neural swelling. Other agents that increase sodium-calcium exchange, such as glutamate, induce neuronal swelling. Disruption of the cell membranes contributes to neuron death, and agents that interfere with membrane peroxidation, such as methylprednisolone and 21-amino steroid tirilazad mesylate, may be useful in spinal cord injury by protecting cell membranes. 
Spinal cord axons also contain sodium and calcium exchange channels. Axonal injury leads to increased intracellular sodium.3 Reducing this sodium is neuroprotective, and increased intracellular sodium exacerbates traumatic axonal injury. Agents that inhibit sodium exchange, such as amiloride and harmaline, are neuroprotective.3 In contrast to neurons, reverse operation of the sodium-calcium exchange does not explain the effects of sodium in white matter injury. Axons in spinal cord white matter lack receptor-coupled and voltage-sensitive calcium channels.3 
The complex fundamental cellular processes initiated by spinal cord injury remain research tools for understanding cell physiology. At this time, this basic science research has not led to any clinical diagnostic or therapeutic interventions. 

Regeneration of Nerve Tissue

Most patients with spinal cord injuries show some neurologic recovery.81,270,274,276 It is not clear whether this recovery is related to resolution of the acute physiologic responses to injury or to active repair mechanisms in the nerve tissue. In animal experiments, ability to regain ambulation correlates with the amount of white matter remaining after the injury.21 The primary injury frequently spares a peripheral rim of white matter. Even a small number of intact axons traversing the injury zone, as few as 5% to 10% in small animal experiments, may be sufficient to support significant functional recovery.291 
This spontaneous regeneration capacity of the central nervous system is more limited than that of the peripheral nervous system.231 Fish and amphibians show successful regeneration of axons in the central nervous system. Higher vertebrates only show this capacity in the embryonic and perinatal periods.133 Adult mammals do retain some capacity for regeneration, and this process may be activated under controlled circumstances. 
Outside the injured spinal cord microenvironment, axons can invade and grow in peripheral nerves.60 Proteins that inhibit axonal growth limit regeneration in the spinal cord.231 Blocking these proteins enhances regeneration.35 
Research involving stem cell implantation relies on pluripotential cells to recreate the complex microenvironment necessary for neural regeneration.6,230,288 Although results in smaller animals and in primates are promising, this technology has not yet advanced to large-scale human trials.132,214 
At least three separate randomized controlled trials of varying levels of evidence took place between 1999 and 2008.9496 Monosialotetrahexosylganglioside GM-1 (Sygen; Sygen International PLC, Berkeley, CA) was given to 697 subjects, divided equally among one of two different drug dosages and a placebo group94,95 Despite an earlier phase 1 trial of 37 patients who suggested encouraging findings,96 this larger investigation failed to demonstrate significance in the predetermined primary efficacy analysis.94,95 All of those subjects received methylprednisolone according to National Acute Spinal Cord Injury Study (NASCIS) II protocol. In a placebo-controlled study examining the effectiveness of nimodipine, the latter was used in combination with methylprednisolone and compared with steroid alone and with placebo.202 No significant differences in sensory or motor recovery were observed 1 year postintervention. Finally, the autologous incubated macrophage trial (Proneuron Biotechnologies Inc., Los Angeles, CA) surgically implanted the patient’s own cells at the level of the spinal cord lesion, necessitating two surgical procedures in a 10- to 14-day window postinjury to accomplish the transplantation. All participants eligible for NASCIS protocol received steroid treatment. Although halted for financial reasons in 2006, preliminary analysis of the 50 subjects who completed the study has not suggested a significant benefit to the procedure.28,137,211 Cellular therapies remain unproven.28,81,150,245,263 

Mechanics of Cervical Spine Injury Fracture

Spine injury dynamics are complex and incompletely understood.188 Injury mechanisms do not have direct or exclusive relationships with injury patterns. Similar injury mechanisms can result in different clinical patterns of spine injury. In addition to the magnitudes and directions of injury forces, the orientation of the spine at the moment of injury and structural predispositions of the vertebral column influence the resulting injury. 
In cervical spine injuries involving direct head impact, the failure of the vertebral column precedes the occurrence of any measurable head motion (Fig. 43-3).187 For a given magnitude, direction, and locale of head impact, variations in the local vertebral alignment at the level of injury at the moment of impact change observed pattern of injury, with facet joint disruptions occurring when the injured vertebrae are in relative flexion and burst-type vertebral body fractures when the vertebrae are in a relatively neutral or extended position. Similar injury patterns of cervical spine fractures and fracture–dislocations can also occur in patients who do not sustain any direct head impact, such as restrained front-seat occupants of motor vehicle crashes.127 These observations explain a long-standing and fundamental problem of spinal injury classification systems based on presumed injury mechanisms: the same injury pattern may result in morphologically different injuries; similar morphologic patterns can be the result of different injury mechanisms, and the patterns of head deflection do not predict the spinal injury patterns. 
Figure 43-3
Timing of head and neck movement in impact injuries of the cervical spine.
 
Spinal column failure precedes head deflection in impact injuries.
Spinal column failure precedes head deflection in impact injuries.
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Figure 43-3
Timing of head and neck movement in impact injuries of the cervical spine.
Spinal column failure precedes head deflection in impact injuries.
Spinal column failure precedes head deflection in impact injuries.
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Another aspect of injuries that limits correlation between injury mechanisms and clinical manifestations is the role played by time during the injury process. Injuries are a series of dynamic events that take place over time, whereas clinical assessment takes place with the patient in a relatively static state with respect to forces and movements. Dynamic events occurring at the time of injury are not reflected in subsequent static anatomic assessments of injured tissues.281,282 For example, the degree of spinal occlusion that occurs during a burst-type fracture of the vertebral body greatly exceeds the amount of spinal canal occlusion seen on computed tomographic (CT) scans obtained after the injury event.50,262 Given this consideration, it is not surprising that radiographic measurements of spinal canal size in patients with cervical spine injuries show an increased likelihood of cord injury for patients with a narrow spinal canal. Poor correlation exists between the severity of spinal canal occlusion and the severity of neurologic deficit.76,78,265 
Time also influences injury severity and injury pattern by way of rate of force application. With faster rates of load application, the transient displacement of failed structural elements is greater, and associated neural space occlusion and spinal cord compression are greater.50 At high loading rates, bone fails first, as opposed to the ligaments or the intervertebral disc. At low loading rates and with rotational forces, the vertebral column fails through the soft tissues.221 
Injuries of the vertebral column tend to cluster at the junctional areas: the craniocervical junction (occiput-C2), the cervicothoracic junction (C7–T1), and the thoracolumbar junction (T11–L2). These areas represent regions of stress concentration, where a rigid segment of the spine meets a more flexible segment. Also contributing to stress concentration in these regions are changes at these levels in the movement constraints of vertebrae. These junctional areas are transition zones where the predominant pattern of movement between vertebrae changes from facet joint orientation allowing side-bending, flexion–extension, and rotation in the cervical spine, to allowing predominantly rotation in the thoracic spine, to permitting no rotation in the lumbar region. Cervical rotational facet injuries are accompanied by facet fractures and bilateral damage of the rotated vertebra.233 
Craniocervical injuries are common in fatalities associated with motor vehicle crashes, and most thoracic–lumbar injuries occur between T11 and L2.7 

Mechanics of Thoracic, Lumbar, and Sacral Fracture

In contrast to cervical fractures, thoracic and lumbar fractures are less likely to have associated neurologic injury. In part, this is because of a high incidence of low-energy thoracic fractures related to osteoporosis, which rarely cause cord injury. Since the spinal cord ends typically at the L1 level, the thecal sac caudal to this level contains only thin nerve roots and has much greater cerebrospinal fluid space than the thoracic or cervical regions. Only 3% of thoracic and lumbar vertebral body fractures are associated with a neurologic deficit.215 
The relationship of neurologic injury to the morphologic characteristics of the vertebral column injury pattern is inconsistent.281,282 In general, fracture–dislocations are associated with a neurologic injury in the majority of cases. Also, burst-type fracture patterns that manifest a neurologic injury demonstrate more severe vertebral column disruption with greater vertebral body collapse, more severe deformity, and greater spinal canal occlusion than burst-type injuries without neurologic involvement. In the lower lumbar vertebrae (L4 and L5), however, severe canal occlusions often have no associated neurologic injury. 
Some thoracic fractures with relatively little displacement of the injured structures may have a severe associated neurologic deficit. This clinical association is consistent with observations from biomechanic studies of injury mechanisms. A high-impact loading rate produces fractures with significant canal encroachment and a high potential for neurologic injury.262 A time interval of 400 ms from zero to peak load results in 7% spinal canal encroachment with fracture fragments.262 Decreasing this interval to 20 ms leads to 48% spinal canal encroachment.262 
Extension-type injuries in the thoracic and lumbar regions are rare in younger trauma patients.100 However, they are common in patients with ankylosing spondylitis or diffuse idiopathic spinal hyperostosis.87 
An injury pattern distinct to the lower thoracic and upper lumbar segments is a “lap belt” or “flexion–distraction” injury.98 In these injuries, the subject’s torso hinges across a lap belt, causing extreme flexion and distraction at a focal vertebral level. Lap belt injuries can cause bowel rupture or major vessel, liver, spleen, and urologic injury, noted in approximately 65% of patients with these injuries.98 In the absence of osteoporosis or neoplastic disease, spinal fracture requires high energy and external trauma. Although rare, forces generated during a tonic–clonic seizure can also result in axial skeletal trauma, including thoracic and lumbar burst fractures.292 Total fracture prevalence is 2.4% in patients with seizure disorders.292 
Sacral fractures are other biomechanic distinct injuries of the caudal spine. They are usually associated with pelvic disruptions or falls. A fall from a height usually results in a transverse sacral fracture.225 The particular sacral fracture pattern, such as vertical, transverse, or combinations such as “H-shaped” or “U-shaped” fracture patterns, is dependent on the sagittal plane position of the lumbar spine at the time of impact.225 

Associated Injuries

Awareness of the patient characteristics that are associated with injury patterns can guide prioritization and sequencing of interventions in the evaluation and management of individual trauma victims. This section presents the different prevalences of vertebral column and spinal cord injuries. 

Vertebral Column Injury

The most common injuries sustained by patients who have been involved in trauma are skeletal injuries and head injuries. The prevalence of skeletal injury is roughly equal to the prevalence of head injury and has been reported to be as high as 78% in multiple injured patients.216 Skeletal injury occurs four times as frequently as abdominal injury and twice as frequently as thoracic injury. 
Injury to the vertebral column occurs much less frequently than injuries to the appendicular skeleton. Vertebral column injuries are reported to occur in approximately 6% of trauma patients, with half of these patients (2.6%) sustaining spinal cord or nerve root–level neurologic injury.44 The vertebral injury can occur at multiple noncontiguous levels in 15% to 20% of the patents sustaining a spinal injury.264 Often, patients with multiple spinal injuries have an injury to the cranial–cervical junction in addition to an injury in the lower cervical, thoracic, or lumbar spine. Chest and abdominal injuries are commonly associated with fractures in the thoracic and lumbar regions. The incidence of concurrent abdominal injury in association with cervical fractures is low, approximately 2.6%.239 
Spinal cord injury rarely occurs in isolation. Of the patients sustaining tetraplegia or paraplegia, 80% have concurrent multiple-system injuries and 40% to 74% have an associated head injury.61,62,260 The presence of a spinal cord injury dramatically affects a patient’s chances of surviving the initial hospitalization and achieving permanent function and quality of life level subsequently. For patients with a spinal cord injury, the overall mortality during the initial hospitalization was 17% based on a study in the early 1980s.44 As of 2008, the National Spinal Cord Injury Statistical Center estimates mortality of traumatic spinal cord injury patients among 15 model systems of care to be 2.6%.12 However, this figure is likely a substantial underestimate because many centers are unable to attribute acute care deaths to spinal cord injury alone. With complete ascertainment, the number is closer to 5% to 10%.272 Improvements in acute care have been partially attributed to this modest improvement in survival following immediate injury.249 
A patient’s eventual function after trauma is determined more by the preservation of neurologic status than by other intermediate results of treatment, such as the quality of long bone and joint reduction in healing, the length of time in the intensive care unit or acute care facility, or by the social and demographic characteristics of the patient. Patients with a permanent residual neurologic deficit require lifelong social adjustments and supportive care. Incremental loss of neurologic function disproportionately increases disability.59,172 Because spinal cord injury primarily affects young individuals, the functional, medical, and social burden of illness of spinal cord injury is amplified in terms of loss of productive life years. 

Cervical Spine Fractures

The prevalence of cervical spine fracture in trauma victims depends on the demographics of the population served by a trauma center. In general, approximately 2% to 6% of trauma patients sustain a cervical spine fracture. Of those trauma patients sustaining a spinal injury, more than half of the spinal injuries involve the cervical region. Various characteristics of the patient and the injury mechanism influence the likelihood of an individual patient having a cervical spine fracture (Table 43-2).27 The highest risk occurs in patients who manifest a focal neurologic deficit (20%).27 Other characteristics associated with an increased risk are age greater than 50 years, an injury mechanism involving high energy, and the presence of a head injury. The same injury mechanism can impart widely different risk of injury to different patients. For example, the risk of a cervical spine fracture from a low-energy mechanism, such as fall from a standing height, in a person younger than 50 years is 0.04%.27 The same mechanism in a person older than 50 years carries a risk of cervical spine fracture of 0.5%, a risk estimate more than 10 times greater than the younger person.27,40 
 
Table 43-2
Risk of Cervical Spine Fracture in Trauma Patients
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Table 43-2
Risk of Cervical Spine Fracture in Trauma Patients
Risk Factor Odds Ratio
Focal neurologic deficit 34
Unconsciousness 14
Skull fracture 9.9
Brain/coma contusion 9.1
Intracranial hematoma 7.8
Loss of consciousness (transient) 5.4
Scalp laceration 5.1
High-speed motor vehicle crash 4.5
Pedestrians struck by a car 3.8
Mandible fracture 2.3
Facial fracture 2.1
Facial laceration 2.1
Intoxication 1.8
Motorcycle crash 1.4
Age 1.04
Fall 1.0
Male sex 1.0
Low-speed motor vehicle crash 0.84
Use of seat belts 0.42
Struck by a blunt object 0.09
 

Data from Blackmore CC, Emerson SS, Mann FA, et al. Cervical spine imaging in patients with trauma: determination of fracture risk to optimize use. Radiology. 1999;211(3):759–765; and Blackmore CC, Ramsey SD, Mann FA, et al. Cervical spine screening with CT in trauma patients: a cost-effectiveness analysis. Radiology. 1999;212(1):117–125.

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Thoracic and Lumbar Fractures

Most isolated thoracic and lumbar spine fractures are related to osteoporosis and involve minimal or no trauma. In fact, osteoporosis-related fractures far outnumber trauma-related thoracic and lumbar fractures. Osteoporosis leads to approximately 750,000 vertebral fractures each year in the United States.175 The annual rate of trauma-related thoracic and lumbar fractures is approximately 15,000.105 Thoracic and lumbar fractures account for 30% to 50% of all spinal injuries in trauma victims. In trauma patients, thoracic and lumbar fractures are concentrated at the thoracolumbar junction, with 60% of thoracic and lumbar fractures occurring between T11 and L2 vertebral levels.214 Although spinal cord injury is exceptionally rare with osteoporotic fractures, neurologic injury occurs in one-fourth of thoracic and lumbar fractures associated with trauma.215 Many of these patients (37%) also sustain concomitant injuries to other regions of the body. 

Spinal Cord Injury

Spinal cord injury occurs predominantly in young males.195,196 The gender ratio is 4:1 (males:females), but data in recent years indicate a growing percentage of females with spinal cord injury.134 The mean age is 39.5 years and the median age is 34 years. Within National Institute on Disability and Rehabilitation Research–funded Model Spinal Cord Injury Care Systems, the percentage of persons older than 60 years with spinal cord injury has increased from 4.7% in 1980 to 11.5% since 2000.12 
The incidence of traumatic spinal cord injury in the United States is estimated to be 525 to 1124 persons per million population.17,151 The incidence of a condition is determined by the size of the affected population and both the incidence rates and the survival rates associated with the condition. Despite changes in automotive technology, such as introduction of seat belts and air bags, and despite changes in laws regulating the use of these safety devices and other safety measures, such as highway speeds, the incidence of trauma-induced spinal cord injury has not changed much over the past 30 years. It is estimated to be between 29 and 50 cases per million persons per year, excluding spinal cord injuries that are fatal at the scene.44 Spinal cord injuries fatal at the scene are estimated to occur at a rate of approximately 20 cases per million persons per year. Each year, 12,000 patients are admitted to trauma centers for acute spinal cord injury.44 Approximately 200,000 persons with trauma-related tetraplegia or paraplegia currently live in the United States, and this population is expected to increase because of an growing number of older patients with spinal cord injury.151 
The most common cause of traumatic spinal cord injury is a motor vehicle crash, which accounts for 42% of all trauma-related cord injuries. Other common causes are falls (27.1%), gunshot injuries (15.3%), and sports injuries (7.4%).12,110,286 Older individuals are more likely to sustain a cord injury from a minor fall, such as a fall from standing height. Falls in persons older than 65 years are 2.8 times more likely to be associated with a spinal cord injury than similar falls in patients younger than 65 years.2 The increasing rates of falls are largely responsible for the shift toward incomplete tetraplegia as the most common neurologic category. 
The most common site of spinal cord injury is the cervical region, accounting for 50% to 64% of traumatic spinal cord injuries,256 with incomplete injuries outnumbering complete ones by nearly a 2:1 ratio.12 Neurologic injury is localized to the lumbar region (conus medullaris or cauda equina) in 20% to 24% of patients and to the thoracic cord in 17% to 19%.256 Approximately 41% of the patients with an acute spinal cord injury have a complete injury on initial evaluation, with no preservation of motor or sensory function in the sacral cord segments. Cervical injuries (tetraplegia) are more often incomplete neurologic deficits than complete, whereas thoracic injuries are more often complete. 
Children younger than 15 years account for 2% to 5% of acute spinal cord injury admissions, whereas up to 60% occur in patients aged 16 to 30 years.18,65,134,195,196 Patients with an immature skeleton can sustain a spinal cord injury without overtly disrupting the structural components of the vertebral column. This type of a cord injury, labeled as spinal cord injury without radiographic abnormality in the publications preceding the use of magnetic resonance imaging, may occur in nearly half of very young spinal cord injury patients (42% of patients younger than 9 years).69 It is present much less frequently in patients with mature skeletons (8% of patients aged 15 to 17 years).69 A majority of the younger patients (70%) with spinal cord injury without radiographic abnormality had an incomplete spinal cord injury.69 
Spinal cord injury without structural disruption of the vertebral column can also occur in older patients who have a narrow spinal canal, either a congenitally narrow spinal canal (spinal canal diameter <80% of the midbody vertebral body diameter) or a pathologically narrow canal from osteophytes and degenerative changes.223 These patients also typically have an incomplete cord injury, usually of a central cord injury pattern. 

Cost of Spinal Cord Injury

Spinal cord injury is an expensive problem from every aspect of cost measurement. Although it is the most difficult cost to measure quantitatively, the greatest cost to society of spinal cord injury is the loss of many years of quality of life in the young population of patients who sustain these injuries, especially since improvements in rehabilitation have resulted in nearly normal life expectancy for many young individuals with a spinal cord injury. The lifetime direct medical cost of spinal cord injury is estimated to be from $680,000 to $3 million for persons injured at 25 years of age and $500,000 for persons experiencing a spinal cord injury at 50 years of age.12 In the United States, the aggregate annual direct medical cost of traumatic spinal cord injury is estimated at $7.74 billion.64 Although high-level tetraplegia (upper cervical segments) represents only 10% of spinal cord injury patients, it accounts for 80% of the direct medical cost of spinal cord injury.64 Paraplegia accounts for 4% of the overall aggregate cost, and incomplete injuries account for approximately 15% of the costs.64 

Initial Assessment and Care

Initial evaluation and management of patients with a spinal injury can be complex, but priorities of Advanced Trauma Life Support still apply.8 Critical decisions are necessary at each step as more information about the patient becomes available. Each subsequent event in the patient’s triage is influenced by the findings of the initial evaluation, both for management of the spinal injury and for management of other potential injuries. 
As a general rule, all trauma patients need to be fully investigated for spinal injury. Even mild complaints of pain or posterior midline tenderness in trauma patients should not be dismissed without full evaluation, including imaging studies. Unclear findings on imaging studies should be assumed to reflect acute injury until further evaluation clarifies their significance. Persistent symptoms despite normal initial imaging studies may require further evaluation with dynamic imaging studies such as upright radiographs or flexion–extension radiographs. Unresolved findings from the patient’s history, physical examination, and imaging studies should be clearly and efficiently communicated to all providers involved in the patient’s care. 

Field Care

All trauma patients are at risk for spinal injury. Field management of trauma victims requires keeping the possibility of an unstable spinal injury in the forefront of active concerns until spinal injury is definitively excluded or treated. Treatment priorities are preserving life, limb, and function. The spine must be protected as these priorities are addressed sequentially. 
Proper extrication of the patient and immobilization of the cervical spine at the accident scene are critical to avoid further neurologic injury.201 The head and the neck need to be aligned with the long axis of the trunk and immobilized in this position.17 Emergency medical technicians are challenged by rescue attempts that entail removal of patients from tight spaces or vertical drops. In such situations, the Kendrick Extrication Device has proven to be an effective means of spinal immobilization.283 It can also be used in pediatric patients needing accommodation for a large occiput while maintaining neutral spine positioning.165 Immobilization with cervical collar, sandbags, tape, and spine board is superior to immobilization with a collar alone.23 For field transportation of injured patients, logrolling still allows motion at the spinal injury site, and a scoop-stretcher is a useful adjunct to the spine board.171 Cervical extension should be avoided because it narrows the spinal canal more than flexion.53 Neutral flexion–extension head and neck alignment is optimal during prehospital transport of cervical spine injury patients.201 To maintain neutral head–neck alignment, the relatively larger head of pediatric patients should be accommodated by elevating the trunk on padding or using a special pediatric spine board containing a cutout for the occiput.14 For injured athletes, motorcycle riders, and cyclists, helmet and shoulder gear should be left in position until personnel trained in safe removal techniques are available.15,71,93,176 
Preliminary assessment of neurologic status in the field helps prioritize subsequent treatment interventions in the emergency room. Observations of the patient’s spontaneous physical movements and function should be recorded in field records and conveyed to subsequent caregivers. These observations are extremely valuable in determining the possible presence and sometimes the general extent of neurologic injury. Eliciting subjective symptoms in alert and communicative patients and specifically asking about neck pain, back pain, numbness, and weakness helps identify and localize spinal injury. 
When a spinal cord injury is suspected, steroids should be started in the field. The steroid dosage and administration schedule was established by three publications of results from three phases of the NASCIS I, II, and III (Table 43-3).3133 
Table 43-3
Summary of National Acute Spinal Cord Injury Study I, II, and III Protocols
Methylprednisolone bolus 30 mg/kg, then infusion 5.4 mg/kg/h
Infusion for 24 h if bolus given within 3 h of injury
Infusion for 48 h if bolus given within 3–8 h after injury
No benefit if methylprednisolone started >8 h after injury
No benefit with naloxone
No benefit with tirilazad
 

Data from Bracken MB, Collins WF, Freeman DF, et al. Efficacy of methylprednisolone in acute spinal cord injury. JAMA. 1984;251(1):45–52; Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med. 1990;322(20): 1405–1411; and 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. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA. 1997;277(20):1597–1604.

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Pharmacologic Intervention

The complexity of interdependent secondary events following spinal cord injury makes it difficult to determine the optimal interruption point for preserving neurologic function.231 The secondary responses to spinal injury are both reparative and contributory to additional injury. Interrupting the cascade of events has the potential to change either aspect of the physiologic response. Experimental treatments have investigated agents that block specific pathophysiologic events occurring after the injury. Only a few of these treatment interventions have shown sufficient promise in laboratory studies to prompt clinical trials (Table 43-4).3133,96,199,200,205 
Table 43-4
Randomized Clinical Trials of Pharmacologic Treatment of Spinal Cord Injury
Year Author Number of Patients Treatment Groups Clinical Neurologic Improvement Functional Improvement
1984 Bracken et al31
(NASCIS I)
306 High-dose methylprednisolone
Low-dose methylprednisolone
No Not measured
1990 Bracken et al32
(NASCIS II)
487 Methylprednisolone
Naloxone
Placebo
Yes Not measured
1991 Geisler et al96 34 Ganglioside GM1
Placebo
Yes Not measured
1995 Pitts et al200 20 Thyrotropin-releasing hormone
Placebo
No Not measured
1997 Bracken et al33
(NASCIS III)
499 Methylprednisolone for 24 h
Methylprednisolone for 48 h
Methylprednisolone and Tirilazad
Yes No (Functional Independence Measure)
1998 Petitjean et al199 166 Nimodipine (calcium channel blocking agent)
Methylprednisolone
Both
No Not measured
1998 Potter et al205 26 Fampridine SR (potassium channel blocking agent)
Placebo
Yes No (Functional Independence Measure)
2001 Geisler et al95 687 Monosialotetrahexosylganglioside GM-1 sodium salt (Sygen) No significance in predefined primary analysis at 26 wk; subgroups showed benefit in selected groups No for primary analysis, yes for selected subgroups (Benzel Scale)
2005 Knoller 8 Incubated autologous macrophages Yes, ASIA grade improvement Not performed
2009 Lammertse 50 Incubated autologous macrophages ASIA grade, analysis pending Analysis pending
 

ASIA, American Spinal Injury Association; NASCIS, National Acute Spinal Cord Injury Study.

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Methylprednisolone shows a protective dose-response curve against neurologic injury in animal experiments.34 High doses are required. Most benefit occurs in the first 8 hours; additional effect occurs within the first 24 hours.112 Three large-scale randomized clinical trials have investigated methylprednisolone in the treatment of spinal cord injury.3133 The first trial compared low-dose to high-dose methylprednisolone administered within 48 hours of injury.31 The results showed no difference in outcome and increased infection rate in the high-dose group. The second trial compared methylprednisolone (30 mg/kg loading dose + 5.4 mg/kg/h for 23 h) with naloxone and placebo.32 Statistically significant improvement in motor and sensory scores in both complete and incomplete injuries occurred in the group given methylprednisolone. The magnitude of effect was small: neurologic change score (improvement in motor score) was 16.0 in the treatment group and 11.2 in the control group, with a P value of 0.03 for the difference. Pinprick score change was 11.4 in the treatment group and 6.6 in the control group (P = 0.02).32 These differences reached statistical significance because of the large sample size of the study but they may have little or no clinical significance. Statistically significant advantage of 3 to 7 points in motor score may have limited functional benefit (see section “Controversies” later in this chapter). A crucial assessment missing from clinical trials of spinal cord injury is measurement of clinically meaningful functional changes. NASCIS trials demonstrate that large-scale, high-quality randomized clinical trials are methodologically feasible, even when addressing difficult problems such as the emergent management of spinal cord injury. This achievement is significant for future work in this area. 
Other pharmacologic treatments have not shown sufficient promise in the clinical trial stage to become established interventions.96,199,200 Lazaroids are one category of candidate drugs. Lazaroids are 21-aminosteroid–free radical scavengers.9 One such agent, 21-aminosteroid U7-4006F, inhibits membrane peroxidation. Another category of potential drugs for spinal cord injury treatment is gangliosides. Gangliosides are large glycolipid molecules found on the outer surface of most cell membranes.96 They are highly concentrated in neural tissues and are involved in immunologic processes, binding, transport, and nerve cytogenesis. Gangliosides have a trophic effect on nerve cells. They can stimulate dendritic outgrowth and neuronal recovery. Further research is needed to understand their application to spinal cord injury treatment. 

Emergency Room Care

Severely injured patients require continuous or serial monitoring to diagnose conditions not readily apparent early in their clinical course. Spinal evaluation is concurrent with resuscitative measures. Spine evaluation within the first few minutes of arrival in the emergency room includes 
  1.  
    assessment of gross neurologic function by reports from field personnel, direct observation, or initial gross examination during primary survey;
  2.  
    diagnosis of severely unstable injuries such as fracture–dislocations or distractive injuries on trauma radiographs that include a lateral cervical spine radiograph and an anteroposterior (AP) chest radiograph; and
  3.  
    assessment of hemodynamic parameters for potential neurogenic shock.
Spinal cord injury can complicate resuscitation.8 Loss of vasoconstrictive sympathetic control of the peripheral vasculature can accentuate the hemodynamic effects of hemorrhage. Nonetheless, recognizing neurogenic shock as distinct from hemorrhagic shock is critical for safe initial resuscitation of a trauma patient (Table 43-5).8,155 Treatment of neurogenic shock is pharmacologic intervention (typically dopamine) to augment peripheral vascular tone. It may be essential for effective resuscitation. Fluid overload from excessive fluid volume administration, typical in treatment of hemorrhagic shock, can result in pulmonary edema in the setting of neurogenic shock. For this reason, clinical practice guidelines have advised the use of vasopressors, rather than large volumes of intravenous fluid, to maintain mean arterial pressure.108 Because of these complicated fluid dynamics, these patients often merit invasive monitors such as central lines or Swan–Ganz catheters to accurately assess fluid status. In a prospective trial that examined aggressive blood pressure management in postinjury days 3 to 7, findings suggest favorable neurologic recovery in patients whose main arterial pressure is maintained above 85 mm Hg.266 
 
Table 43-5
Comparison of Neurogenic and Hypovolemic Shock
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Table 43-5
Comparison of Neurogenic and Hypovolemic Shock
Neurogenic Shock Hypovolemic Shock
Etiology Loss of sympathetic outflow Loss of circulating blood volume
Blood pressure Hypotension Hypotension
Heart rate Bradycardia Tachycardia
Skin temperature Warm extremities Cold extremities
Urine output Normal Low
 

Data from Piepmeier JM, Lehmann KB, Lane JG. Cardiovascular instability following acute cervical spinal cord trauma. Cent Nerv Syst Trauma. 1985;2:153–160; Zipnick RI, Scalea TM, Trooskin SZ, et al. Hemodynamic responses to penetrating spinal cord injuries. J Trauma. 1993;35:578–582; and Ducker TB, Salcman M, Perot PL Jr, et al. Experimental spinal cord trauma, I: correlation of blood flow, tissue oxygen and neurologic status in the dog. Surg Neurol. 1978;10:60–63.

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Spinal cord injury itself increases the risk of multiple organ system failure in polytrauma patients.16 Presence of severe hemodynamic parameter abnormalities in the initial phases of resuscitation is associated with a poor prognosis for neurologic recovery.155 Normal hemodynamics, on the contrary, do not predict neurologic recovery. 
Although all patients are observed for spontaneous activity during resuscitation, complete spine examination and neurologic assessment follows resuscitation. The spine assessment begins with a review of the reports from the field. The sequence of evaluation and intervention steps differs in unresponsive patients from awake and cooperative patients. Assessment of acute symptoms is critical in evaluation of awake patients. Neurologic examination should be performed concurrently with resuscitation and hemodynamic stabilization of the patient. Perineal reflex assessment and rectal examination are essential components of the physical examination in every trauma patient (Tables 43-6 and 43-7). 
 
Table 43-6
Spinal Cord and Conus Medullaris Reflex Pathways
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Table 43-6
Spinal Cord and Conus Medullaris Reflex Pathways
Reflex Location of Lesion Stimulus Normal Response Abnormal Response
Babinski Upper motor neuron Stroking the plantar aspect of foot proximal lateral to distal medial Toes plantarflex Toes extend and splay
Oppenheim Upper motor neuron Rubbing the tibial crest proximal to distal Toes plantarflex Toes extend and splay
Cremasteric T12–L1 Stroking the medial thigh proximal to distal Upward motion of the scrotum No motion of the scrotum
Anal wink S2–S4 Stroking skin around anus Anal sphincter contracts No anal sphincter contraction
Bulbocavernosus S3–S4 Squeezing the penis in males, applying pressure to clitoris in females, or tugging the bladder catheter in either Anal sphincter contracts No anal sphincter contraction
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Table 43-7
Assessments During Rectal Examination in a Trauma Patient
Neurologic function
 Touch
 Pinprick
 Spontaneous tone
 Maximal voluntary contraction
 Deep pressure sensation
Severity of pelvic trauma
 Gross hemorrhage
 Occult hemorrhage
 High riding prostate
 Rectal tear
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Awake and cooperative patients require a complete neurologic examination. The American Spinal Injury Association (ASIA) has identified essential minimal elements of neurologic assessment recommended for all patients with a spinal injury (Fig. 43-4).13,138,169,183 The essential elements of neurologic function are strength assessment of five specific muscles in each limb and pinprick discrimination assessment at 28 specific sensory locations on each side of the body. On each side of the body, five muscles representing the segments of the cervical cord and five muscles representing segments of the lumbar cord are scored on a 5-point muscle grading scale (Fig. 43-4). The sum of all 20 muscles yields a total motor score for each patient, with a maximum possible score of 100 points for patients with no weakness. For the 28 sensory dermatomes on each side of the body, sensory levels are scored on a 0- to 2-point scale. A patient with normal sensation would be assigned a maximum possible light touch score of 112 points and a similar pinprick score of 112 points. The findings of sensory testing of the sacral segments distinguish complete from incomplete spinal cord injury. The sensory examination and motor strength testing allow designation of sensory and motor levels for each side of the body and of the overall neurologic level.138,169,183 
Figure 43-4
Neurologic examination recommended by ASIA.
 
ASIA, American Spinal Injury Association.
ASIA, American Spinal Injury Association.
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Figure 43-4
Neurologic examination recommended by ASIA.
ASIA, American Spinal Injury Association.
ASIA, American Spinal Injury Association.
View Original | Slide (.ppt)
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The spine examination includes inspection of the spine and palpation of the spine. The patient must be rolled on his or her side using a logrolling maneuver. The patient’s head and neck are supported by one assistant and the patient’s trunk is supported by two to three other assistants. The head and trunk are then rolled by the assistants in unison while the examiner inspects and palpates the spine to check for hemorrhage, abrasion, laceration, malalignment, or palpable gap in the spinous processes. The chest and abdomen are also examined for contusions or abrasions suggestive of a seat belt– or steering wheel–induced injury. 
The elements of neurologic examination selected as minimum necessary assessment by ASIA were chosen because of their reproducibility.13,138,169,183 They constitute a minimal data set desirable in all spinal injury patients for accurate communication, particularly for clinical research study populations. Clinical management, however, requires neurologic assessment extending beyond essential examination elements recommended by ASIA. In fact, the examination elements considered optional by ASIA are often necessary components for actual patient care. Assessment of lower extremity and perineal reflexes is important in determining the severity of neurologic involvement. These elements are considered optional in the ASIA standards because they do not meet sufficient reproducibility standards to allow categorization of spinal cord injury patients for objective comparisons. Although categorization of injury severity is essential to allow comparisons, guide treatment, and determine prognosis, neurologic deficits span a continuous spectrum of severity and may not always fit into clean, distinct categories (Table 43-8). 
 
Table 43-8
Impairment Scale Categories
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Table 43-8
Impairment Scale Categories
A Complete No motor or sensory function in the lowest sacral segment (S4–S5)
B Incomplete Sensory function below neurologic level and in S4–S5, no motor function below neurologic level
C Incomplete Motor function is preserved below neurologic level and more than half of the key muscle groups below neurologic level have a muscle grade lower than 3
D Incomplete Motor function is preserved below neurologic level and at least half of the key muscle groups below neurologic level have a muscle grade of at least 3
E Normal Sensory and motor function is normal
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Categorization of a specific patient into a specific division of a classification requires some arbitration and judgment. The variability in these judgments sometimes makes comparisons across different research studies difficult. Older spinal cord injury literature contains variable interpretations of many commonly used terms but the modern literature provides greater clarity (Table 43-9). These specific definitions will hopefully improve categorization of spinal cord injury patients in scientific communication and allow more meaningful analyses of collective experience. 
 
Table 43-9
Definitions of Terms Describing Spinal Cord Injury
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Table 43-9
Definitions of Terms Describing Spinal Cord Injury
Impairment Loss of motor and sensory function
Disability Loss in daily life functioning
Tetraplegia Loss of motor and/or sensory function in the cervical segments
Paraplegia Loss of motor and/or sensory function in the thoracic, lumbar, or sacral segments
Dermatome Area of skin innervated by sensory axons within each segmental nerve
Myotome Collection of muscle fibers by the motor axons within each segmental nerve
Neurologic level The most caudal segment with normal sensory and motor function on both sides
Sensory level The most caudal segment with normal sensory function on both sides
Motor level The most caudal segment with normal motor function on both sides
Skeletal level Radiographic level of greatest vertebral damage
Sensory score Numerical summary value of sensory impairment
Motor score Numerical summary value of motor impairment
Incomplete injury Partial preservation of sensory and/or motor function below the neurologic level and sensory and/or motor preservation of the lowest sacral segment
Complete injury Absence of sensory and motor function in the lowest sacral segment
Zone of partial preservation Dermatomes and myotomes caudal to the neurologic level that remain partially innervated
Only used in complete injuries.
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Neurological injury level is the most common caudal segment of the spinal cord with normal motor and sensory function on both sides: right and left sensation, right and left motor function (Table 43-8).119,169,183 Complete injury is defined by the absence of sensory and motor function in the lowest sacral segment.13,18,119,138,276 Sacral sensation refers to sensation at the anal mucocutaneous junction and deep anal sensation. Sacral motor function is voluntary anal sphincter contraction on digital examination. Incomplete injuries have partial preservation of sensory or motor function in the lowest sacral segment. For a patient to be classified as sensory incomplete, he or she must demonstrate either sensory preservation (light touch, pinprick, or both) in the S4–S5 dermatome or deep anal sensation. To be considered motor incomplete, a patient must demonstrate either voluntary anal sphincter contraction or a combination of sacral sensory sparing and presence of lower extremity motor function more than three levels below the designated motor level of injury (Table 43-10). Details of the examination grading are described in Fig. 43-4
 
Table 43-10
Descriptions of Incomplete Spinal Cord Injury Patterns
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Table 43-10
Descriptions of Incomplete Spinal Cord Injury Patterns
Syndrome Lesion Clinical Presentation
Bell cruciate paralysis Long-tract injury at the level of decussation in brain stem Variable cranial nerve involvement, greater upper extremity weakness than lower, greater proximal weakness than distal
Anterior cord Anterior gray matter, descending corticospinal motor tract, and spinothalamic tract injury with preservation of dorsal columns Variable motor and pain and temperature sensory loss with preservation of proprioception and deep pressure sensation
Central cord Incomplete cervical white matter injury Sacral sparing and greater weakness in the upper limbs than in the lower limbs
Brown-Sequard Injury to one lateral half of cord and preservation of contralateral half Ipsilateral motor and proprioception loss and contralateral pain and temperature sensory loss
Conus medullaris Injury to the sacral cord (conus) and lumbar nerve roots within the spinal canal Areflexic bladder, bowel, and lower limbs. May have preserved bulbocavernosus and micturition reflexes
Cauda equina Injury to the lumbosacral nerve roots within the spinal canal Areflexic bladder, bowel, and lower limbs
Root injury Avulsion or compression injury to single or multiple nerve roots (brachial plexus avulsion) Dermatomal sensory loss, myotomal motor loss, and absent deep tendon reflexes
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Distal motor function and sacral sparing are important for prognosis.242 Sacral sensory sparing predicts improvement in neurologic status.145 Sacral pinprick sensation at 4 weeks postinjury carries an improved prognosis of regaining the ability to walk even in patients who are initially motor complete.58,192 In addition, pinprick preservation in more than 50% of the lower extremity dermatomes L2–S1 in the first 72 hours of injury is associated with improved prognosis for ambulation.192 
Neurologic assessment in unresponsive patients includes a review of observations recorded in the field and during transport by emergency medical system personnel. The neurologic assessment must be systematically reevaluated and updated over time in unresponsive patients until a complete examination is possible. 
Radiographic studies are the primary modalities for identifying a spine injury in unresponsive patients. Spine injury precautions are maintained in effect until a spine injury is identified and treated or until assessment is complete and injury excluded. If imaging studies identify a spinal column injury, the treating spine surgeon makes a decision regarding the urgency of assessing the integrity of neurologic structures. In an unresponsive patient, the options for this assessment are serial neurologic examinations, magnetic resonance imaging (MRI) to identify structural neural tissue disruption, and sensory or motor evoked potentials to assess function in neural pathways.8890 Several reports suggest that presence of intramedullary hemorrhage at the time of initial spinal cord injury is indicative of a poor prognosis,228,229,232 with many subjects remaining complete89 or at least motor complete.164 Although the degree of bone or soft tissue injury did not correlate with injury severity, rostral extent of edema and total length of cord edema did have prognostic value.29,89 One report found that a hemorrhage longer than 4 mm suggested poor neurologic recovery, but smaller ones were not as ominous for prognosis.29 Miyanji et al.180 recently demonstrated that degree of spinal cord compression had greater predictive value than the amount of canal compromise. 
Although somatosensory evoked potentials may help differentiate sensory complete from incomplete in the nonresponsive patient126 or in children,183 findings may not translate to motor function, given the location of assessment at the dorsal columns. 
“Spinal shock” is a term that accounts for much confusion in the assessment of spinal cord injury patients.70 Spinal shock refers to depressed spinal reflexes caudal to spinal cord injury. First, spinal shock should be distinguished from neurogenic shock, which refers to hypotension associated with loss of peripheral vascular resistance in spinal cord injury. Second, the etiology and significance of spinal shock are unclear.70 The confusion surrounding the concept of spinal shock is responsible for some complacency in the management of spinal cord injury patients during the initial few hours following injury, the time interval in which intervention may have the most beneficial results. Spinal shock may involve immediate depolarization of the axonal membranes from kinetic energy of the injury. Spinal shock disrupts all cord function distal to injury, including reflexes. Although many effects of spinal shock, such as return of deep tendon reflexes, may take weeks or even months, early effects of spinal shock typically resolve within 24 hours of injury.139 The difficulty for practitioners is the varying definitions of spinal shock and different interpretations of its resolution.70 In addition, the delayed plantar reflex, the first sign of emergence from spinal shock, is present only transiently and can easily be missed during the focus of immediate lifesaving measures. Moreover, it may be several days before the next series of reflexes (bulbocavernosus, cremasteric, or anal wink) are observed. 
During the first 24 hours, prognosis for neural recovery may not be reliable due to issues of somnolence, pain, and possible substance abuse withdrawal.45 Patients have also been known to worsen in the first 72 hours as maximal cord swelling is reached.38,45 Examinations conducted between 72 hours and 1 week after injury more accurately predict functional muscle recovery than examinations conducted within the first 24 hours.38 For this reason, distinction of spinal cord injury as complete or incomplete on the basis of clinical examination is problematic.273 Suspending treatment interventions until resolution of this depressed reflex state may waste a potentially time-sensitive opportunity to arrest or diminish the secondary injury process in patients with spinal cord injury.179 

Imaging and Diagnostic Studies

A cleared spine in a patient implies that diligent spine evaluation is complete and the patient does not have a spinal injury requiring treatment. Because all trauma patients are at risk of spinal injury, systematic evaluation is necessary to achieve the goal of no missed injuries. Based on mechanism of injury and physical examination, physician judgment alone is not accurate in predicting cervical spine fractures.135 Clinical prediction rules are based on measurement of patient characteristics, injury circumstances, and findings on initial evaluation associated with spinal injuries. These measures, in combination with physician clinical judgment, allow efficient utilization of radiologic imaging studies (Table 43-11).27 
Table 43-11
Concepts Underlying the White and Panjabi Instability Checklist for the Lower Cervical Spine (C3–C7)
Point Value Criterion
2 Anterior elements destroyed or unable to function
2 Anterior elements destroyed or unable to function
2 Positive stretch test
Dynamic flexion–extension radiographs
2 Sagittal plane translation >3.5 mm or 20%
2 Sagittal plane rotation >11 degrees
On resting static radiographs
2 Sagittal plane displacement 3.5 mm or 20%
2 Relative sagittal plane angulation >20 degrees
1 Abnormal disc narrowing
1 Developmentally narrow spinal canal sagittal diameter <13 mm or Torg-Pavlov ratio <0.8
2 Spinal cord damage
1 Nerve root damage
1 Dangerous anticipated loading
Total of 5 or more = unstable
Explanations and additional guidelines from the formulators of the checklist:
  1.  
    Total score: For borderline decision on any element, add half the value to the sum.
  2.  
    Anatomic criteria: If all anterior or all posterior elements are destroyed, the spine is potentially unstable. If anterior elements are destroyed, the spine is more unstable in flexion. If posterior elements are destroyed, the spine is more unstable in extension. If the spinal canal is developmentally narrow, the threshold for neurologic problems with spinal injury is lower.
  3.  
    Radiographic criteria: These criteria are not applicable to children younger than 7 years. Translation: measurements assume a tube to film distance of 72 in. Threshold for sagittal plane translation is 3.5 mm on a static film or flexion–extension views, and it is based on a 2.7-mm laboratory measured value plus 30% for magnification. Rotation threshold is >20 degrees on flexion–extension views or at least 11 degrees more than functional spinal unit above or functional spinal unit below the injured level on a static view.
  4.  
    Criteria for a positive stretch test: >1.7-mm difference in interspace separation pre- and posttest or >7.5 degrees angulation with 25 lb of cervical traction incrementally applied.
  5.  
    Disc space height: Disc narrowing may suggest annulus disruption and instability; disc space widening may also indicate annulus disruption and instability.
  6.  
    Canal width: Canal anteroposterior diameter <15 mm or Torg-Pavlov ratio <0.80 (normal > 1), where Torg-Pavlov ratio = distance from midlevel posterior vertebral body to nearest point on spinolaminar line/midlevel vertebral body anteroposterior diameter.
  7.  
    Neurologic criteria: If the trauma is severe enough to cause initial neurologic damage, the support structures have probably been altered sufficiently to allow subsequent neurologic damage; clinically unstable, root involvement is a weaker indicator for clinical instability (one point) versus cord injury (two points
     
    ).
  8.  
    Physiologic criteria: Anticipated dangerous loads such as heavy labor occupation, contact sport athlete, and motorcyclist; also, intractable, progressive pain may suggest instability.
 

From White AA III, Johnson RM, Panjabi MM, et al. Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop Relat Res. 1975;109:85–96.

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The necessary elements for a complete spine evaluation are 
  1.  
    history focused on high-risk events and high-risk factors;
  2.  
    physical examination to check for physical signs of spinal injury or neurologic deficit; and
  3.  
    imaging studies based on an initial evaluation.
Radiographs are not necessary for alert patients who are not intoxicated, provided they have had an isolated blunt trauma and have no neck tenderness on physical examination.124 However, this estimate of “no false negatives” is based on small numbers of patients with fractures. Each patient with a diagnosed fracture had at least one of the following four characteristics: midline neck tenderness, evidence of intoxication, abnormal level of alertness, or several painful injuries elsewhere.124 Lack of these clinical findings suggests absence of a spine fracture but does not definitively exclude injury. To reduce routine cervical spine imaging in trauma patient, two competing prediction rules have been developed and validated: the National Emergency X-ray Utilization Study (NEXUS) criteria123 and the Canadian C-spine Rule247 (Fig. 43-5). The Canadian C-spine injury prediction rules have better sensitivity and specificity and reduce unnecessary imaging to a greater extent,246,247 but they are more complex to apply routinely.120124 Applying Canadian C-spine Rules in the field may prevent 38% of out-of-hospital spine immobilizations.27 
NEXUS, National Emergency X-ray Utilization Study.
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Figure 43-5
Comparison of NEXUS Criteria and Canadian C-spine Rule for avoiding imaging in alert, examinable trauma patients.
NEXUS, National Emergency X-ray Utilization Study.
NEXUS, National Emergency X-ray Utilization Study.
View Original | Slide (.ppt)
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Spine injury may be difficult to recognize in a patient with altered mental status.161 Therefore, cervical spine injury should be considered in an unconscious patient even in the absence of a definitive history of trauma.1 The clinical presentation of an unrecognized spinal cord injury, such as a neurologic deficit from a cervical injury, may be misinterpreted as a stroke.135 In obtunded patients found unresponsive at the scene, spinal cord injury may present as a medical emergency, such as bradycardia with hypotension, hydronephrosis, renal failure, or pyelonephritis associated with urinary retention. Focused emergency room evaluation of medical symptoms may overlook the underlying spinal cord injury.20 Spinal cord injury without an associated cervical fracture or dislocation, advanced age, unusual or changing neurologic deficits, intoxication, and psychiatric problems all contribute to clinical confusion and missed diagnoses of cervical fracture.25 Neurologic problems in these patients may be attributed to hysteria, intoxication, or other disease. 
The process of clearing the thoracolumbar spine is similar to that for clearing the cervical spine. Only AP and lateral view radiographs are necessary. Patients with a clear mental status, no back pain, and no other major injuries do not need radiographs of the spine to exclude a spinal fracture.174 The spine in these patients can be safely cleared by a physical examination alone. Any physician with adequate training and experience can clear the spine following a directed spine and neurologic examination of the patient and careful review of appropriate and adequate-quality imaging.220 

Diagnostic Imaging

Ideally, no patient undergoing care for trauma should deteriorate from a missed spine injury. To meet this goal, immediate recognition of a potential cervical spine injury is essential.77 Patients with missed fractures can develop neurologic deterioration.77,272 Assessment of the cervical spine is an essential component of the advanced trauma life support system of trauma care.8 Every trauma patient requires a definitive decision regarding the presence or absence of spine injury. At minimum, the assessment requires a careful review of history and a thorough examination. Usually, spine evaluation involves serial clinical examinations and review of cervical spine radiographs. 
The prevalence of cervical spine fractures is 1% to 5% in screening radiographs.77 Standard imaging (three views of the cervical spine and computed tomography as necessary) has a false-negative rate of 0.1%. The radiographic evaluation should be correlated to clinical considerations. The aim of careful decision making is to have a zero missed injury rate. 

Plain Radiography

Plain radiographs, if they show complete lateral visualization of the cervical spine and include an open-mouth view, are fairly sensitive in identifying cervical spine fractures. The risk of missing significant fractures is less than 1% of patients.77 The sensitivity of the lateral radiograph alone is 83% and specificity is 97%. The addition of open-mouth and AP views increases the sensitivity to approximately 100%.160 
Cervical radiographs in a trauma patient are obtained with the patient supine and secure on a backboard. The patient is not moved to different positions for the various views; rather, the x-ray beam and film position is adjusted to provide the desired image perspective. Opinions for minimum number of plain radiographs necessary in trauma patients range from 0 to 7 (AP, lateral, open-mouth, oblique, flexion–extension) (Figs. 43-6 and 43-7).116 
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Figure 43-6
Standard radiographs of the cervical spine.
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Figure 43-7
Flexion–extension radiographs.
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Accurate interpretation of the lateral cervical spine radiograph is essential, yet this interpretation may frequently be erroneous because of the stressed circumstances in an emergency setting and inexperience of the individuals responsible for initial care. The first step in interpreting radiographs is to make sure that they are of adequate quality for the intended purpose. Lower-quality films significantly increase error rates.198 Adequate lateral cervical spine radiographs require clear visualization of the spine from the occiput to the first thoracic vertebra. If the lower cervical spine is not visualized on a lateral radiograph, a swimmer’s lateral view or a CT scan can visualize this region (Fig. 43-8). 
Figure 43-8
Images from a screening cervical spine computed tomographic scan.
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The AP cervical spine view is less helpful in diagnosing acute injuries. A change in alignment of the uncovertebral joints and spinous processes can indicate an acute injury. The open-mouth view is essential for excluding a C1 arch or C2 odontoid process fractures. Tomograms or a CT scan may be necessary to substitute for the open-mouth view in unresponsive patients. Oblique views can identify injuries of the facet joints, pedicles, and lateral masses, particularly at the cervicothoracic junction. For this reason, oblique views in the trauma setting can increase the diagnostic sensitivity of cervical radiographs. 
Most spine injuries occur at the junctions: craniocervical, cervicothoracic, and thoracolumbar. They are often the most difficult to see on standard radiographs. Among these injuries, the most serious and most frequently missed is craniocervical dissociation. Harris et al117 measurements based on the distance between the dens and the basion are probably the simplest and most reliable measurements for identifying craniocervical dissociation. Suspicion of injury and careful scrutiny of radiographs minimize errors of missed injury.208 
In patients with cervical tenderness and normal plain radiographs, flexion–extension views can identify occult cervical ligamentous injury (see Fig. 43-7). Flexion–extension views in the acute setting of an emergency room, however, can be nondiagnostic or even dangerous. Patients in acute pain may have limited mobility related to muscle spasm, limiting cervical spine motion on dynamic views. Unsupervised or forceful flexion in a patient with an occult ligamentous injury may precipitate a neurologic injury. When necessary, flexion–extension radiographs should be obtained in alert patients, under supervision, and with voluntary unassisted positioning by the patient. 
Interpretation of radiographs has limitations. Knowledge of anatomy and clinical experience are important for accurate interpretation of radiographs.185 Landmarks for measurements can be difficult to identify. A systematic approach to reading cervical radiographs can help reduce the chances of missing an important injury. Alignment of the cervical vertebrae is assessed by examining longitudinal lines along vertebral bodies, lamina, and spinous processes. Examining alignment of the lamina in the upper cervical vertebrae is particularly helpful in excluding injuries of the craniocervical junction in both children and adults. 
The prevertebral soft tissues can be useful as an indicator of swelling from acute hemorrhage. Increased thickness and altered contour of the pharyngeal tissue anterior to C2 (i.e., convexity instead of concavity caudal to the C1 anterior arch) suggest acute craniocervical injury. The prevertebral soft tissue shadow thickness, however, becomes unreliable in the presence of oropharyngeal tubes. Also, soft tissue swelling can occur without bony injury, and conversely, bony injuries can occur without significant soft tissue swelling.178 Prevertebral soft tissue widening resolves to normal after 2 weeks in 50% of patients and in 3 weeks in 90% of patients.198 

Computed Tomography

Computed tomography and MRI may be useful together in determining the presence and extent of spinal column injury.156 MRI is superior in demonstrating spinal cord pathology and intervertebral disc herniation. Computed tomography is superior to MRI in demonstrating osseous injury. However, injuries purely localized to the transverse plane, such as odontoid fracture, can be missed on axial CT scans. For these types of injuries, direct coronal CT scan can provide superior demonstration of skeletal features in the upper cervical spine.197 

Magnetic Resonance Imaging

MRI is useful for imaging soft tissues and bone. MRI can expose edema and hemorrhage associated with acute spinal cord injury. Increased cord signal and parenchymal cord hemorrhage indicate poor prognosis for neurologic recovery.29,89,90,164,228,229 MRI is particularly useful for assessing the craniocervical junction. Edema in the occipitocervical facet capsules and basicervical ligaments or acute cervicomedullary angulation suggests craniocervical injury.42 While MRI can offer exceptional imaging of soft tissues and may prove valuable in the management of spinal injuries, its use for primary spine clearance is limited. MRI (usually with sagittal short tau inversion recovery images) is very sensitive to muscular and soft tissue injury and often does not correlate with clinical instability.259 MRI has high sensitivity for identifying injuries to the disc space, posterior longitudinal ligament, facet joint, and posterior interspinous tissues; it is less sensitive for the anterior longitudinal ligament and ligamentum flavum. In unstable injuries, MRI within 24 hours of injury may show edema across the entire vertebral column: prevertebral space, disc space, facet joints, and interspinous ligaments. If increased MRI signal is not present in all four regions, correlation with unstable injury is lower.102 
MRI also provides noninvasive assessment of the vertebral artery blood flow in cervical trauma, which can be frequently disrupted in cervical spine injuries.92 MRI angiograms are abnormal in 24% of patients.92 However, MRI diagnosis of arterial artery may not be functionally significant.237 

Sequence of Imaging Studies

Clearing the spine frequently requires considerable time, with one study reporting a median time of 15 hours.56 Patients often need emergent care and transport prior to the spine being cleared. Emergent lifesaving interventions, such as intubation, anesthesia, and abdominal or chest surgery, can be performed relatively safely using appropriate precautions in a patient with incompletely evaluated cervical spine. 
Obtaining a lateral cervical spine radiograph is part of initial evaluation of a trauma patient. Obtaining an AP chest radiograph, AP pelvis radiograph, and a lateral cervical spine radiograph does not interfere with the urgent management of multiple injured patients during resuscitation. These three images provide crucial information that facilitates resuscitation and comprise the standard “trauma series” in trauma centers. Additional emergent spinal imaging is necessary only if these initial views demonstrate a spine injury or if the primary survey examination suggests a neurologic deficit. Otherwise, further spinal imaging can follow resuscitation and hemodynamic stabilization. Plain radiographic studies are increasingly being replaced by computed tomography for initial cervical spine imaging in trauma patients. Cervical spine CT scan is frequently obtained in conjunction with head CT scan. CT scanning adds diagnostic information in approximately half of the injuries identified on plain radiographs.55 
Complete cervical spine radiographs in addition to the initial trauma lateral radiograph are completed once the patient is medically stable (see Fig. 43-5). These additional views include open-mouth, AP, and in some institutions, right and left oblique radiographs. Alternatively, trauma patients at high risk for cervical spine injury can be screened for a cervical injury with a rapid-sequence helical CT scan (see Fig. 43-8).115 Patients with an incomplete spinal cord injury may require an emergent MRI to identify the source of cord injury, if radiographs and CT scans do not show vertebral column injury consistent with the neurologic examination.219 
MRI should be performed urgently in any patient with a progressive neurologic deficit. In an important publication that stimulated debate about acute MRI, 6 patients were described as having an unrecognized disc herniation that potentially contributed to neurologic worsening after reduction of a cervical spine facet dislocation.75 Many surgeons cite this report as justification for obtaining prereduction magnetic resonance image of patients with spinal cord injury associated with cervical facet dislocation. However, this report acknowledged other treatment-related complications that may have also contributed to deterioration in three of the six reported cases. 
Most traumatic disc injuries associated with cervical fractures and dislocations do not adversely influence neurologic function.104 In patients with spinal cord injury associated with cervical spine fracture–dislocations, the most urgent priority after lifesaving measures is mechanical decompression of the spinal cord. This is most expeditiously and efficiently achieved through closed reduction. Rapid closed reduction is successful and safe.104 Waiting for MRI in this setting should not delay closed reduction. Other interventions or other diagnostic tests for non–life-threatening conditions also should not supersede the priority for closed reduction. Postreduction MRI, however, is useful to look for disc extrusion, if neurologic deterioration occurs or if planning approach for definitive surgical treatment is required.222 
Neurologically intact patients with a cervical spine dislocation do not have the time–urgency of spinal cord injury. In these patients, magnetic resonance imaging may be obtained prior to reduction without adversely influencing outcome. The disc at the level of dislocation is usually abnormal on these images.73 Such disc abnormalities have been advanced as an argument for decompressing the damaged disc prior to reduction. However, induction of anesthesia and positioning for surgery remain challenging in a patient with a dislocated cervical spine. Furthermore, performing an open reduction through an anterior approach is a difficult task. Neck swelling occurs more commonly after an anterior approach, leading to potential swallowing deficits or prolonged intubation postoperatively. The improved stability gained from reduction, safer induction of anesthetic, and the option of posterior surgery are arguments for attempted closed reduction even in neurologically intact patients. 
Patients with pain and normal initial imaging studies may have an occult fracture or ligamentous injury. Also, fractures may be difficult to see if patients have severe degenerative disease, osteoporosis, or ankylosis of the spine. In these settings, magnetic resonance imaging or a technetium bone scan can facilitate diagnosis of occult injuries.22,87 

Unresponsive Patients

Spine clearance is a difficult issue in obtunded patients with high-energy injury mechanisms. In these patients, the spine is sometimes deferred until the patient is examinable. However, that may be weeks to months in some patients. Meanwhile, these patients may develop complications associated with external bracing and mobility restrictions imposed by spine precautions. If a CT scan is completely normal, the spine may be cleared without further imaging or examination.118 When the CT scan is difficult to interpret because of severe degeneration, osteoporosis, diffuse idiopathic spinal hyperostosis, or ankylosing spondylitis, then additional imaging such as MRI, clinical examination, or dynamic imaging such as a traction test may be needed to rule out injury of the cervical spine. Thoracic and lumbar injuries can be reliably excluded by radiographs alone. 

Patient Care Until the Spine is Cleared

An important publication that led to delayed reduction of cervical spine injuries suggested that neurologic deterioration occurred after admission in 5% of spine injury patients.166 An identifiable specific management event is associated with 86% of these deteriorations. Unstable spinal injury should be assumed and the patient protected.106 Logrolling does not keep the spine immobile, and unstable injuries should be stabilized immediately when the patient’s medical condition permits doing so safely.171 Extremely combative patients with a closed head injury may require intubation and chemical paralysis to protect against neurologic injury from an associated spine fracture. Fiberoptic intubation or laryngeal mask airway should be considered in the management of patients with cervical spine instability.37 

Missed Injuries

The rate of missed or delayed diagnosis of cervical spine injury at trauma centers is from less than 1% to 4.9%.63,77,166 Most patients with missed injuries or delayed diagnosis (71%) suffer no adverse consequences. However, patients who deteriorate from a missed injury (29%) may have severe complications. These complications range from death (20%) to quadriplegia (40%) or other new neurologic deficit (40%).63 
The most frequent reasons for missed injuries are inadequate radiographs (44%) and misinterpretation of adequate-quality radiographs (47%). More frequently than cervical injuries, the diagnosis of thoracolumbar fractures may be delayed in 11% of trauma patients and missed in 5.5%.174 A thoracolumbar fracture may not be recognized despite complaints in 66% of these patients during their initial evaluation. Patients with a missed thoracolumbar fracture who do not complain of back pain have either altered mental status or other major associated injuries.174 Back pain in trauma patients should be taken seriously and evaluated thoroughly, and the evaluation should include radiographic imaging. 

Current Treatment Options

The goal of treatment of every spinal injury is restoration of the patient to maximal possible function (Table 43-12). In trauma care, this goal implies protecting all patients until a spinal injury is definitively excluded or identified and treated. Also, caring for a trauma patient requires that associated injuries be expeditiously identified and appropriately addressed. For patients sustaining a spinal column injury, the treatment focus is protecting uninjured neural tissues, maximizing recovery of injured neural tissues, and optimizing conditions for the musculoskeletal portions of the spinal column to heal in a satisfactory position. 
 
Table 43-12
Goals of Spine Trauma Care
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Table 43-12
Goals of Spine Trauma Care
Protect against further injury during evaluation and management
Expeditiously identify spine injury or document absence of spine injury
Optimize conditions for maximal neurologic recovery
Maintain or restore spinal alignment
Minimize loss of spinal mobility
Obtain a healed and stable spinal column
Facilitate rehabilitation
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Treatment Priorities

Errors in the initial care of spinal injury patients can have catastrophic or fatal outcomes.63 Minimizing these errors requires management of spinal injury patients at highly specialized centers with experienced personnel. Spinal cord injury patients, in particular, benefit from early transfer to a trauma center with a spinal cord injury unit.190 Early referral to a spinal cord injury center improves patient survival and neurologic recovery.108,144 
Management of spinal injuries in multiply injured patients requires the concerted activity of a trauma team. Experienced field personnel, emergency room physicians, general surgeons, orthopedic surgeons, neurosurgeons, radiologists, anesthesiologists, physiatrists, and nursing personnel are integral members of this team. The overriding general principle in efficient care for trauma patients is early involvement by appropriate members of this team. Physicians ultimately assuming the long-term management of trauma patients and frequently orthopedic surgeons and physiatrists are particularly critical in directing optimal initial care.103 

Provisional Stabilization

Trauma patients require protection and immobilization of the spine until spinal injury is definitively excluded or treated. This general principle has specific patient-care implications commonly referred to as “spine precautions.” All trauma patients should be maintained in the supine position on strict bed rest with the bed flat, transfers with a spine board, and frequent logrolling for decubitus ulcer prophylaxis. Alternatively, patients may be placed in a rotating frame for improved pulmonary mechanics and skin care. 
Cervical injuries associated with malalignment require skull traction, except injuries with complete ligamentous disruption, usually indicated by distraction between vertebrae on imaging studies. Distraction injuries are the most unstable spine injuries. Skull traction in these patients will lead to catastrophic neurologic deterioration or even fatal vascular injury. Patients with distraction injuries are best immobilized with sandbags and tape or a halo apparatus. Even when immobilized in the halo apparatus, these patients should be maintained on strict bed rest with full spine precautions until definitive surgical stabilization. 
Traction pins or skull tongs are placed in-line with the external auditory meatus, 1 cm above the pinna. Carbon fiber tongs with titanium pins should be used initially to permit subsequent MRI evaluation if necessary. Carbon fiber tongs, however, grip the skull less strongly than steel tongs. Pins in carbon fiber tongs may pull out of the skull with traction weights above 80 lb. Pins in steel tongs can withstand traction up to 140 lb.147 On occasion, if closed reduction in a cervical injury requires weights greater than 80 lb, carbon fiber tongs may be exchanged for steel tongs before applying heavier weights. 

Closed Reduction

Closed reduction in cervical spine injuries is safe and effective.104,146 Successful reduction may require weights as high as 140 lb. In young patients with no osteoporosis, traction weight up to 70% of body weight is generally safe, provided steel tongs are used and pins are properly placed.226 Cervical traction at weights larger than 80 lb should not be applied to most carbon fiber MRI compatible tongs; traditional steel Gardner-Wells tongs are less likely to slip with larger weights.147 Traction should not be applied in injuries showing distraction of the spinal column. 
Decompression of spinal cord injury should proceed as soon as the patient can medically tolerate it.66 The window of opportunity for maximal neurologic improvement through decompression may be as short as the first few hours following spinal cord injury.4749,66 Spinal cord injury patients may have an excellent capacity for spinal cord recovery regardless of initial presentation.39 Reduction within the first few hours of injury may lead to dramatic improvement in neurologic status. Reduction within 2 hours of injury has been reported to reverse tetraplegia.252 Emerging evidence from the Surgical Treatment of Acute Spinal Cord Injury Study indicates that decompression within 24 hours is associated with improved neurologic recovery. Although results of this observational study are preliminary, investigators found a 2- to 3-grade improvement in the ASIA impairment score in those decompressed within 24 hours. Moreover, higher rates of surgical complications were found in subjects who underwent surgery after the first 24 hours.84,150 
In cervical injuries, closed reduction can achieve decompression. Emergent attempted closed reduction is the treatment of choice for alert cooperative patients with acute spinal cord injury from a cervical spine dislocation.241 In these patients, MRI is not necessary prior to reduction and should not delay reduction.153 Reduction in an unconscious or unexaminable patient should be preceded by magnetic resonance imaging. In this situation, the presence of a herniated disc may be treated with surgical decompression before reduction.75,219 
Patients with highly unstable injuries, such as craniocervical dissociation or a cervical injury that shows distraction at the injured segment, require compression for reduction, not further traction. Compression across the cervical spine can be applied by a halo vest.182 
Reduction improves stability, preventing neurologic deterioration in the interval preceding definitive treatment.41 Closed reduction can also improve neurologic recovery.236 Although case reports have described neurologic deterioration during reduction,191 larger series of closed reductions have not observed neurologic deterioration.57,104 In fact, a case in one of these series was of a patient with a large disc herniation seen on a prereduction magnetic resonance image that resolved with closed reduction. Closed reduction also decreases the need for more complicated surgical procedures later.251 

Definitive Treatment

Nonsurgical Options

Closed treatment remains the standard of care for most spinal injuries. Clinical observation reports, biomechanical investigations of stability, and radiographic measurements of stability have not produced definitive recommendations applicable to specific cases in deciding closed or operative treatment. The only consistent indication for surgical treatment may be skeletal disruption in the presence of a neurologic deficit. A consistent contraindication to closed treatment is an unstable purely ligamentous spinal column injury in a skeletally mature patient. Although these injuries may heal sufficiently in pediatric patients with significant growth remaining, in adult patients the healing response does not restore sufficient strength to provide spinal column stability, regardless of the length of bed rest or external immobilization. Unstable ligamentous injuries require fusion. Osseous injuries heal adequately but require treatment to control deformity. 
Closed treatment options are bed rest, halo apparatus, external orthosis, or cast.78 Bed rest as definitive treatment may be indicated in rare cases of patients unable or unwilling to undergo bracing or surgery: severe preexisting deformity, morbid obesity, medical comorbidity, or personal preference. Bed rest for the initial few weeks preceding bracing is an option for severely unstable injuries. If bed rest is determined as a treatment option, measures must be taken to provide pressure relief to areas at risk for skin breakdown. Sacral, calcaneal, and occipital pressure ulcers are particularly problematic in persons with spinal cord injury remaining on bed rest for undefined periods of time.108,149 
The level of injury serves as a guide for the category of external orthosis. Most commercially available braces within each category are equivalent.24 Custom-molded trunk orthoses provide added rotational control. Casts can be applied in hyperextension to improve kyphosis. Bracing is continued until bone healing is sufficient for load bearing: 8 weeks in cervical injuries and 12 weeks in thoracolumbar injuries. 

Surgical Options

Surgical management of spinal cord injury patients is based on reports of experience and observation, not rigorous clinical trials. Surgical stabilization of the spinal column can prevent further mechanical injury to the damaged cord tissue. Removing a residual compressive mass effect may additionally allow better neurologic recovery. Closed treatment of unreduced injuries may lead to chronic pain requiring later surgical treatment.24 
The critical role of time is increasingly being recognized as potentially pivotal in affecting neurologic recovery. Early intervention in this setting is not defined in days after the injury but rather in minutes and hours. Animal studies have suggested a potential window of opportunity in the first 3 to 6 hours after injury in which significant neurologic recovery may be possible (Fig. 43-9).47,48,66 
Figure 43-9
Electrophysiologic recovery diminishes with longer duration of cord compression.
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Surgery in spinal injuries involves fusion with two rare exceptions: odontoid fractures and C2 arch fractures. These two injuries in specific circumstances may be treated with internal fixation (osteosynthesis). Open reduction and instrumentation may be just as effective as fusion for spinal fractures.193 Early surgery reduces hospital stay. 
Earlier studies reported high complication rates with anterior cervical surgery.243 Injured vertebrae are associated with injury to nearby soft tissues. Anterior interbody grafts without fixation may work for anterior cervical fusion following discectomy. However, grafts of this nature are prone to displacement if there is posterior instability or gross deformity of the vertebral body, unless supplemented by fixation.267 Anterior plating and posterior plating are equally successful in cervical trauma.83,101 Anterior plating provides immediate stabilization even with posterior ligamentous injury.51 Although the strength of the fixed spine is relatively unchanged by corpectomy and anterior grafting, anterior grafting improves alignment and fixation maintains alignment.162,181 Anterior fusion allows early mobilization, shorter stay, and less cost.253 Spinal cord blood flow may, however, be adversely affected by an anterior surgical approach. 
For thoracolumbar injuries, a three-column injury treated with anterior instrumentation should be either augmented with posterior instrumentation or postoperatively immobilized in a rigid external brace.163 In burst fractures, anterior reconstruction with fixation is more stable than the posterior instrumentation systems in all loading conditions.235 
The choice of the operative method in thoracolumbar fractures should not be based on any hypothetical differences in reductive power.79,269 Canal clearance is most effective when carried out in the first 4 days after injury and in patients with an initial canal compromise of 34% to 66%.99 Percentage of encroachment decrease in posterior systems is small.52 Laminectomy increases deformity and neurologic deficit unless combined with internal stabilization.243 Traumatic dural tears should be repaired before any anterior or posterior spinal reduction maneuver.68 
If spinal canal decompression is the goal, this is best achieved through an anterior approach.11,140 Primary anterior decompression and fusion is preferred in an axial loading or flexion compression injury with a large midline retropulsed fragment that produces a significant neurologic deficit.170,216 
Transpedicular fixation provides solid internal fixation that is circumscribed to the injured vertebral segments.177 As injury progresses to involve all three structural columns, the ability of the transpedicular constructs to restore preinjury stiffness decreases. Several reports have identified failure of fixation when thoracolumbar vertebral body fractures are treated with short-segment posterior fixation.74,173 One option to reduce the risk of hardware failure prior to solid fusion is to augment transpedicular constructs with anterior bone grafting.46,234,238 However, external bracing to protect posterior fixation during healing remains an alternative to anterior surgery. 

Authors’ Preferred Treatment

 
 

We recommend discontinuing routine administration of steroids in acute spinal cord injury. The magnitude of observed neurologic improvement is minimal and controversial compared with risk of infection and gastrointestinal bleeding complications. We recommend a screening CT scan to image the cervical spine in obtunded patients and discontinuing cervical spine immobilization and mobility precautions if the study is normal (Fig. 43-10). Decompression should be achieved expediently in patient with spinal cord injury, whether complete or incomplete. For medically stable, examinable patients with cervical spine dislocation and severe neurologic injury, such as complete tetraplegia, we recommend emergent closed reduction prior to MRI or other time-consuming interventions.

 
Figure 43-10
Dartmouth Spine Clearance Protocol.
 
CT, computed tomography; MRI, magnetic resonance imaging; NEXUS, National Emergency X-ray Utilization Study.
CT, computed tomography; MRI, magnetic resonance imaging; NEXUS, National Emergency X-ray Utilization Study.
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Figure 43-10
Dartmouth Spine Clearance Protocol.
CT, computed tomography; MRI, magnetic resonance imaging; NEXUS, National Emergency X-ray Utilization Study.
CT, computed tomography; MRI, magnetic resonance imaging; NEXUS, National Emergency X-ray Utilization Study.
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Pearls and Pitfalls
 

Errors in the emergency room management of patients have serious adverse consequences for subsequent care. For optimal spine evaluation of trauma patients and reducing risk of complications, we recommend observing the following principles.

  1.  
    Solicit observations of neurologic function at the scene and en route from the field personnel and the paramedic team. Suspicion of neurologic injury may help prioritize subsequent care. Record the source of information in medical record notes.
  2.  
    Personally review outside imaging studies; do not assume that studies were adequate or interpretation was accurate.
  3.  
    Convey your level of concern for potential spine injury clearly to all members of the team caring for the patient. Trauma care is multidisciplinary; coordination of care is critical for successful outcomes, both when spinal injury is identified and also when spinal injury is excluded.
  4.  
    Do not accept inadequate-quality radiographs or other imaging for definitive decision making. An initial lateral radiograph “clear to C5” does not mean “no cervical spine injury.”
  5.  
    Look for thoracic fracture–dislocation on the trauma AP chest radiograph: lateral translation between vertebrae and widened disc space.
  6.  
    Perform a neurologic examination unobtrusively during resuscitation, if possible, prior to intubation or pharmacologic paralysis. Identifying a neurologic deficit may change treatment priorities.
  7.  
    Record personal neurologic examination accurately in the medical record: moving all extremities, neurovascular intact, and “wiggle your toes” are not adequate assessment or documentation of neurologic function.
  8.  
    Check sacral pinprick sensation. Sacral sparing assessment is essential for distinguishing a complete spinal cord injury from an incomplete injury, and this distinction is important for prognosis of neurologic recovery.
  9.  
    Do not attribute neurologic deficit to intoxication, the effect of drugs, or pain from extremity injuries. This dangerous assumption may limit proper management of neurologic injury.
  10.  
    Do not dismiss unusual or complex neurologic deficits as nonphysiologic. Incomplete spinal cord injury can present with complex neurologic deficits, and not recording or investigating them urgently can delay the appropriate acute treatment of spinal cord injury.
  11.  
    Pay careful attention to any discrepancy between neurologic level on examination and radiographic level of injury. The difference may be due to another vertebral injury level, hemorrhage, ligamentous disruption, or other process causing cord compression.
  12.  
    Differentiate between neurogenic shock and hypovolemic shock. Treating neurogenic shock with fluid resuscitation instead of vasopressors may result in volume overload, pulmonary edema, or adult respiratory distress syndrome.
  13.  
    Do not delay closed reduction of a dislocated cervical spine in a patient with complete tetraplegia. Delay to obtain CT scan, magnetic resonance image, or other diagnostic tests not essential to reduction may miss an opportunity to decompress the spinal cord during an early postinjury period when it has the best potential for recovery.
  14.  
    Do not apply cranial traction pins in a patient with a skull fracture without consulting a neurosurgeon. Placing pins in fracture fragments may exacerbate cranial injury.
  15.  
    Use traction tongs, weights, and pins compatible with MRI. Some pins and tongs may develop heat, displace, or cause interference with the image.
  16.  
    Do not apply cervical traction in an injury that shows widened disc space or other distraction. Overdistraction and vertebral artery injury is a potentially fatal complication.
  17.  
    Look for associated injury patterns. A patient with a flexion–distraction injury will frequently have lap belt marks and abdominal injury, bilateral calcaneus fractures may be associated with a lumbar burst fracture, a thoracic fracture–dislocation may be associated with a vascular injury, and cervical fracture in ankylosing spondylitis may be associated with esophageal injury.
  18.  
    Look for additional levels of spinal injury. Approximately 15% of patients have multiple discontiguous levels of spinal injury.
  19.  
    Remove the backboard within 2 hours of application; pressure sores can develop in patients laying on a backboard for more than 2 hours.
  20.  
    Consider age and mechanism of injury before allowing a patient to be discharged home without additional evaluation.

Complications

The first principle of all medical treatment is “do no harm.”80 Harm to a patient with spine injury takes the form of missed diagnosis, missed associated injuries such as an aortic tear with a thoracic fracture–dislocation, a missed abdominal injury with a lumbar flexion–distraction injury, or marked neurologic deterioration in a neurologically intact patient. The frequency of complications during acute hospitalization is increased in the presence of a neurologic deficit (Table 43-13).91 Even when they are not life-threatening, complications can prolong hospitalization and compromise outcome. Complications during initial hospitalization add $1.5 billion annually to the cost of caring for patients with vertebral fractures in the United States.91 
 
Table 43-13
Complications in Spine Injury Patients
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Table 43-13
Complications in Spine Injury Patients
Complication Cord Injury (%) No Cord Injury (%)
Overall 52.9 20.6
Urinary tract infection 24.0 8.6
Respiratory 23.1 56
Cardiac 11.5 3.2
Decubitus ulcer 7.7 1.0
Pneumonia 13.5 7.3
Mortality 9.6 4.8
 

From Fletcher DJ, Taddonio RF, Byrne DW, et al. Incidence of acute care complications in vertebral column fracture patients with and without spinal cord injury. Spine. 1995;20:1136–1146.

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Outcomes of Spine Injury

Pain and Function

Neurologic status determines end-results following spinal injury.172,186 Function after spinal injury seems dependent primarily on the injury itself and less on the method of treatment, residual spinal mobility, or the radiographic results.36,154,203,204 Nonsurgical treatment of neurologically intact patients is associated with results equivalent to surgical treatment.54,184,284 Anterior and posterior surgical procedures yield equivalent function in neurologically intact patients.285 In the absence of neurologic injury, pain and function approach population norms at 3 to 8 years following the injury.154 
Despite strong convictions of surgeons who treat patients with spinal cord injury, clinical studies have not shown an association between neurologic and skeletal outcome.72 Clinical outcome in general is not related to deformity.11,186,254 Kyphosis of more than 30 degrees may increase pain, but this threshold is based on a impressions of surgeons, not rigorous clinical research.97 Residual canal occlusion does not result in late symptoms of spinal stenosis. 

Neurologic Recovery

Outcome of spinal cord injury is predominantly determined by patient’s age and severity of neurologic injury.12,248 Most common causes of death are respiratory disease, sepsis, and cardiovascular disease.12 A recent report identified several important secondary health predictors that significantly improved prediction models of mortality when compared with injury severity models alone.148 Secondary health conditions thought to influence mortality include surgery to repair pressure ulcers (which strongly correlates with severity of pressure ulcer); infection symptoms, notably urinary tract infections; amputations; additional bone fractures remote from acute injury; and probable major depression. Older patients with complete tetraplegia have very high acute mortality (60% to 100%).5,278 In contrast, more than 90% of patients with central cord injury survive the initial hospitalization. Life expectancy following spinal cord injury is related to the severity of neurologic deficit, with decreased survival in patients with more severe deficits (Table 43-14).248 Older age at the time of spinal cord injury is also associated with decreased survival (Table 43-15). 
Table 43-14
Life Expectancy, in Years, Following Spinal Cord Injury for Those Surviving the Initial 24 Hours
Age at Injury (y) No Injury Incomplete Motor SCI (ASIA C) Complete Paraplegia Complete Tetraplegia with NLI C5–C8 Complete Tetraplegia with NLI C1–C4 Ventilator-Dependent at Any Level
20 58.4 52.6 45.2 40.0 35.7 17.1
40 39.5 34.1 27.6 23.3 19.9 7.3
60 22.2 17.7 12.8 9.9 7.7 1.5
 

From University of Alabama. Spinal Cord Injury: Facts and Figures at a Glance. Birmingham, AL: University of Alabama SCI National Statistical Center; 2008.

 

ASIA, American Spinal Injury Association; NLI, neurologic level of injury; SCI, spinal cord injury.

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Table 43-15
Life Expectancy, in Years, for Patients with Spinal Cord Injury Surviving at Least 1 Year Postinjury
Age at Injury (y) No Injury Incomplete Motor SCI (ASIA C) Complete Paraplegia Complete Tetraplegia With NLI C5–C8 Complete Tetraplegia With NLI C1–C4 Ventilator-Dependent at Any Level
<30 43 53.0 45.5 40.8 36.9 25.1
30–50 24 34.5 27.9 23.9 20.8 12.2
>50 11 18.1 13.1 10.3 8.4 3.6
 

From University of Alabama. Spinal Cord Injury: Facts and Figures at a Glance. Birmingham, AL: University of Alabama SCI National Statistical Center; 2008.

 

ASIA, American Spinal Injury Association; NLI, neurologic level of injury; SCI, spinal cord injury.

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Prognosis for neurologic recovery is determined by the nature and magnitude of the initial injury. The pattern of spinal cord injury does not correlate with the pattern of skeletal injury on plain radiographs.248 Cord hemorrhage is associated with less neurologic recovery. When controlling for neurologic level (paraplegia vs. tetraplegia) and completeness of spinal cord injury, motor recovery does not differ for type of injury (penetrating vs. nonpenetrating) or type of fracture.275 Complete cord injuries are more likely in flexion–rotation patterns of injury, bilateral facet dislocation, and gunshot injury, with the bullet traversing the canal. Incomplete injuries are associated with preexisting spondylosis and gunshot injury, with the bullet not traversing the canal.275 The initial motor index score correlates with overall function at the time of discharge from rehabilitation in tetraplegia and complete injuries but not in paraplegia and incomplete injuries.152 Levels that have some voluntary motor function at 1 week after injury are likely to achieve three-fifths of original strength by 1 year postinjury.70 Pediatric patients with incomplete injuries have a good prognosis; neurologic deficit improves in 74% and resolves in 59%. Pediatric patients with complete injuries show improvement in 10% and resolution in none.114 
Some complete lesions show recovery. Patients with complete injuries frequently gain one or two levels: 32% gain one level and 18% gain two levels. The average motor score increase after complete tetraplegia is nine points at 1 year.276 Although a large multicenter trial by Fawcett et al81 found conversion rates of complete to incomplete injuries as high as 20% within the first month, the study included patients before and after the shift in the ASIA definitions which were changed in the year 2000. Burns and colleagues45 found that up to 9.3% of subjects initially considered complete at 72 hours were reclassified as motor complete, sensory incomplete (ASIA impairment score B) in the first week of injury because of challenges affecting the reliability of the early examination. In contrast, only 2.6% of subjects without factors impeding accuracy of early examination converted to sensory incomplete and no subjects were upgraded to motor incomplete.45 
Late conversion of complete to incomplete spinal cord injury can occur. Early studies suggest that approximately 4% of injuries complete at 21 days convert to incomplete. Three of six patients with late conversion regained bladder and bowel control and two regained the ability to ambulate.276 In the largest series to date, 987 subjects were evaluated for changes in ASIA impairment score, Motor Index score, motor level, and neurologic level of injury. Of the 539 subjects who were neurologically complete at 1 year, 94.4% remained complete at 5 years postinjury, with 3.5% converting to motor complete sensory incomplete and only 2.1% improving to motor incomplete.143 Complete paraplegia at 1 month following injury is associated with essentially no motor recovery in the lower extremities if the injury level is cephalad to T9. With a more caudal level, 38% regain some lower extremity motor function.276 Of patients with neurologic levels at or below T12, 20% gained sufficient lower extremity motor function to reciprocally ambulate with conventional orthoses. 
A direct relationship exists between the ASIA motor score and walking ability.274 Incomplete injuries carry a much better prognosis for recovery than complete injuries. For example, most patients with Brown-Sequard type of incomplete tetraplegia ambulate independently (75%) and nearly all regain bladder and bowel control.224 Patients with ASIA impairment score B incomplete paraplegia, motor complete but preserved bilateral sacral pin sensation, gained an average of 12 motor score points at 1 year. Nearly half (46%) of these patients are able to ambulate with a reciprocal gait.274 

Special Considerations

Children

Significant spinal cord injury can result from trauma without any fractures or ligamentous ruptures.219 Spinal cord injury without radiographic abnormality commonly occurs in children younger than 10 years.69 The mechanism of injury is usually physeal failure through a fracture in the hypertrophic zone of the endplate, leading to distraction of the cord and ischemic injury. Children have a greater capacity for neurologic recovery following spinal cord injury than adults, and the recovery can continue over prolonged periods.271 Studies on the use of methylprednisolone in spinal cord injury did not include children and, therefore, no data exist to comment on the use of such agents in the pediatric population. 

Elderly

Spinal cord damage can also occur without instability because of bulging ligamentum flavum.258 Two-thirds of patients are older than 50 years.25 The diagnosis is often missed. The patients are sent home as normal, called hysterical, or undiagnosed during stupor or coma. Cervical spine injury commonly occurs with relatively minor trauma in patients older than 65 years.159 C2 injuries, especially odontoid fractures, must be ruled out in older patients with neck pain after even a minor injury.159,240 Overall mortality rate in these patients is 26%.5 Patients older than 50 years with complete spinal cord injury have a 60% mortality rate.4,5,240 Injury severity decreases survival, particularly in older patients.107 Bed rest, traction, and halo immobilization are poorly tolerated by older people.157 

Gunshot Injuries

Gunshot injuries rarely cause spine instability.30 Bullet location is not associated with the neurologic prognosis.275 Decompression does not improve recovery if the projectile traverses the canal without a residual mass effect on the neural elements.244 Surgery risks neurologic deterioration.289 Surgery may be necessary for dural repair in patients with a cerebrospinal fluid leak or fistula. Debridement and bullet removal is an option if laparotomy for abdominal injury exposes the spinal injury area without added surgical morbidity. If the projectile traverses the oropharynx or the colon, intravenous antibiotics should be administered for 7 to 14 days for infection prophylaxis.30 NASCIS trials excluded penetrating spinal injury and no data exist as to the efficacy in such patients. 

Controversies

Problems with Stability Assessment in and Instability of Vertebral Column Spinal Injuries

The concept of spinal stability is central to the field of spine surgery. Spinal fusion and fixation surgery, in fact, is performed primarily to restore stability of the spinal column following instability from injury, degeneration, or decompression. It is natural to expect that a concept so integral to the daily work of spine surgeons would be well understood and well defined. Unfortunately, the contrary is true: spinal instability is variably defined, widely interpreted, and inconsistently measured. The components included in the list of “spine instability” are so wide-ranging that the concept has little meaning without specific definition in each context of its use. Stable and unstable lesions can have an associated neurologic injury. Stable and unstable lesions are reported to be equivalently managed with surgery and nonsurgical treatments and are reported to have similar results of treatment. Attempts to assign universal meaning to the term “instability” have rendered it useless. It should be explicitly defined wherever it is used. Because treatment and outcome of spine injuries are integrally related to the neurologic status, definition of spinal stability in trauma should be centered on preservation of neural function. 
Historically, discussions of spinal stability have focused on the vertebral column and not on neural structures or neural function.67,86,125,277 For the cervical spine, a commonly advanced principle is that the functional spinal unit, composed of two adjacent vertebrae and their intervening ligaments and intervertebral disc, is stable if all anterior structures plus one posterior structure are intact or, alternatively, if all posterior structures and one anterior structure are intact.279 In this enticingly elegant rule, anterior structures are the vertebral body and the intervertebral disc and posterior structures are facet joints, laminae, spinous processes, and the posterior intervertebral ligaments. The rule is based on biomechanical laboratory studies where investigators applied opposing anteriorly and posteriorly directed forces to adjacent cadaveric vertebrae and sequentially sectioned each structure.279 This work was later summarized into a checklist to help clinicians evaluate cervical spine stability (see Table 43-13).280 
The White and Panjabi280 checklist for instability assessment is helpful in providing a framework for evaluating a spinal injury or other destructive lesions of the vertebral column. Although the elements scored in the assessment were compiled for the cervical region of the spine, similar anatomic, functional, and physiologic considerations also apply to the evaluation of thoracic and lumbar lesions. The checklist organizes the various considerations necessary in thoroughly analyzing a spinal injury and formulating the treatment plan for an individual patient. Calculation of a specific numerical instability score, however, does not provide a reliable cookbook formula for treatment determination. The scores are difficult to confidently calculate in actual patients with real injuries, and no clinical studies have confirmed the validity of the numerical score method for determining which injuries should be surgically stabilized. Also, in our opinion, neurologic considerations are likely to be undervalued in the checklist scoring method. If a patient has vertebral column disruption associated with a spinal cord injury, the stabilizing role of the vertebral column has failed, and in this setting, we most often will prefer surgical stabilization over nonsurgical treatments. 

Administration of Steroids in Acute Spinal Cord Injury

Three large-scale randomized clinical trials have investigated methylprednisolone in the treatment of spinal cord injury.3133 The first trial (NASCIS I) compared low-dose (100-mg bolus and 25 mg every 6 hours for 10 days) with high-dose (1000-mg bolus and 250 mg every 6 hours for 10 days) methylprednisolone administered within 48 hours of injury.31 The results showed no difference in motor or sensory outcome at 6 weeks, 6 months, and 1 year following injury. An increased infection rate was seen in the high-dose group. 
The second trial (NASCIS II) compared methylprednisolone (30 mg/kg loading dose and 5.4 mg/kg/h every 23 hours) with naloxone and placebo.32 The authors claimed statistically significant improvements in motor and sensory scores in both complete and incomplete injuries in the group receiving steroids. The magnitude of effect was small: neurologic change score (improvement in motor score) was 16.0 in the treatment group and 11.2 in the control group, with a P value of 0.03 for the difference. Pinprick score change was 11.4 in the treatment group and 6.6 in the control group (P = 0.02).32 These differences reached statistical significance because of the large sample size for the study. 
The third trial (NASCIS III) was reported in 1998 and compared the motor and sensory outcomes from spinal cord injuries when treated with the dose regimen shown effective in NASCIS II (30 mg/kg bolus followed by 5.4 mg/kg/h for 23 hours) versus an extended dose of methylprednisolone (same bolus dose with the infusion lasting 48 hours) versus an initial bolus of methylprednisolone with a 48-hour administration of tirilazad (a lazaroid with free radical scavenging benefit). The authors concluded that all three arms achieved equal benefit if the treatment was started within 3 hours of the injury. After 3 hours, but within 8 hours of injury, the extended dose regimen of 48 hours of methylprednisolone gave superior results. 
After their publications, the NASCIS trials were generally accepted by medical practitioners, and the dosing regimens of either NASCIS II or III were widely adopted. However, several limitations were brought forth by critics, and an ongoing conflict has yet to be resolved regarding the utility of steroids in spinal cord injuries. 
Critiques of the NASCIS trials are well developed in a number of publications.109,111,129131,227,255,257 In brief, the articles were criticized on a number of issues: statistical analyses, lack of standardizations in treatment, failure to show significant functional recovery, lack of minimum injury inclusion criteria, and an inability for independent reviewers to access the raw data for further investigation. 
In terms of statistical analyses, one key component was the development of the 8-hour cutoff in NASCIS II and the 0- to 3-hour and 3- to 8-hour window in NASCIS III. The original NASCIS II hypothesis included a plan for analysis of early versus late treatments. Although the critics are correct in stating that the exact times were selected from post hoc analyses, the 8-hour window was created since the median time to treatment was 8.5 hours. A similar argument concerns the development of the 0- to 3-hour and 3- to 8-hour window in NASCIS III. Researchers have requested the data to see whether the treatment is a time-limited effect (i.e., the earlier steroids are received, the more likely a better outcome regardless of a hard 3-hour or 8-hour window). Unfortunately, to date, no independent assessment of the data has been published. 
Function in both NASCIS II and III was measured as a motor score of seven muscle groups (using a 0- to 5-point scale) on both sides of the body. Only the scores from the right side were used for analyses. Improvement was graded as a percentage and not evaluated as a functional gain in NASCIS II. Although function was evaluated in NASCIS III, the improvements are modest and need to be weighed against the potential complications. 
No standard medical or surgical treatment regimen was created in any of the trials. Although this may reflect the implementations of the treatments in real-world settings, it opens the data to potential bias with unaccounted interventions. 
Finally, the use of high-dose steroids is not without a risk. National Acute Spinal Cord Injury Study III data showed the 48-hour regimen to result in a statistically significant increase in pneumonia and a trend toward increased severe sepsis. Further reports have additionally shown higher rates of complications (infection, pulmonary, gastrointestinal bleeding) in patients receiving high-dose steroids.167,202 
In short, since their publication, the NASCIS trials have undergone continued reevaluation with continued critiques and rebuttals from the lead author. As the criticisms mounted against the articles and the request for third-party review of the data has yet to appear, the acceptance of steroid use has declined. Hurlbert, one of the most vocal critics of the trials, and Hamilton131 document a dramatic turn in the use of steroids in spinal cord injury in Canada. Their survey suggests that in 2001, 76% of surgeons prescribed steroids for spinal cord injury (concerningly, many for reasons of “being sued or from peer pressure”). Five years later, the number had dropped to 24%. Similar trends are occurring in the United States, perhaps the most notable being the American Association of Neurological Surgeons/Congress of Neurological Surgeons joint statement on the Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries in which they concluded that there is insufficient evidence to support treatment standards or guidelines and the use of “methylprednisolone for either 24 or 48 hours is recommended as an option in the treatment of patients with acute spinal cord injuries that should be undertaken only with the knowledge that the evidence suggesting harmful side effects is more consistent than any suggestion of clinical benefit.”109 
The use of high-dose steroids in the setting of acute spinal cord injury is far from accepted. In patients evaluated after 8 hours from injury, the consensus is clear that there is no indication for steroid use. However, the use within 8 hours is still hotly debated and will likely require further randomized controlled studies for clarification of the issue. 

Limitations of Inferences from Biomechanical Studies

Biomechanical studies have advanced the understanding of much of orthopedics, including spinal injuries. These studies usually yield isolated observations related to injury mechanisms and their consequences, or the effects of various fixation constructs used to reconstruct the vertebral column. It is difficult to assemble these isolated observations into a cohesive or simple conceptualization of the mechanics of the spine. In fact, sometimes the results of experiments lead to seemingly contrary conclusions. For example, fractures of the C2 arch may result from hyperextension, hyperflexion, or both. The cervical spine facet joint capsules provide resistance to disruption in both flexion and extension. These differing results are partly due to the artificial conditions selected in the experimental design of biomechanical studies. Experiments are designed to answer individual questions, and experimental models simplify conditions in order to clarify interpretation of the results. Another limitation on the generalizability of experimental findings is the aim of homogeneity in experimental protocols. For practical considerations of limited time and resources, biomechanical experiments seek to minimize variation among individual specimens. Real-life injuries, on the contrary, may occur under conditions that are much more complex than experimental setups, and they may be highly influenced by individual variations. 
Despite these limitations of interpretability, some general principles are clear from biomechanical studies. Injuries with distraction between adjacent vertebrae require near complete disruption of essentially all intervening structural elements. As such, distraction injuries represent the most unstable injury pattern. Examples of these injuries are craniocervical dissociation, distracted fracture–dislocations, and displaced extension fractures in patients with ankylosing spondylitis or diffuse idiopathic spinal hyperostosis. These injuries are often associated with severe neurologic deficits, vascular disruption, stroke, and death. In these types of injuries, the static views in imaging studies are useful for identifying distraction as a crucial component of injury categorization, but the particular direction of displacement is not indicative of any mechanistic anterior, posterior, or lateral displacement; it is simply a reflection of the particular position of the patient at the moment the image was obtained. Patients with these injuries are susceptible to further deterioration during physical transfers for diagnostic studies. Furthermore, application of cervical traction, for obvious reasons, would exacerbate the injury. 

Future Directions

Injury prevention offers the best value return for interventions aimed at decreasing the medical and social burden of injuries.217,218 Strategies to prevent or minimize the functional loss include changing modifiable risk factors, altering the mechanics of the injury event, mechanisms of initial injury, or interrupting the ensuing deleterious biologic responses. Implementing injury prevention measures requires a high initial investment of resources. Success in these efforts is difficult to achieve and difficult to measure.287 

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