Principles of Spine Trauma Care

By admin Last updated May 2, 2024

Ovid: Rockwood And Green’s Fractures In Adults

Editors: Bucholz, Robert W.; Heckman, James D.; Court-Brown, Charles M.; Tornetta, Paul

Title: Rockwood And Green’s Fractures In Adults, 7th Edition

> Table of Contents > Section Three – Spine > 41 – Principles of Spine Trauma Care

Principles of Spine Trauma Care

Christina V. Oleson

Nathan E. Simmons

Sohail K. Mirza

INTRODUCTION

An undiagnosed or suboptimally managed spine injury can
result in a neurologic deficit and permanently impair a patient’s
function and quality of life, and in some cases may lead to death.
Additionally, 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 over 45,000 years ago are noted to forewarn that paralysis is incurable¹³⁷
and this remains true today, but that does not 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

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level continues to improve our understanding of the fundamental processes,²²²
and clinical research methods to study spinal cord injury in real
patient populations have improved, renewing optimism for novel spinal
cord injury treatments.²⁷⁸ 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

The meaning of terms commonly used to describe spinal cord injury depends on the context of the discussion.¹⁸⁴
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
etiologybased 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).
Or laceration, which describes 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 typically 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.²⁹⁵

FIGURE 41-1
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.

Mechanics of Neural Injury

Structural failure of the spinal column displaces 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.²⁵ 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.¹⁵¹

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.¹⁵⁰ 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.²⁵,²⁹⁰ Spinal cord tolerance for compression decreases as the velocity of compression increases (Fig. 41-1).¹⁵⁰ Minimum compression of the cord at high-contact velocity may produce severe anatomic injury and limited functional recovery.¹⁵⁰ At about 50% cord compression, functional recovery is minimal regardless of the contact velocity.¹⁵⁰
Although this threshold effect denotes an upper limit of compression in
the acute injury model, it is not apparent in 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 and yet
manifest minimal clinical symptoms.

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.²²⁸
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.²²⁸ Maximum stretching occurs between C2 and T1. Cord deformations may be more severe

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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.⁸²,²⁸¹
The preinjury spinal canal diameter, as measured on lateral radiographs
or sagittal magnetic resonance images (MRI), and the cross sectional
spinal canal area are important in determining the severity of cord
injury.¹⁸³,²⁸¹
A narrow spinal canal is associated with a greater likelihood of
neurologic injury and a higher probability of complete cord injury.
Cervical spondylosis can severely decrease the size of the spinal
canal, further predisposing 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.”¹⁴⁸ Although the mechanism of spinal shock is not established, it may relate to immediate depolarization of the entire cord.⁷⁵
The clinical examination more accurately reflects the neural injury
when spinal shock resolves and uninjured neural tissues neural
structures repolarize.

Blunt trauma to the spinal cord causes contusion of the neural tissue.²²⁵
As physical displacement of the spinal cord damages neural tissue, the
inner most regions of the spinal cord sustain the most severe injury.⁴²,²²⁶
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 41-1).
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.

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 dura can also lead to an apparent expansion of the
cord or progressive noncystic myelomalacia. These mechanisms may
contribute 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.²⁴⁹ The initial mechanical tissue disruption triggers a cascade of interrelated processes (see Table 41-1).
Local tissue elements undergo structural and chemical changes. These
changes in turn 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.²⁴⁹

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).¹⁷¹
Apoptosis depends on active protein synthesis and begins to occur as
early as 4 hours after injury. Programmed cell death 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.²²³
Cytoskeletal protein disruption in the axon membranes causes separation
of axons and necrosis ascending from the injury site (Wallerian
degeneration).²²³ Axons die back at approximately 1 mm per month.²²³
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).²²³

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.⁴⁸,⁴⁹ Ischemia also contributes to delayed secondary injury.⁹²,²⁷⁶ Severity of neurologic injury is also proportional to the duration of spinal cord deformation.²⁰⁹
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.²⁰³
Inflammatory response consists of polymorphonuclear cell infiltration
within 6 hours of injury and macrophage infiltration beginning at 24
hours following injury (Fig. 41-2).⁵⁰

The mechanism of cellular injury differs between white matter and gray matter.²²⁷ In the gray matter, disruption of the electrolyte balance may lead to anoxic cell injury.²⁶⁹ Intercellular sodium and calcium influx are key events in the pathogenesis of hypoxic-ischemic injury to neurons.⁹⁰,¹⁰⁸ Influx of these ions disrupts mitochondria and uncouples oxidative phosphorylation.¹⁴⁵ Some injury models have shown reversal of the normal sodium calcium exchange processes in anoxic cell injury.²⁶⁸
Incomplete conversion of oxygen to carbon dioxide in water results in
free radical formation, lipid poor oxidation, and membrane breakdown.¹²²,³¹⁴

Sodium and calcium exchange processes in injured neurons and axons have received a great deal of attention in spinal cord

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injury research. Sodium-calcium exchange mechanisms have been noted to operate in reverse following an acute injury.²⁶⁸
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 glutamic, 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.

TABLE 41-1 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 hour	Endothelial cell disruption
		Separation of endothelial junctions
		Vacuolation and swelling of endothelial cells
		Craters in capillary endothelium
1 to 6 hours	Necrotic changes in gray matter
		Cytoplasmic eosinophiliain in gray matter neurons
		Ghost cells
		Shrunken neurons, loss of Nissl bodies, irregular shape
		Eosinophilic changes in perikarya
		Apoptosis
4 to 8 hours	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 hours to 1 week	Edema formation
		Vasogenic edema
		Filtration edema
6 hours to 1 week	Inflammatory cell infiltration
		Neutrophil infiltration
		Monocyte infiltration
2 days to 2 weeks	Central nervous system reactivity
		Activation of microglia
		increased number of processes (pseudopods)
		Upregulation of surface antigens
		Phagocytic vacuoles
1 week to 4 weeks	Activation of astrocytes
		Hypertrophy
		Proliferation
		accumulation at margins of lesion
		Apoptosis in white matter
After 2 weeks	Cavity and scar formation (gliosis)
		Demyelination
		Inflammatory angiogenesis
		Formation of network of astrocyte processes
		Wallerian degeneration

Spinal cord axons also contain sodium and calcium exchange channels. Axonal injury leads to increased intracellular sodium.³
Reduction of extracellular sodium is a 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 voltagesensitive calcium
channels.³

The complex fundamental cellular processes initiated by spinal cord injury remain research tools for understanding cell

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physiology. At this time, this basic science research has not led to any clinical diagnostic or therapeutic interventions.

FIGURE 41-2 The inflammatory response begins within 4 hours of injury. Neutrophil infiltration precedes macrophage accumulation.

Regeneration of Nerve Tissue

Most patients with spinal cord injuries show some neurologic recovery.⁸⁸,²⁹²,²⁹⁶,²⁹⁷
It is not clear whether this recovery is related to resolution to 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.³¹⁵
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.³¹⁵

This spontaneous regeneration capacity of the central nervous system is more limited than that of the peripheral nervous system.²⁴⁹
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.¹⁴² 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.⁶⁴ Proteins that inhibit axonal growth limit regeneration in the spinal cord.²⁴⁹ Blocking these proteins enhances regeneration.³⁵

Research involving stem cell implantation relies on
pluripotential cells to recreate the complex microenvironment necessary
for neural regeneration.⁶,²⁴⁸,³¹¹
Although results in smaller animals and in primates are promising, this
technology has not yet advanced to large scale human trials.¹⁴¹,²²⁹

At least three separate randomized controlled trials of varying levels of evidence took place between 1999 to 2008.¹⁰³,¹⁰⁴,¹⁰⁵
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 group.¹⁰³,¹⁰⁴ Despite an earlier phase 1 trial of 37 patients that suggested encouraging findings,¹⁰⁵ this larger investigation failed to demonstrate significance in the predetermined primary efficacy analysis.¹⁰³,¹⁰⁴
All of those subjects received methylprednisolone according to National
Acute Spinal Cord Injury Study II protocol (NASCIS). In a
placebo-controlled study examining effectiveness of nimodipine, the
latter was used in combination to methylprednisolone and compared with
steroid alone and with placebo.²¹⁸
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 surgeries 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.⁷,²⁷,¹⁴⁶,¹⁶⁰,¹⁶¹ Cellular therapies remain unproven.²⁷,⁸⁸,¹⁶²,²⁶³,²⁸³

Mechanics of Cervical Spine Injury Fracture

Spine injury dynamics are complex and incompletely understood.²⁰¹
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. 41-3).²⁰²
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 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.¹³⁶
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.

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

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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.³⁰⁴,³⁰⁵
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 tomography (CT) scans performed
after the injury event.⁵¹,²⁸²
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.⁸²,⁸⁵,²⁸⁶

FIGURE 41-3
Timing of head and neck movement in impact injuries of the cervical
spine. Spinal column failure precedes head deflection in impact
injuries.

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.⁵¹ 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.²³⁸

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.²⁵¹

Craniocervical injuries are common in fatalities
associated with motor vehicle crashes, and most thoracic-lumbar
injuries occur between T11 and L2.⁸,¹¹⁴

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.²³⁰

The relationship of neurologic injury to the morphologic characteristics of the vertebral column injury pattern is inconsistent.³⁰⁴,³⁰⁵
In general, fracture-dislocations are associated with a neurologic
injury in majority of the 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 severe associated
neurologic deficit. This clinical association is consistent
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.²⁸² A time interval of 400 msec from zero to peak load results in 7% spinal canal encroachment with fracture fragments.²⁸² Decreasing this interval to 20 msec leads to 48% spinal canal encroachment.²⁸²

Extension-type injuries in the thoracic and lumbar region are rare in younger trauma patients.¹⁰⁹ However, they are common in patients with ankylosing spondylitis or diffuse idiopathic spinal hyperostosis (DISH).⁹⁴

An injury pattern distinct for the lower thoracic and upper lumbar segments is a “lap-belt” or “flexion-distraction” injury.⁵⁵,¹⁰⁷
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.¹⁰⁷ 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.³¹⁶ Total fracture incidence is 2.4% in patients with seizure disorders.³¹⁶

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.²⁴³ 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.²⁴³

ASSOCIATED INJURIES

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

Vertebral Column Injury

The most common injury sustained by patients that 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 multiply
injured patients.²³² 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.⁴³ The vertebral injury can occur at multiple noncontiguous levels in 15% to 20% of the patents sustaining a spinal injury.²⁸⁵ Often, patients with multiple spinal injuries have an injury to the cranial-cervical

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junction in addition to an injury in the lower cervical, thoracic, or
lumbar spine. Chest and abdominal injuries are common with fractures in
the thoracic and lumbar region. The incidence of concurrent abdominal
injury in association with cervical fractures is low, approximately
2.6%.²⁵⁷

Spinal cord injury rarely occurs in isolation. Of the
patients sustaining tetraplegia or paraplegia, 80% have concurrent
multiple system injuries and 40%-74% have associated head injury.⁶⁵,⁶⁶,²⁷⁹
The presence of a spinal cord injury dramatically affects a patient’s
chances of surviving the initial hospitalization and in achieving the
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.⁴³
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%.²⁸⁴
However, this figure is a substantial underestimate since many centers
are unable to attribute acute care deaths to spinal cord injury alone.
With complete ascertainment, the number is closer to 5%-10%.²⁹⁴ Improvements in acute care have been partially attributed to this modest improvement in survival following immediate injury.²⁶⁷

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 life-long social adjustments and supportive
care. Incremental loss of neurologic function disproportionately
increases disability.⁶³,¹⁸⁷
Since 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 41-2).²⁶ The highest risk occurs in patients who manifest a focal neurologic deficit (20%).²⁶
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 aged less than 50 years is 0.04%.²⁶
The same mechanism in a person aged greater 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.²⁶,⁴⁰

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.²³¹ The annual rate of trauma-related thoracic and lumbar fractures is approximately 15,000.¹¹⁴ Thoracic and lumbar fractures account for 30% to 50% of all spinal injuries in trauma victims.¹¹⁴
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.²²⁹
Although spinal cord injury is exceptionally rare with osteoporotic
fractures, neurologic injury occurs in one fourth of thoracic and
lumbar fractures associated with trauma.²³⁰ Many of these patients (37%) also sustain concomitant injuries to other regions of the body.

TABLE 41-2 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
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.

Spinal Cord Injury

Spinal cord injury occurs predominantly in young males.²¹⁰,²¹¹
The gender ratio is 4:1 (males:females), but data in recent years
indicate a growing percentage of females with spinal cord injury.¹⁴³ The mean age is 39.⁵
years and the median age 34. Within National Institute on Disability
and Rehabilitation Research funded Model Spinal Cord Injury Care
Systems, the percentage of persons over age 60 with spinal cord injury
has increased from 4.7% in 1980 to 11.5% since 2000.²⁸⁴

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Prevalence of traumatic spinal cord injury in the United States is estimated to be 525 to 1124 persons per million population.¹⁷,¹⁶³
Prevalence 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 seatbelts 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 which are fatal at the
scene.⁴³ 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.⁴³
Approximately 200,000 persons with trauma-related tetraplegia or
paraplegia currently live in the United States, and this population is
expected to increase due to an growing number of older patients with
spinal cord injury.¹⁶³

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%).¹¹⁹,²⁸⁴,³⁰⁹
Older individuals are more likely to sustain a cord injury from a minor
fall, such as a fall from standing height. Falls in persons of age
greater 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,²⁷⁴ with incomplete injuries outnumbering complete ones by nearly a 2:1 ratio.²⁸⁴
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%.²⁷⁴ 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 under age 15 account for 2%-5% of acute spinal
cord injury admissions, while 15%-20% of spinal cord injuries occur in
persons under age.¹⁸,⁷²,¹⁴³,²¹⁰,²¹¹
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 (SCIWORA) in the publications
preceding the use of MRI, may occur in nearly half of very young spinal
cord injury patients (42% of patients aged less than 9 years).⁷³ It is present much less frequently in patients with mature skeletons (8% of patients aged 15 to 17 years).⁷³ A majority of the younger patients (70%) with SCIWORA had an incomplete spinal cord injury.⁷³

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 less than 80% of the midbody vertebral body diameter) or a
pathologically narrow canal from osteophytes and degenerative changes.²⁴¹ 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 for 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-$3 million for persons injured at age 25 and $500,000 for
persons experiencing a spinal cord injury at age 50.²⁸⁴ In the United States, the aggregate annual direct medical cost of traumatic spinal cord injury is estimated at $7.74 billion.⁷¹
Although high-level tetraplegia (upper cervical segments) only
represents 10% of spinal cord injury patients, it accounts for 80% of
the direct medical cost of spinal cord injury.⁷¹ Paraplegia accounts for 4% of the overall aggregate cost, and incomplete injuries account for approximately 15% of the costs.⁷¹

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.¹⁴ 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 spine 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.²¹⁷ The head and 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

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drops. In such situations, the Kendrick Extrication Device has proven to be an effective means of spinal immobilization.³⁰⁶
It can also be used in pediatric patients needing accommodation for a
large occiput while maintaining neutral spine positioning.¹⁸⁰ Immobilization with cervical collar, sandbags, tape, and spine board is superior to immobilization with a collar alone.¹¹⁵
For field transportation of injured patients, log-rolling still allows
motion at the spinal injury site, and a scoop-stretcher is useful
adjunct to the spine board.¹⁸⁶ Cervical extension should be avoided since it narrows the spinal canal more than flexion.⁵⁶ Neutral flexion-extension head and neck alignment is optimal during prehospital transport of cervical spine injury patients.²¹⁷
To maintain neutral head-neck alignment, the relatively larger head of
pediatric patients should be accommodated with elevating the trunk on
padding or using a special pediatric spine board containing a cutout
for the occiput.¹² 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.¹³,⁷⁶,¹⁰²,¹⁹⁰

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 41-3).³⁰,³¹,³³

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.²⁴⁹
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 41-4).³¹,³²,³³,¹⁰⁵,²¹⁵,²¹⁶,²²¹

TABLE 41-3 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 hours if bolus given within 3 hours of injury.

Infusion for 48 hours if bolus given within 3 to 8 hours after injury.

No benefit if methylprednisolone started more than 8 hours after injury.

No benefit with naloxone.

No benefit with tirilzad.

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.

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.¹²¹ Three large-scale randomized clinical trials have investigated methylprednisolone in the treatment of spinal cord injury.³¹,³²,³³ 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 23h) to
naloxone and placebo.³²
Statistically significant improvement in motor and sensory scores in
both complete and incomplete injuries occurred in the group given
methylprednisolone.³² 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.³² 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; 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 on
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
as significant for future work in this area.

Other pharmacologic treatments have not shown sufficient
promise in the clinical trial stage to become established interventions.¹⁰⁵,²¹⁵,²¹⁶ Lazaroids are one category of candidate drugs. Lazaroids are 21-amino-steroid 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.¹⁰⁵
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:

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TABLE 41-4 Randomized Clinical Trials of Pharmacologic Treatment of Spinal Cord Injury

Year	Author	Number of Patients	Treatment Groups	Clinical Neurologic Improvement	Functional Improvement
1984	Bracken³¹ (NASCIS I)	306	High-dose methylprednisolone Low-dose methylprednisolone	No	Not measured
1990	Bracken³² (NASCIS II)	487	Methylprednisolone Naloxone Placebo	Yes	Not measured
1991	Geisler¹⁰⁵	34	Ganglioside GM1 Placebo	Yes	Not measured
1995	Pitts²¹⁶	20	Thyrotropin Releasing Hormone (TRH)	No	Not measured
			Placebo
1997	Bracken³³ (NASCIS III)	499	Methylprednisolone for 24 hours Methylprednisolone for 48 hours Methylprednisolone and Tirilazad	Yes	No (FIM: Functional Independence Measure)
1998	Petitjean²¹⁵	166	Nimodipine (calcium channel blocking agent)	No	Not measured
			Methylprednisolone
			Both
1998	Potter²²¹	26	Fampridine SR (potassium channel blocking agent)	Yes	No (FIM: Functional Independence Measure)
			Placebo
2001	Geisler¹⁰⁴	687	Monosialotetrahexosylganglioside GM-1sodium salt (Sygen)	No significance in predefined primary analysis at 26 weeks; subgroups showed benefit in selected groups	No for primary analysis, yes for selected subgroups (Benzel Scale)
2005	Knoller¹⁵⁶	8	Incubated autologous macrophages	Yes, ASIA grade improvement	Not performed
2009	Lammertse¹⁶⁰	50	Incubated autologous macrophages	ASIA grade, analysis pending	Analysis pending

Assessment of gross neurologic function
by report from field personnel, direct observation, or initial gross
examination during primary survey,
Diagnosis of severely unstable injuries
such as fracture-dislocations or distractive injuries on trauma
radiographs that include lateral cervical spine radiograph and
anteroposterior (AP) chest radiograph, and
Assessment of hemodynamic parameters for potential neurogenic shock.

Spinal cord injury can complicate resuscitation.¹⁴
Loss of vasoconstrictive sympathetic control of the peripheral
vasculature can accentuate hemodynamic effects of hemorrhage.
Nonetheless, recognizing neurogenic shock as distinct from hemorrhagic
shock is critical for safe initial resuscitation of a trauma patient (Table 41-5).¹⁴,¹⁶⁷
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.⁶⁰ Because of these complicated

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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 3-7, findings suggest favorable
neurologic recovery in patients whose main arterial pressure is
maintained above 85 mm Hg.²⁸⁸

TABLE 41-5 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
^*Penetrating spinal cord injuries rarely cause neurogenic shock.³¹⁷ The injured spinal cord cannot autoregulate blood flow.⁷⁹
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.

TABLE 41-6 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

Spinal cord injury itself increases the risk for 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.¹⁶⁷ Normal hemodynamics, on the other hand, 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 41-6 and 41-7).

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. 41-4).¹⁵,¹⁴⁷,¹⁸⁴,¹⁹⁷
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 (Table 41-8).
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.¹⁴⁷,¹⁸⁴,¹⁹⁷

TABLE 41-7 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

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 log-rolling 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 seatbelt or
steering-wheel induced injury.

The elements of neurologic examination selected as
minimum necessary assessment by ASIA were chosen because of their
reproducibility.¹⁵,¹⁴⁷,¹⁸⁴,¹⁹⁷
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

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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 since 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 41-9).

FIGURE 41-4 Neurologic examination recommended by ASIA.

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. The ASIA definitions have provided guidance for use of these
terms with greater clarity (Table 41-10). These
specific definitions will hopefully improve categorization of spinal
cord injury patients in scientific communication and allow more
meaningful analyses of collective experience.

According to ASIA definitions, neurologic injury level
is the most caudal segment of the spinal cord with normal motor and
sensory function on both sides: right and left sensation, right and
left motor function (see Tables 41-8 and 41-9).¹²⁸,¹⁸⁴,¹⁹⁷ Complete injury is defined by the absence of sensory and motor function in the lowest sacral segment.¹⁵,¹⁸,¹²⁸,¹⁴⁷,²⁹⁵
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 3 levels below the designated motor level of
injury (Table 41-11). Details of the examination grading are described in Table 41-8.

Distal motor function and sacral sparing are important for prognosis.²⁶⁰ Sacral sensory sparing predicts improvement in neurologic status.¹⁵⁴ Sacral pinprick sensation at 4 weeks postinjury

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carries an improved prognosis of regaining the ability to walk even in patients who are initially motor complete.⁶²,²⁰⁶
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 (Table 41-12).²⁰⁶

TABLE 41-8 Neurologic Assessment Recommended by the American Spinal Injury Association

Examination	Method	Testing Locations	Grading
*Required Elements of ASIA Neurologic Impairment Assessment*
Pinprick (sharp/dull)	Discriminate sharp and dull ends of a standard safety pin	28 dermatomes specified by designated bony prominences	0, 1, 2, NT
Light touch	Identify contact with a cotton swab tip
Deep anal sensation	Digital rectal examination	Pressure on rectal wall	0, 1 (absent, present)
Key muscles	Patient is in supine position	10 key muscles	0, 1, 2, 3, 4, 5, 5^*, NT
*Optional Elements of ASIA Neurologic Impairment Assessment*
Joint movement appreciation (proprioception)	Support proximal portion and move distal portion by gripping medial and lateral edges	Wrist Thumb interphalangeal joint Small finger proximal interphalangeal joint Knee Ankle Great toe interphalangeal joint	0, 1, 2, NT
Deep pressure sensation	Apply pressure with thumb or index finger	Wrist radial styloid Thumb nailbed Small finger nailbed Ankle medial malleolus Great toe nailbed Small toe nailbed	0, 1 (absent, present)
Diaphragm	Observe under fluoroscopy	Movement over two or more interspaces	0, 1 (absent, present)
Deltoids	Shoulder abduction	C5-C6 ± 4	0, 1, 2, 3, 4, 5, 5^*, NT
Abdominal muscles	Observe movement of umbilicus (Beevor sign: umbilicus moves up in T9-T11 lesions)	T6-T12	0, 1, 2, 3, 4, 5, 5^*, NT
Hip adductors	Palpate adductor longus	L2-L3	0, 1, 2, 3, 4, 5, 5^*, NT
Hamstrings	Knee flexion	Pleurisegmental	0, 1, 2, 3, 4, 5, 5^*, NT
Motor Grades
Score	Description
0	No visible or palpable contraction
1	Any visible or palpable contraction
2	Able to move full range of motion of joint with gravity eliminated
3	Able to move full range of motion of joint against gravity
4	Able to move full range of motion of joint against some resistance
5	Able to exert sufficient resistance to be normal according to examiner’s judgement
5^*	Normal according to examiner’s judgement if inhibiting factors were not present
NT	Not testable
Sensory Grades
Score	Description
0	Absent → unable to distinguish
1	Impaired → able to distinguish but intensity is abnormal
2	Normal
NT	Not testable
From American Spinal Injury Association. Standards for neurological classification of spinal injury. Chicago: Author; 1996.

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TABLE 41-9 Definitions of American Spinal Injury Association Impairment Scale Categories

A	Complete	No motor or sensory function in the lowest sacral segment (S4-S5)
B	Incomplete	Sensory function below neurological 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
From American Spinal Injury Association. International standards for neurological classification of spinal injury. Atlanta, GA: Author, 2008.

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 re-evaluated 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, MRI to
identify structural neural tissue disruption, and sensory or motor
evoked potentials to assess function in neural pathways.⁹⁵,⁹⁶,⁹⁷
Several reports suggest that presence of intramedullary hemorrhage at
the time of initial spinal cord injury is indicative of a poor
prognosis,²⁴⁶,²⁴⁷,²⁵⁰ with many subjects remaining complete⁹⁶ or at least motor complete.¹⁷⁹
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.²⁸,⁹⁶
One report found that a hemorrhage longer than 4 mm suggested poor
neurologic recovery, but smaller ones were not as ominous for prognosis.²⁸ Miyanji et al.¹⁹⁴ 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 patient¹³⁵ or in children,¹⁹⁷ findings may not translate to motor function, given the location of assessment at the dorsal columns.

TABLE 41-10 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
Neurological 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.
From American Spinal Injury Association. International standards for neurological classification of spinal injury. Atlanta, GA: Author, 2008.

Spinal shock is a term that accounts for much confusion in the assessment of spinal cord injury patients.⁷⁵ Spinal shock refers to depressed spinal reflexes caudal to spinal cord injury.⁷⁵
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.⁷⁵ The
confusion surrounding the concept of spinal shock is responsible for
some complacency during the management of spinal cord injury patients
during the initial few hours following injury, the time interval where
intervention may have the most beneficial results. Spinal shock may
involve immediate depolarization of the axonal membranes from kinetic
energy of the injury.¹⁴⁸ 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.¹⁴⁸

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The difficulty for practitioners is the varying definitions of spinal shock and different interpretations of its resolution.⁷⁵
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 life-saving measures. Moreover, it may be
several days before the next series of reflexes (bulbocavernosus,
cremasteric, or anal wink) are observed.

TABLE 41-11 Descriptions of Incomplete Spinal Cord Injury Patterns

Syndrome	Lesion	Clinical Presentation
Bell cruciate paralysis	Long tract injury at the level of decussation in brainstem	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 the lower limbs
Brown-Séquard	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
From American Spinal Injury Association. International standards for neurological classification of spinal injury. Atlanta, GA: Author, 2008.

During the first 24 hours, prognosis for neural recovery may not be reliable due to issues of somnolence, pain, and possible

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substance abuse withdrawal.⁴⁵ Patients have also been known to worsen in the first 72 hours as maximal cord swelling is reached.³⁸,⁴⁴,⁴⁵
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.²⁹⁵
Suspending treatment interventions until resolution of this depressed
reflex state may waste a potentially timesensitive opportunity to
arrest or diminish the secondary injury process in patients with spinal
cord injury.¹⁹³

TABLE 41-12 Ambulation According To ASIA Grade

ASIA Grade	Baseline Exam	Rates of Ambulation
ASIA A tetraplegia²⁹⁶	<30 days	0% community at 1 year
ASIA A paraplegia²⁹⁵	<30 days	5% community at 1 year (no subjects above T9 NLI)
ASIA B with Pinprick in: >50% LE dermatomes	<72 hrs	67% household only at 1 yr 40% community & HH at 1 yr
ASIA B with Pinprick in: <50% LE dermatomes²⁰⁶	<72 hrs	16% community & HH at 1 yr 40 % household only at 1 yr
ASIA C^45a Under age 50	<72 hrs	91% at least HH at time of discharge from rehab hospital
ASIA C^45a Age 50 or older	<72 hrs	42% at least HH at time of discharge from rehab hospital
ASIA D^45a All ages	<72 hrs	>95% community ambulation at discharge from rehab hospital
HH, household; NLI, neurological level of injury.

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. All trauma patients are at risk for spinal injury.
Two to 4.6% of patients presenting with blunt trauma have cervical
spine injuries.⁵³ 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.¹⁴⁴
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 41-13).²⁶

The necessary elements for a complete spine evaluation are:

History to assess for high-risk events and high-risk factors.
Physical examination to check for physical signs of spinal injury or neurologic deficit.
Imaging studies based on an initial evaluation.

Radiographs are not necessary for alert patients who are
not intoxicated, provided they have an isolated blunt trauma without
neck tenderness on physical examination.¹³³ However, this estimate of “no false negatives” is based on small numbers of patients with fractures.¹³³
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.¹³³ 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)
criteria¹³² and the Canadian C-spine Rule²⁶⁵ (Fig. 41-5).
The Canadian C-spine injury prediction rules have better sensitivity
and specificity and reduce unnecessary imaging to a greater extent,²⁶⁴,²⁶⁵ but they are more complex to apply routinely.¹²⁹,¹³⁰,¹³¹,¹³²,¹³³ Applying Canadian C-spine rules in the field may prevent 38% of out-of-hospital spine immobilizations.²⁶

Spine injury may be difficult to recognize in a patient with altered mental status.¹⁷⁴,¹⁷⁵ 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.²¹⁴ 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.²⁴ 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.¹⁸⁹
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.²³⁷

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.⁸³ Patients with missed fractures can develop neurologic deterioration.⁸³,²⁹⁴ Assessment of cervical spine is an essential component of the advanced trauma life support system of trauma care.¹⁴
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 is 1% to 5% in screening radiographs.⁸³
Standard imaging (three views of the cervical spine and CT 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.⁸³ The sensitivity of the lateral radiograph alone is 83% and specificity is 97%.¹⁷³ The addition of open-mouth and AP view increases the sensitivity to approximately 100%.¹⁷³

Cervical radiographs in a trauma patient are performed
with the patient supine and secure on a backboard. The patient is not
moved to position 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. 41-6 and 41-7).¹²⁵

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 they are of
adequate quality for the intended purpose. Lower

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quality films significantly increase error rates.²¹³
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. 41-8).

TABLE 41-13 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 old. 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 greater than 20 degrees on flexion-extension views or at least 11 degrees more than functional spinal unit (FSU) above or FSU below the injured level on a static view.
4.	Criteria for a positive stretch test: more than 1.7 mm difference in interspace separation pre- and posttest or more than 7.5 degrees angulation with 25 pounds 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 AP diameter less than 15 mm or Torg-Pavlov ratio less than 0.80 (Normal > 1), where: Torg-Pavlov ratio = (distance from midlevel posterior vertebral body to nearest point on spinolaminar line)/(midlevel vertebral body AP 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, 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.

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.

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FIGURE 41-5 Comparison of NEXUS Criteria and Canadian C-spine Rule for avoiding imaging in alert, examinable trauma patients.

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 measurements based on the distance between the
dens and the basion are probably the simplest and most reliable
measurements for identifying craniocervical dissociation.¹²⁶ Suspicion of injury and careful scrutiny of radiographs minimizes errors of missed injury.²²⁴

In patients with cervical tenderness and normal plain
radiographs, flexion-extension views can identify occult cervical
ligamentous injury (see Fig. 41-7).
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
performed in alert patients, under supervision, and with voluntary
unassisted positioning by the patient.

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FIGURE 41-6 Standard radiographs of the cervical spine.

Interpretation of radiographs has limitations. Knowledge
of anatomy and clinical experience are important for accurate
interpretation of radiographs.¹⁹⁹
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.¹⁹² Prevertebral soft tissue widening resolves to normal after 2 weeks in 50% of patients, and in 3 weeks in 90%.²¹³

FIGURE 41-7 Flexion-extension radiographs.

Computed Tomography

CT and MRI may be useful together in determining presence and extent of spinal column injury.¹⁶⁹
MRI is superior in demonstrating spinal cord pathology and
intervertebral disc herniation. CT 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 images. For

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these types of injuries, direct coronal CT can provide superior demonstration of skeletal features in the upper cervical spine.²¹²

FIGURE 41-8 Images from a screening cervical spine CT.

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.²⁸,⁹⁶,⁹⁷,¹⁷⁹,²⁴⁶,²⁴⁷
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.⁴¹
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.²⁷⁸
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 anterior longitudinal
ligament and ligamentum flavum.¹¹¹
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.¹¹¹ If increased MRI signal is not present in all four regions, correlation with unstable injury is lower.¹¹¹

MRI also provides noninvasive assessment of the
vertebral artery blood flow in cervical trauma, which can be frequently
disrupted in cervical spine injuries.¹⁰⁰ MR angiograms are abnormal in 24% of patients.¹⁰⁰ However, MR diagnosis of arterial artery may not be functionally significant.²⁵⁵

Sequence of Imaging Studies

Clearing the spine frequently requires considerable time, with one study reporting a median time of 15 hours.⁵⁹
Patients often need emergent care and transport prior to the spine
being cleared. Emergent life-saving 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.¹⁴
Obtaining an AP chest radiograph, AP pelvis radiograph, and a lateral
cervical spine radiograph does not interfere the urgent management of
multiply 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 only necessary 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 CT for initial cervical spine imaging in trauma
patients since radiographs. Cervical spine CT is frequently performed
in conjunction with head CT. CT imaging adds diagnostic information in
approximately half of the injuries identified on plain radiographs.⁵⁸

Complete cervical spine radiographs in addition to the
initial trauma lateral radiograph are completed once the patient is
medically stable (see Fig. 41-5). 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. 41-7).¹²⁴
Patients with an incomplete spinal cord injury may require an emergent
MRI to identify the source of cord injury, if radiographs and CT do not
show vertebral column injury consistent with the neurologic exam.²³⁶

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.⁸¹ Many surgeons cite
this report as justification for obtaining prereduction MRI in 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.¹¹³
In patients with spinal cord injury associated with cervical spine
fracture-dislocations, the most urgent priority after life-saving
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.¹¹³
Waiting for MRI in this setting should not delay closed reduction.
Other interventions or other diagnostic tests for nonlife-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.²³⁹

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Neurologically intact patients with a cervical spine
dislocation do not have the time-urgency of spinal cord injury. In
these patients, MRI may be obtained prior to reduction without
adversely influencing outcome. The disc at the level of dislocation is
usually abnormal on these images.⁷⁸
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, MRI or a
technetium bone scan can facilitate diagnosis of occult injuries.²²,⁹⁴

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.¹²⁷
When the CT scan is difficult to interpret due to severe degeneration,
osteoporosis, DISH, 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 neurologic deterioration occurred
after admission in 5% of spine injury patients.¹⁸¹ An identifiable specific management event is associated with 86% of these deteriorations.¹⁸¹ Unstable spinal injury should be assumed and the patient protected.¹¹⁶
Log-rolling does not keep the spine immobile, and unstable injuries
should be stabilized immediately when the patient’s medical condition
permits doing so safely.¹⁸⁶
Extremely combative patients with 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 for missed or delayed diagnosis of cervical spine injury at trauma centers is from less than 1% to 4.9%.⁶⁷,⁸³,¹⁸¹ Most patients with missed injuries or delayed diagnosis (71%) suffer no adverse consequences.⁶⁷ However, patients who deteriorate from a missed injury (29%) may have severe complications.⁶⁷ These complications range from death (20%) to quadriplegia (40%) or other new neurologic deficit (40%).⁶⁷

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%.¹⁸⁹ A
thoracolumbar fracture may not be recognized despite complaints of back
pain by 66% of these patients during their initial evaluation.¹⁸⁹
Patients with a missed thoracolumbar fracture that do not complain of
back pain have either altered mental status or other major associated
injuries.¹⁸⁹ 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 41-14).
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.

Treatment Priorities

Errors in the initial care of spinal injury patients can have catastrophic or fatal outcomes.⁶⁷ Minimizing these errors requires management of spinal injury patients at highly specialized centers with experienced personnel.²⁴⁰ Spinal cord injury patients in particular benefit from early transfer to a trauma center with a spinal cord injury unit.²⁰⁴ Early referral to a spinal cord injury center improves patient survival and neurologic recovery.⁶⁰,¹⁵³

Management of spinal injuries in multiply injured
patients requires concerted activity of a trauma team. Experienced
field personnel, emergency room physicians, general surgeons,
orthopaedic 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,
frequently orthopaedic surgeons

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and physiatrists, are particularly critical in directing optimal initial care.¹¹²

TABLE 41-14 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

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 at strict bedrest with the bed flat,
transfers with a spine board, and frequent log-rolling 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 in strict bedrest with full spine precautions
until definitive surgical stabilization.

Traction pins for 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 pounds. Pins in steel tongs
can withstand traction up to 140 pounds.¹⁵⁷
On occasion, if closed reduction in a cervical injury requires weights
greater than 80 pounds, carbon fiber tongs may be exchanged for steel
tongs prior to applying heavier weights.

Closed Reduction

Closed reduction in cervical spine injuries is safe and effective.¹¹³,¹⁵⁵ Successful reduction may require weights as high as 140 pounds.²⁴⁴
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.²⁴⁴ Cervical
traction at weights larger than 80 pounds should not be applied to most
carbon fiber MRI compatible tongs; traditional steel Gardner-Wells
tongs are less like to slip with larger weights.¹⁵⁷ 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.⁶⁸
The window of opportunity for maximal neurologic improvement through
decompression may be as short as the first few hours following spinal
cord injury.⁴⁸,⁴⁹,⁵⁰,⁶⁸ 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.²⁷⁰
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 2-3 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.⁸⁹,^91a,¹⁶¹,^162a

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.²⁵⁹ In these patients, MRI is not necessary prior to reduction and should not delay reduction.¹⁶⁵
Reduction in an unconscious or unexaminable patient should be preceded
by an MRI scan. In this situation, the presence of a herniated disc may
be treated with surgical decompression before reduction.⁸¹,²³⁶

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.¹⁹⁶

Reduction improves stability, preventing neurologic deterioration in the interval preceding definitive treatment.¹⁷⁶ Closed reduction can also improve neurologic recovery.²⁵⁴ Although case reports have described neurologic deterioration during reduction,²⁰⁵ larger series of closed reductions have not observed neurologic deterioration.⁶¹,¹¹³
In fact, a case in one of these series was of patient with a large disc
herniation seen on a prereduction MRI scan resolved with closed
reduction.¹¹³ Closed reduction also decreases the need for more complicated surgical procedures later.²⁶⁹

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 bedrest or external immobilization. Unstable ligamentous injuries
require fusion. Osseous injuries heal adequately but require treatment
to control deformity.

Closed treatment options are bedrest, halo apparatus, external orthosis, or cast.⁸⁴
Bedrest as definitive treatment may be indicated in rare cases of
patients unable or unwilling to undergo bracing or surgery: severe
pre-existing deformity, morbid obesity, medical comorbidity, or
personal preference. Bedrest for the initial few weeks preceding
bracing is an option for severely unstable injuries. If bedrest 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 bedrest for undefined periods of
time.⁶⁰,¹⁵⁹

The level of injury serves as a guide for the category of external orthosis. Most commercially available braces within each

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category are equivalent.²³
Custom molded trunk orthosis 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 residual
compressive mass effect may additionally allow better neurologic
recovery. Closed treatment of unreduced injuries may lead to chronic
pain requiring later surgical treatment.²³

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. 41-9).⁴⁸,⁴⁹,⁶⁸

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 fusion for spinal fractures.²⁰⁸ Early surgery reduces hospital stay.²⁰⁷

Earlier studies reported high complication rates with anterior cervical surgery.²⁶¹
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.²⁸⁹ Anterior plating and posterior plating are equally successful in cervical trauma.⁹¹,¹¹⁰ Anterior plating provides immediate stabilization even with posterior ligamentous injury.⁵²
Although the strength of the fixated spine is relatively unchanged by
corpectomy and anterior grafting, anterior grafting improves alignment.¹⁷⁷ Fixation maintains alignment.¹⁹⁵ Anterior fusion allows early mobilization, shorter stay, and less cost.²⁷¹ Spinal cord blood flow may, however, be adversely affected by an anterior surgical approaches.

FIGURE 41-9 Electrophysiologic recovery diminishes with longer duration of cord compression.

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.¹⁷⁸ In burst
fractures, anterior reconstruction with fixation is more stable than
the posterior instrumentation systems in all loading conditions.²⁵³

The choice of the operative method in thoracolumbar
fractures should not be based on any hypothetical differences in
reductive power.⁸⁶,²⁹¹
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%.¹⁰⁸ Percentage of encroachment decrease in posterior systems is small.⁵⁵ Laminectomy increases deformity and neurologic deficit unless combined with internal stabilization.⁴⁶,²⁶¹ Traumatic dural tear should be repaired before any anterior or posterior spinal reduction maneuver.⁷⁰

If spinal canal decompression is the goal, this is best achieved through an anterior approach.¹¹,¹⁴⁹
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.¹⁸⁵,²³²

Transpedicular fixation provides solid internal fixation that is circumscribed to the injured vertebral segments.¹⁹¹
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.⁸⁰,¹⁸⁸
One option to reduce risk of hardware failure prior to solid fusion is
to augment transpedicular constructs with anterior bone grafting.⁴⁷,²⁵²,²⁵⁶ 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 to risk of
infection and gastrointestinal bleeding complications. We recommend a
screening CT to image the cervical spine in obtunded patients, and
discontinuing cervical spine immobilization and mobility precautions if
the study is normal (Fig. 41-10). 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.

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.

Solicit observations of neurologic function at the scene and en route from the field personnel and the paramedic team.

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Suspicion of neurologic injury may help prioritize subsequent care. Record the source of information in medical record notes.
Personally review outside imaging studies; do not assume studies were adequate or interpretation was accurate.
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.
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.”
Look for thoracic fracture-dislocation on
the trauma AP chest radiograph: lateral translation between vertebrae
or widened disc space.

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Perform a neurologic examination
unobtrusively during resuscitation, if possible, prior to intubation or
pharmacologic paralysis. Identifying a neurologic deficit may change
treatment priorities.
Record personal neurologic examination
accurately in the medical record: moving all extremities (MAE),
neurovascular intact (NVI), and “wiggle your toes” are not adequate
assessment or documentation of neurologic function.
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.
Do not attribute neurologic deficit to
intoxication, effect drugs, or pain from extremity injuries. This
dangerous assumption that may limit proper management of neurologic
injury.
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 appropriate acute treatment of
spinal cord injury.
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.
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.
Do not delay closed reduction of a
dislocated cervical spine in a patient with complete tetraplegia. Delay
to obtain CT, MRI, 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.
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.
Use traction tongs, weights, and pins
compatible with MR. Some pins and tongs may develop heat, displace, or
cause interference with the image.
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.
Look for associated injury patterns. A
patient with a flexion-distraction injury will frequently have lapbelt
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.
Look for additional levels of spinal injury. Approximately 15% of patients have multiple discontiguous levels of spinal injury.
Remove the backboard within 2 hours of
application; pressure sores can develop in patients laying on a
backboard for more than 2 hours.
Consider age and mechanism of injury before allowing a patient to be discharged home without additional evaluation.

FIGURE 41-10 Dartmouth Spine Clearance Protocol.

COMPLICATIONS

This first principle of all medical treatment is “do no harm.”⁸⁷
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 41-15).⁹⁸
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.⁹⁸

TABLE 41-15 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.

OUTCOMES OF SPINE INJURY

Pain and Function

Neurologic status determines end-results following spinal injury.¹⁸⁷,²⁰⁰
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.³⁶,¹⁶⁶,²¹⁹,²²⁰ Nonsurgical treatment of neurologically intact patients is associated results equivalent to surgical treatment.⁵⁷,¹⁹⁸,³⁰⁷ Anterior and posterior surgery yield equivalent function in neurologically intact patients.³⁰⁸ In the absence of neurologic injury, pain and function approach population norms at 3 to 8 years following the injury.¹⁶⁶

Despite strong convictions of surgeons who treat
patients with spinal cord injury, clinical studies have not shown an
association between neurologic and skeletal outcome.⁷⁷ Clinical outcome in general is not related to deformity.¹¹,²⁰⁰,²⁷²
Kyphosis of more than 30 degrees may increase pain, but this threshold
is based on a impressions of surgeons, not rigorous clinical research.¹⁰⁶ Residual canal occlusion does not result in late symptoms of spinal stenosis.

Neurologic Recovery

Outcome of spinal cord injury is predominantly determined by patient age and severity of neurologic injury.²⁶⁶,²⁸⁴ Most common causes of death are respiratory disease, sepsis, and cardiovascular disease.¹⁶⁸,²⁸⁴
A recent report identified several important secondary health
predictors that significantly improved prediction models of mortality
when compared with

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injury severity models alone.¹⁵⁸
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%-100%).⁴,³⁰¹
In contrast, over 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 41-16).²⁶⁶ Older age at time of spinal cord injury is also associated decreased survival (Table 41-17).¹⁶⁸

TABLE 41-16 Life Expectancy Following Spinal Cord Injury, for Those Surviving the Initial 24 Hours

Age at injury (years)	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.) NLI, neurological level of injury.

Prognosis for neurologic recovery is determined by
nature and magnitude of initial injury. The pattern of spinal cord
injury does not correlate with the pattern of skeletal injury on plain
radiographs.²⁶⁶ Cord hemorrhage is
associated with less neurologic recovery. When controlling for
neurologic level (paraplegia versus tetraplegia) and completeness of
spinal cord injury, motor recovery does not differ for type of injury
(penetrating versus nonpenetrating) or type of fracture.²⁹⁸
Complete cord injuries are more likely in flexion-rotation patterns of
injury, bilateral facet dislocation, and gunshot injury with bullet
traversing the canal. Incomplete injuries are associated with
pre-existing spondylosis and gunshot injury with bullet not traversing
the canal.²⁹⁸ 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.¹⁶⁴
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.⁷⁵ Pediatric patients with incomplete injuries have a good prognosis; neurologic deficit improves in 74% and resolves in 59%.¹²³ Pediatric patients with complete injuries show improvement in 10% and resolution in none.¹²³

TABLE 41-17 Life Expectancy for Persons with SCI Surviving at least 1 Year Postinjury

Age at injury (years)	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
<30y	43	53.0	45.5	40.8	36.9	25.1
30-50y	24	34.5	27.9	23.9	20.8	12.2
>50y	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.) NLI, neurological level of injury.

Some complete lesions show recovery.⁹⁹ Patients with complete injuries frequently gain one or two levels: 32% gain one level and 18% gain 2 levels.³¹² The average motor score increase after complete tetraplegia is 9 points at 1 year.²⁹⁶ While a large multicenter trial by Fawcett et al.⁸⁸
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, due to challenges
affecting the reliability of the early examination. In contrast, only
2.6% of subjects without factors impeding accuracy of early exam
converted to sensory incomplete and no subjects were upgraded to motor
incomplete.⁴⁵

Late conversion of complete to incomplete spinal cord injury

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can occur. Early studies suggest approximately 4% of injuries complete
at 21 days convert to incomplete. Three of 6 patients with late
conversion regained bladder and bowel control and 2 regained the
ability to ambulate.²⁹⁹
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.¹⁵²
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 T9.²⁹⁹ With a more caudal level, 38% regain some lower extremity motor function.²⁹⁹
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 ASIA motor score and walking ability (see Table 41-12).²⁹⁷
Incomplete injuries carry a much better prognosis for recovery than
incomplete injuries. For example, most patients with Brown-Séquard type
of incomplete tetraplegia ambulate independently (75%) and nearly all
regain bladder and bowel control.²⁴²
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.²⁹⁷ Nearly half (46%) of these patients are able to ambulate with a reciprocal gait.²⁹⁷

SPECIAL CONSIDERATIONS

Children

Significant spinal cord injury can result from trama without any fractures or ligamentous ruptures.²³⁶ SCIWORA commonly occurs in children less than 10 years old.⁷³
Mechanism of injury is likely physeal failure through a fracture in
hypertrophic zone of endplate, leading to distraction of 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.²⁹³
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 due to bulging ligamentum flavum.²⁷⁶ Two thirds of patients are over 50 years old.²⁴
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 more than 65
years of age.¹⁷² C2 injuries, especially odontoid fractures, must be ruled out in older patients with neck pain after even a minor injury.¹⁷²,²⁵⁸ Overall mortality rate these patients is 26%.⁴ Patients older than 50 years of age with complete spinal cord injury have a 60% mortality rate.⁴,⁵,²⁵⁸ Injury severity decreases survival, particularly in older patients.¹¹⁷ Bedrest, traction, and halo immobilization are poorly tolerated by older people.¹⁷⁰

Gunshot Injuries

Gunshot injuries rarely cause spine instability.²⁹ Location of bullet is not associated with neurologic prognosis.²⁹⁸ Decompression does not improve recovery if the projectile traverses the canal without residual mass effect on neural elements.²⁶² Surgery risks neurologic deterioration.³¹³
Surgery may be necessary for dural repair in patients with a
cerebrospinal fluid leak or fistula. Débridement 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
orophrynx or colon, intravenous antibiotics should be administered for
7 to 14 days for infection prophylaxis.²⁹ NASCIS trials excluded penetrating spinal injury and no data exists 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 to address
neural tissue. 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. Since treatment and outcome of spine injuries is 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.⁶⁹,⁹³,¹³⁴,³⁰⁰
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
is intact.³⁰² 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 force to adjacent
cadaveric vertebrae and sequentially sectioned each structure.³⁰² This work was later summarized into a checklist to help clinicians evaluate cervical spine stability (see Table 41-13).³⁰³

The White and Panjabi³⁰³
checklist for instability assessment is helpful in providing a
framework for evaluating a spinal injury or other vertebral column
destructive lesions. 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

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necessary
in thoroughly analyzing a spinal injury and formulating the treatment
plan for an individual patient. Calculation of 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 (the authors’) opinion, neurologic considerations are
likely 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.³¹,³²,³³
The first trial (NASCIS I) compared low-dose (100 mg bolus and 25 mg
every 6 hours for 10 days) to 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) to 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.³²
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.³² 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/hr 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.¹¹⁸,¹²⁰,¹³⁸,¹³⁹,¹⁴⁰,²⁴⁵,²⁷³,²⁷⁵
In brief, the papers 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 0-3-hour and
3-8-hour window in NASCIS III. The original NASCIS II hypothesis
included a plan for analysis of early versus late treatments. While the
critics are correct in stating 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 0-3-hour and 3-8-hour window in NASCIS III. Researchers have
requested the data to see if 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 7 muscle groups (using a 0-5 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. While 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. While this may reflect the
implementations of the treatments in real world settings, it opens the
data to potential bias with unaccounted interventions.

Lastly, the use of high-dose steroids is not without a
risk. NASCIS 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.¹⁸²,²¹⁸

In short, since their publication, the NASCIS trials
have undergone continued re-evaluation with continued critiques and
rebuttals from the lead author. As the criticisms mounted against the
papers 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 Hamilton¹⁴⁰
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”).¹⁴⁰
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 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.”¹¹⁸

Thus, as of this publication, 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

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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 orthopaedics, 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. Partly, these differing
results are 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. Reallife injuries, on
the other hand, 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 DISH. These injuries are often
associated with severe neurologic deficits, vascular disruption,
stroke, and death. In these types 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 of posterior or lateral
displacement; it is simply a reflection of the particular position of
the patient at the moment the image was taken. 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 medical and social burden of injuries.²³⁴,²³⁵
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.³¹⁰

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