MEDICAL SURGICAL NURSING

TERM PAPER

SPINAL CORD INJURY

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 INDEX
SI NO CONTENT PAGE
NUMBER
1. INTRODUCTION
2. EPIDEMIOLOGY
3. REVIEW OF ANATOMY OF SPINE AND SPINAL CORD
4. DEFINITION- SPINAL CORD INJURY
5. CLASSIFICATION OF SPINAL CORD INJURY
6. ETIOLOGY
7. PATHOPHYSIOLOGY
8. CLINICAL MANIFESTATIONS AND COMPLICATIONS
9. ASSESMENT OF SPINAL CORD INJURY
10. MANAGEMENT OF SPINAL CORD INJURY
11. REHABILITATION AND PATIENT OUTCOME
12. COLLABORATIVE CARE
13. NURSING DIAGNOSIS
14. NURSING ROLES AND RESPONSIBILITIES IN
REHABILITATION
15. JOURNAL ARTICLES
16. CONCLUSION
REFERENCES

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 SPINAL CORD INJURY
INTRODUCTION
Spinal cord injury (SCI) is a non - progressive neurological impairment which can result
from a range of traumatic and non - traumatic causes. It predominates amongst adult males
but could affect any one of us, or our children, at any time. Thanks to our modern
understanding and management of this condition it has a low mortality and a reasonably
good life expectancy.
EPIDEMIOLOGY OF SPINAL CORD INJURY
The incidence of spinal cord injury ranges between 27 and 47 cases per million per year.
Road traffic accidents remain the leading cause of spinal cord injuries worldwide. Males in
the third decade of life are the most likely group to sustain serious spinal cord injury. .
Significant spinal column injuries can be presentin up to 10% of all trauma admissions and
up to 20% of severely injured patients (NCEPOD,2007 ) whose injuries have the potential to
result in damageto the underlying spinal cord. 71% of spinal cord injuries are due to trauma
(SIA, 2009 ). However, traumatic spinal cord injury is still a relatively rare event,
representing approximately 2% of current trauma admissions . There is a 7:3 male:female
ratio amongst current new SCI centre admissions. SCI is not confined to any particular age
group; acute admissions to SCI centres ranged between 3 and 103 years in 2007 – 2008,
with 20% of new injuries occurring between 21 and 30 years of age. The area of the spinal
column most commonly involved in the incidence of traumatic SCI is the cervical spine
(50% of all SCI centre admissions) . The most common levels of cervical trauma resulting in
SCI are C5 – C8 (26% of all SCI centre admissions) with 37% of SCI admissions involving
the thoracic spinal cord (T1 – T12) and 11% involve the lumbar spinal cord (L1 – L5).
Mortality amongst children and older people sustaining SCI is higher than other age groups
as they are more susceptible to the effects of severe multi - trauma. Older people are much
more vulnerable to cervical spinal cord compression resulting from minor trauma because of
the presence of pre - existing age - related diseases such as ankylosing spondylitis and spinal
stenosis .

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REVIEW OF ANATOMY
SPINE
The spine is a flexible column
formed by a series of bones called
vertebrae, each stacked one on
another tosupport the head and
trunk. The vertebral column is
made The axis has a
perpendicular projection called
the odontoid process on which
the atlas sits . The thoracic or
dorsal vertebrae are intermediate
in size, becoming larger as they descend the vertebral column. The lumbar vertebrae are
the largest segments in the spine. The vertebral bodies are the largest part of the vertebrae,
above and below which flattened
surfaces are found for attachmentof
fibrocartilage. There are apertures for
spinal nerves, veins, and arteries. The
vertebrae are connected by means of the
articular processes and the intervertebral
fibrocartilage. The arch of the vertebrae
is composed of two pedicles, two
laminae, a spinous process, four articular
processes, and two
transverse processes. The two pedicles
are short, thick pieces of bone. The
concavity above and below the pedicles
creates the intervertebral notches from
which the spinal nerves emanate. The
two laminae are broad plates of bone.

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 CERVICAL SPINE
They complete the neural arch by
fusing in the midline and enclose the
spinal foramen, which protects the
spinal cord. The upper and lower
borders are rough in order to allow for
the attachment of the ligament
subflava. The spinous process
projects backward from the laminae
and serves as the attachment for
muscles and ligaments. The four
articular processes (two on either
side) provide stability for the spine.
The two transverse processes provide
stability for the spine and serve as points of attachment for muscles and ligaments.

LIGAMENTS OF THE SPINE

The most important ligaments of the vertebral column are the anterior and posterior
longitudinal ligaments and the ligamenta flava . The anterior longitudinal ligament
consists of longitudinal fibers firmly attached to the anterior surface of the vertebral bodies
and intervertebral discs. The posterior longitudinal ligament is attached to the posterior
surface of the vertebral bodies within the spinal canal. The ligamentum flavum consists of
yellow elastic fibers that connect the laminae of adjacent vertebrae. The attachment pattern
is unique in that the attachment is from the lower margin of the anterior surface of the
superior lamina to the posterior surface of the upper margin of the inferior lamina.
The supraspinous ligament joins the spinous process tips from C7 to the sacrum. The
interspinous ligaments connect adjacent spinous processes from their tips to their roots.
The interspinals fuse with the supraspinals posteriorly and with the ligamentum flavum
anteriorly. Such an arrangement controls vertebral movement to prevent excessive flexion. If
violent force in any direction occurs, these ligaments can be ruptured, possibly causing
injury to the vertebrae and spinal cord

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INTERVERTEBRAL DISCS
The intervertebral discs are fibrocartilaginous disc-shapedstructures located between the
vertebral bodies from the second cervical vertebra to the sacrum. They vary in size,
thickness,and shape at different levels of the spine. The purpose of the intervertebral disc is
to cushion movement. The central core, the nucleus pulposus, is surrounded by a fibrous
capsule
called the annulus fibrosus. As a result of aging and trauma, discs lose their water content
and the tissue is more prone to injury.
MENINGES
Meninges cover both the brain and spinal cord.
The layers, from the outermost layer inward,
are called the dura mater, the arachnoid, and
the pia mater .
The dura mater is a double-layer, whitish,
inelastic, fibrous membrane that lines the
interior of the skull. The outer layer of the dura
is actually the periosteum of the bone. The
inner layer is the thick membrane that extends
throughout the skull and creates compartments.
The dura lines various foramina that exit at the
base of the skull. Sheaths for the nerves passing
through these foramina are also formed by the
dura. Four folds of dura are situated within the
skull cavity to support and protect the brain.
They include the following:
Falx cerebri, a double fold of dura, descends
vertically into the longitudinal fissure between
the two hemispheres of the brain and partially divides the frontal lobe into a left and right
side.
Tentorium cerebelli is a tent-like double fold of dura that covers the upper surface of the
cerebellum, supports the occipital lobes, and prevents them from pressing on the cerebellum.

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The falx cerebri attaches midline to the tentorium. (The tentorium is an important anatomic
point to note. The area above the tentorium is termed supratentorial, whereas the area
below it is called infratentorial. In addition, the opening in the tentorium from which the
brainstem emerges is called the tentorial notch. Herniation through this opening is called
uncal herniation.
Falx cerebelli is found between the two lateral lobes of the cerebellum.
Diaphragma sella is a horizontal process that forms a small circular fold, thus creating a
roof for the sella turcica. The spinal dura is a continuation of the inner layer of the cerebral
dura. The outer layer of the dura terminates at the foramen magnum, where it is replaced by
the periosteal lining of the vertebral canal. The spinal dura encases the spinal roots, spinal
ganglia, and spinal nerves. The spinal dural sac terminates at the second or third sacral level.
The second meningeal layer, the arachnoid membrane, is an extremely thin, delicate layer
that loosely encloses the brain. The subdural space separates the dura mater from the
arachnoid layer. Bleeding within this space (subdural hemorrhage) can occur with head
injury. The subarachnoid space is not really a clear space because there is much spongy,
delicate connective tissue between the arachnoid and pia mater layers. CSF flows in the
subarachnoid space. The cisterna magnum is a space between the hemispheres of the
cerebellum and the medulla oblongata. The arachnoid layer of the spinal meninges is a
continuation of the cerebral arachnoid . The arachnoid is a delicate, gossamer network of
fine, elastic, fibrous tissue; it also contains blood vessels of varying sizes, which may be
damaged by lumbar or cisternal puncture, resulting in hemorrhage.
The innermost layer of the meninges is called the pia mater. It is a mesh-like, vascular
membrane that derives its blood supply from the internal carotid and vertebral arteries. The
pia mater covers the entire surface of the brain, dipping down between the convolutions of
the surface. Because the pia covers the gray matter, vascularity increases and minute
perpendicular vessels extend for some distance into the cerebrum. The pia mater of the
spinal cord is thicker, firmer, and less vascular than that of the brain.
Vertebral Arteries
The vertebral arteries, originating from the subclavian arteries, enter the skull through the
foramen magnum, ventrolateral to the spinal cord. The two vertebral arteries unite at the
level

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of the pons to become the singular basilar artery . The basilar artery subdivides into the
two posterior cerebral arteries that supply part of the cerebrum . In general, the vertebral
arteries and their branches supply the cerebellum, the brainstem, the spinal cord, the
occipital lobes, the medial and inferior surfaces of the temporal lobes, and the posterior
diencephalon. Before they begin to supply blood to the brain, the vertebral arteries give off
recurrent branches that anastomose with the anterior and posterior spinal arteries and with a
posterior meningeal branch. In its intracranial course, the vertebral arteries give rise to direct
bulbar arteries to the
medulla, the anterior spinal artery, the posterior inferior cerebellar artery (PICA),
sometimes the posterior spinal artery, and small branches to the basal meninges. The first
branch off the basilar artery is the anterior inferior cerebellar artery (AICA). The basilar
artery is also the origin of the pontine arteries, the internal auditory arteries, the superior
cerebellar arteries, and the posterior cerebral arteries.
Blood Supply to the Spinal Cord, Spinal Roots, and Spinal Nerves
The upper cervical cord receives its arterial blood supply from the vertebral arteries through
recurrent branches. Below this region, the spinal cord receives its arterial blood supply, in
part, from the anterior spinal artery and the two posterior spinal arteries, which arise from
the vertebral arteries. The anterior spinal artery runs the full length of the cord
midventrally, whereas the two posterior spinal arteries run full length along each row of
the dorsal roots. As these three vessels pass down the cord, they receive feeders from deep
cervical, intercostal, lumbar, and sacral arteries. Additional blood supply comes from
radicular arteries (which supply blood to only one nerve root) and radiculospinal arteries
(which supply blood to about six spinal cord segments). The large artery of Adamkiewicz
originates from the aorta and enters the cord at about the second lumbar (L-2) ventral root
level (range, T-10 to L-2) and supplies most of the caudal third of the cord. The venous
system of the spine includes an intradural and extradural system. The intradural veins follow
the pattern of the arteries, whereas the extradural intravertebral veins form a plexus
extending from the cranium to the pelvis and having many communications along the way
with veins of the neck, thorax, and abdomen

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SPINAL CORD
The spinal cord and medulla form a continuous structure extending from the cerebral
hemispheres and serving as the connection between the brain and the periphery.
Approximately 45 cm (18 in) long and about the thickness of a finger, it extends from the
foramen magnum at the base of the skull to the lowerborder of the first lumbar vertebra,
where it tapers to a fibrousband called the conus medullaris. Continuing below the second
lumbar space are the nerve roots that extend beyond the conus, which are called the cauda
equina because they resemble a horse’stail. Similar to the brain, the spinal cord consists of
gray and white matter. Gray matter in the brain is external and white matter is internal; in
the spinal cord, gray matter is in the center and is surrounded on all sides by white matter.

The spinal cord is surrounded by the meninges, dura, arachnoid, and pia layers. Between the
dura mater and the vertebral canal is the epidural space. The spinal cord is an H-shaped
structure with nerve cell bodies (gray matter) surrounded by ascending and descending tracts
(white matter) . The lower portion of the H is broader than the upper portion and
corresponds to the anterior horns. The anterior horns contain cells with fibers that form the
anterior (motor) root end and are essential for the voluntary and reflex activity of the

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muscles they innervate. The thinner posterior (upper horns) portion contains cells with fibers
that enter over the posterior (sensory) root end and thus serve as a relay station in the
sensory/reflex pathway. The thoracic region of the spinal cord has a projection from each
side at the crossbar of the H of gray matter called the lateral horn. It contains the cells that
give rise to the autonomic fibers of the sympathetic division. The fibers leave the spinal cord
through the anterior roots in the thoracic and upper lumbar segments
Neuronal cell groups of the spinal cord
The grey matter of the spinal cord may be divided, on
the basis of cytoarchitecture, into 10 zones, known as
Rexed’s laminae, which are numbered sequentially
from dorsal to ventral. The laminae are defined on the
basis of neuronal size, shape, cytological features and
density. Some of these lamina are equated with cell
groupings of particular functional types. Laminae I–IV
correspond to the dorsal part of the dorsal horn, and
are the main site of termination of cutaneous primary
afferent terminals and their collaterals. Many complex
polysynaptic reflex paths (ipsilateral, contralateral,
intrasegmental and intersegmental) start from
this region, as also do many long ascending tract fibres, which pass to higher levels. Lamina
I (lamina marginalis) is a very thin layer with an ill-defined boundary at the dorsolateral tip
of the dorsal horn. It has a reticular appearance, reflecting its content of intermingling
bundles of coarse and fine nerve fibres. It contains small, intermediate and large neuronal
somata, many of which are fusiform in shape. The much larger lamina II consists of densely
packed small neurones, responsible for its dark appearance in Nissl-stained sections. With
myelin stains, lamina II is characteristically distinguished from adjacent laminae by the
almost total lack of myelinated fibres. Lamina II corresponds approximately to the
substantia gelatinosa. Lamina III consists of somata that are mostly larger, more variable and
less closely packed than those in lamina II. It also contains many myelinated fibres. The
ill-defined nucleus proprius of the dorsal horn corresponds to some of the cell constituents
of laminae III and IV. Lamina IV is a thick, loosely packed, heterogeneous zone permeated

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by fibres. Its neuronal somata vary considerably in size and shape, from small and round,
through intermediate and triangular, to very large and stellate.
Laminae V and VI lie at the base of the dorsal horn. They receive most of the terminals of
proprioceptive primary afferents, profuse corticospinal projections from the motor and
sensory cortex, and input from subcortical levels, suggesting their involvement in the
regulation of movement. Lamina V is a thick layer, divisible into a lateral third and medial
two-thirds. Both have a mixed cell population but the former contains many prominent well-
staining somata interlaced by numerous bundles of transverse, dorsoventral and longitudinal
fibres. Lamina VI is most prominent in the limb enlargements. It has a densely staining
medial third of small, densely packed neurones and a lateral two-thirds containing larger,
more loosely packed, triangular or stellate somata. Lamina VII occupies the region just
ventral to lamina VI and extending across the spinal grey matter on each side. This region is
known as the intermediate zone and within the thoracic cord includes the lateral horn. The
size of lamina VII varies at different spinal levels. In the cervical and lumbar enlargements,
lamina VII extends laterally and ventrally throughout the ventral horn containing cell groups
of lamina IX neurons embedded within it. In the thoracic region, lamina VII occupies
the intermediate zone and the dorsal part of the ventral horn only.Three important nuclear
groups are contained within lamina VII: the posterior thoracic nucleus (nucleus thoracicus
posterior, Clarke’s column), which extends throughout the thoracic and upper lumbar
segments and gives rise to the dorsal spinocerebellar tract; the intermediolateral nucleus,
which is located between T1 and L2 and gives rise to the preganglionic sympathetic fibres;
and the intermediomedial nucleus, which extends the full length of the cord and may be
involved in the control of visceral motor neurones .
Lamina VIII spans the base of the ventral horn in the thoracic region but is restricted to the
medial aspect of the ventral horn in the cervical and lumbar enlargements. Its neurones
display a heterogeneous mixture of sizes and shapes from small to moderately large. Lamina
VIII is a mass of propriospinal interneurones. It receives terminals from the adjacent
laminae, many commissural fibres from the contralateral lamina VIII, and descending
connections from the interstitiospinal, reticulospinal and vestibulospinal tracts and the
medial longitudinal fasciculus. The axons from these interneurones influence α motor

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neurone activity bilaterally, perhaps directly but more probably by excitation of small γ
motor neurones supplying efferent fibres to muscle spindles.
Lamina IX consists of several distinct groups of somatic motor neurons located throughout
the ventral horn. In the thoracic cord, these nuclear groups are embedded within lamina VIII,
whereas in the cervical and lumbar enlargements, the lamina IX cell groups are embedded
within both lamina VII and lamina VIII. Lamina IX is a complex array of cells consisting of
α and γ motor neurones and many interneurones. The large α motor neurones supply motor
end-plates of extrafusal muscle fibres in striated muscle. Recording techniques have
demonstrated tonic and phasic α motor neurones. The former have a lower rate of firing and
lower conduction velocity, and tend to innervate type S muscle units. The latter have higher
conduction velocity and tend to supply fast twitch (type FR, FF) muscle units. The smaller γ
motor neurons give rise to small-diameter efferent axons (fusimotor fibres), which innervate
the intrafusal muscle fibres in muscle spindles. There are several functionally distinct types
of γ motor neurone. The ‘static’ and ‘dynamic’ responses of muscle spindles have separate
controls mediated by static and dynamic fusimotor fibres, which are distributed variously to
nuclear chain and nuclear bag fibres . Lamina X surrounds the central canal and consists of
the dorsal and ventral grey commissures.
Sensory and Motor Pathways: The Spinal Tracts.
The white matter of the cord is composed of myelinated and unmyelinated nerve fibers. The
fast conducting myelinated fibers form bundles that also contain glial cells. Fiber bundles
with a common function are called tracts. There are six ascending tracts. Two conduct
sensation, principally the perception of touch, pressure, vibration, position, and passive
motion from the same side of the body. Before reaching the cerebral cortex, these fibers
cross to the opposite side in the medulla. The two spinocerebellar tracts conduct sensory
impulses from muscle spindles, providing necessary input for coordinated muscle
contraction. They ascend essentially uncrossed and terminate in the cerebellum.
The last two spinothalamic tracts are responsible for conduction of pain, temperature,
proprioception, fine touch, and vibratory sense from the upper body to the brain. They
ascend, cross to the opposite side of the brain, and terminate in the thalamus There are eight
descending tracts, seven of which are engaged in motor function. The two corticospinal
tracts conduct motor impulses to the anterior horn cells from the opposite side of the brain

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and control voluntary muscle activity. The three vestibulospinal tracts descend uncrossed
and are involved in some autonomic functions (sweating, pupil dilation, and circulation and
involuntary muscle control. The corticobulbar tract conducts impulses responsible for
voluntary head and facial muscle movement and crosses at the level of the brain stem. The
rubrospinal and reticulospinal tracts conduct impulses involved with involuntary muscle
movement.

Vertebral Column.
The bones of the vertebral column surround and protect the spinal cord and normally
consist of 7 cervical, 12 thoracic, and 5 lumber vertebrae, as well as the sacrum (afused mass
of five vertebrae), and terminate in the coccyx. Nerve roots exit from the vertebral column
through the intervertebral foramina (openings). The vertebrae are separated by disks, except
for the first and second cervical, the sacral, and
the coccygeal vertebrae. Each vertebra has a
ventral solid body and a dorsal segment or arch,
which is posterior to the body. The arch is
composed of two pedicles and two laminae
supporting seven processes. The vertebral body,
arch, pedicles, and laminae all encase the
vertebral canal.
The Peripheral Nervous System
The peripheral nervous system includes the
cranial nerves, the spinal nerves, and the
autonomic nervous system.
CRANIAL NERVES
There are 12 pairs of cranial nerves that emerge from the lowersurface of the brain and pass
through the foramina in the skull.Three are entirely sensory (I, II, VIII), five are motor (III,
IV, VI, XI, and XII), and four are mixed (V, VII, IX, and X) as they have both sensory and
motor functions. The cranial nerves are numbered in the order in which they arise from the
brain. For example, cranial nerves I and II attach in the cerebral hemispheres, whereas
cranial nerves IX,

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X, XI, and XII attach at the
medulla .Most cranial nerves
innervate the head, neck, and
special sense structures.
SPINAL NERVES
The spinal cord is composed of
31 pairs of spinal nerves: 8
cervical, 12 thoracic, 5 lumbar,
5 sacral, and 1 coccygeal. Each
spinalnerve has a ventral root
and a dorsal root The dorsal
roots are sensory and transmit
sensory impulses from specific
areas of the body known as
dermatomes . to the dorsal
ganglia. The sensory fiber may be somatic, carrying information about pain, temperature,
touch, and position sense (proprioception) from the tendons, joints, and body surfaces; or
visceral, carrying information from the internal organs. The ventral roots are motor and
transmit impulses from the spinal cord to the body. These fibers are also either somatic or
visceral.The visceral fibers include autonomic fibers that control the cardiac muscles and
glandular secretions.
AUTONOMIC NERVOUS SYSTEM
The autonomic nervous system regulates the activities of internal organs such as the heart,
lungs, blood vessels, digestive organs, and glands. Maintenance and restoration of internal
homeostasis is largely the responsibility of the autonomic nervous system. There are two
major divisions: the sympathetic nervous system with predominantly excitatory responses,
most notably the “fight or flight” response, and the parasympathetic nervous system,
which controls mostly visceral functions. The autonomic nervous system innervates most
body organs.

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Although usually considered part of the peripheral nervous system, it is regulated by centers
in the spinal cord, brain stem, and hypothalamus. The autonomic nervous system has two
neurons in a series extending between the centers in the CNS and the organs innervated. The
first neuron, the preganglionic neuron, is located in the brain or spinal cord, and its axon
extends to the autonomic ganglia. There, it synapses with the second neuron, the
postganglionic neuron, located in the autonomic ganglia, and its axon synapses with the
target tissue and innervates the effector
organ. Its regulatory effects are exerted not on individual cells but on large expanses of
tissue and on entire organs. The responses elicited do not occur instantaneously but after a
lag period. These responses are sustained far longer than other neurogenic responses to
ensure maximal functional efficiency on the part of receptor organs, such as blood vessels.
The quality of these responses is explained by the fact that the autonomic nervous system
transmits its impulses by way of nerve pathways, enhanced by chemical mediators,
resembling in this respect the endocrine
system. Electrical impulses, conducted
through nerve fibers, stimulate the
formation of specific chemical agents at
strategic locations within the muscle
mass; the diffusion of these chemicals
within the muscle is responsible for the
contraction.
The hypothalamus is the major
subcortical center for the regulation of
visceral and somatic activities, with an
inhibitory– excitatory role in the
autonomic nervous system. The
hypothalamus has connections that link
the autonomic system with the
thalamus, the cortex, the olfactory
apparatus, and the pituitary gland.
Located here are the mechanisms for the

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control of visceral and somatic reactions that were originally important for defense or attack,
and are associated with emotional states (eg, fear, anger, anxiety); for the control of
metabolic processes, including fat, carbohydrate, and water metabolism; for the regulation
of body temperature, arterial pressure, and all muscular and glandular activities of the
gastrointestinal tract; for control of genital functions and for the sleep cycle.
The autonomic nervous system is separated into the anatomically and functionally distinct
sympathetic and parasympathetic divisions. Most of the tissues and the organs under
autonomic
control are innervated by both systems. Sympathetic stimuli aremediated by norepinephrine
and parasympathetic impulses are mediated by acetylcholine. These chemicals produce
opposing and mutually antagonistic effects. Both divisions produce stimulatory and
inhibitory effects. For example, the parasympathetic division causes contraction
(stimulation) of the urinary bladder muscles and a decrease (inhibition) in heart rate,
whereas the sympathetic division produces relaxation (inhibition) of the urinarybladder and
an increase (stimulation) in the rate and force of the heartbeat. compares the sympathetic
and the parasympathetic effects on the different systems of the body.
Sympathetic Nervous System.
The sympathetic division of the autonomic nervous system is best known for its role in the
body’s “fight-or-flight” response. Under stress conditions from either physical or emotional
causes, sympathetic impulses increase greatly. As a result, the bronchioles dilate for easier
gas exchange; the heart’s contractions are stronger and faster; the arteries to the heart and
voluntary muscles dilate, carrying more blood to these organs; peripheral blood vessels
constrict, making the skin feel cool but shunting blood to essential organs; the pupils dilate;
the liver releases glucose for quick energy; peristalsis slows; hair stands on end; and
perspiration increases. The sympathetic neurotransmitter is norepinephrine (noradrenaline),
and this increase in sympathetic discharge is the same as if the body has been given an
injection of adrenalin—hence, the term adrenergic is often used to refer to this division.
Sympathetic neurons are located in the thoracic and the lumbar segments of the spinal cord;
their axons, or the preganglionic fibers, emerge by way of anterior nerve roots from the
eighth cervical or first thoracic segment to the second or third lumbar segment. A short
distance from the cord, these fibers diverge to join a chain, composed of 22 linked ganglia,

16
that extends the entire length of the spinal column, adjacent to the vertebral bodies on both
sides. Some form multiple synapses with nerve cells within the chain. Others traverse the
chain without making connections or losing continuity to join large “prevertebral” ganglia in
the thorax, the abdomen, or the pelvis or one of the “terminal” ganglia in the vicinity of an
organ, such as the bladder or the rectum. Postganglionic nerve fibers originating in the
sympathetic chain rejoin the spinal nerves that supply the extremities and are distributed to
blood vessels, sweat glands, and smooth muscle tissue in the skin. Postganglionic fibers
from the prevertebral plexuses (eg, the cardiac, pulmonary, splanchnic, and pelvic plexuses)
supply structures in the head and neck, thorax, abdomen, and pelvis, respectively, having
been joined in these plexuses by fibers from the parasympathetic division. The adrenal
glands, kidneys, liver, spleen, stomach, and duodenum are under the control of the giant
celiac plexus, commonly known as the solar plexus. This receives its sympathetic nerve
components by way of the three splanchnic nerves, composed of preganglionic fibers from
nine segments of the spinal cord (T4 to L1), and is joined by the vagus nerve, representing
the parasympathetic division. From the celiac plexus, fibers of both divisions travel along
the course of blood vessels to their target organs. Sympathetic Syndromes. Certain
syndromes are distinctive to diseases of the sympathetic nerve trunks. Among these are
dilation of the pupil of the eye on the same side as a penetrating wound of the neck
(evidence of disturbance of the cervical sympathetic cord); temporary paralysis of the bowel
(indicated by the absence of peristaltic waves and the distention of the intestine by gas) after
fracture of any one of the lower dorsal or upper lumbar vertebrae with hemorrhage into the
base of the mesentery; and the marked variations in pulse rate and rhythm that often follow
compression fractures of the upper six thoracic vertebrae.

Parasympathetic Nervous System.

The parasympathetic nervous system functions as the dominant controller for most visceral
effectors. During quiet, nonstressful conditions, impulses from parasympathetic fibers
(cholinergic) predominate. The fibers of the parasympathetic system are located in two
sections, one in the brain stem and the other from spinal segments below L2. Because of the
location of these fibers, the parasympathetic system is referred to as the craniosacral
division, as distinct from the thoracolumbar (sympathetic) division of the autonomic nervous

17
system.The parasympathetic nerves arise from the midbrain and the medulla oblongata.
Fibers from cells in the midbrain travel with the third oculomotor nerve to the ciliary
ganglia, where postganglionic fibers of this division are joined by those of the sympathetic
system, creating controlled opposition, with a delicate balance maintained between the two
at all times.
Motor and Sensory Functions of the Nervous System
MOTOR SYSTEM FUNCTION
The motor cortex, a vertical band within each cerebral hemisphere, controls the voluntary
movements of the body. The exact locations within the brain at which the voluntary
movements of the muscles of the face, thumb, hand, arm, trunk, and leg originate are known
. To initiate muscle movement, these particular cells must send the stimulus down along
their fibers.
Stimulation of these cells with an electric current will also result in muscle contraction. En
route to the pons, the motor fibers converge into a tight bundle known as the internal
capsule. A comparatively small injury to the capsule causes paralysis in more muscles than
does a much larger injury to the cortex itself. Within the medulla, the motor axons from the
cortex form the motor pathways or tracts, notably the corticospinal or pyramidal tracts.
Here, most of the fibers cross (or decussate) to the opposite side, continuing as a crossed
pyramidal tract. The remaining fibers enter the spinal cord on the same side as the direct
pyramidal tract. Each fiber in this tract finally crosses to the opposite side of the cord and
terminates within the gray matter of the anterior horn on that side, in proximity to a motor
nerve cell. Fibers of the crossed pyramidal tract terminate within the anterior horn and make
connections with anterior horn cells on the same side. All of the motor fibers of the spinal
nerves represent extensions of these anterior horn cells, with each of these fibers
communicating with only one particular muscle fiber.
The motor system is complex, and motor function depends on the integrity of the
corticospinal tracts, the extrapyramidal system, and cerebellar function. A motor impulse
consists of a two-neuron pathway (described below). The motor nerve pathways are
contained in the spinal cord. Some represent the pathways of the so-called extrapyramidal
system, establishing connections between the anterior horn cells and the automatic control
centers located in the basal ganglia and the cerebellum. Others are components of reflex

18
arcs, forming synaptic connections between anterior horn cells and sensory fibers that have
entered adjacent or neighboring segments of the cord.
Upper and Lower Motor Neurons
The voluntary motor system consists of two groups of neurons: upper motor neurons and
lower motor neurons. Upper motor neurons originate in the cerebral cortex, the cerebellum,
and the brain stem and modulate the activity of the lower motor neurons. Upper motor
neuron fibers make up the descending motor pathways and are located entirely within the
CNS. Lower motor neurons are located either in the anterior horn of the spinal cord gray
matter or within cranial nerve nuclei in the brain stem. Axons of both extend through
peripheral nerves and terminate in skeletal muscle. Lower motor neurons are located in both
the CNS and the peripheral nervous system.
The motor pathways from the brain to the spinal cord, as well as from the cerebrum to the
brain stem, are formed by upper motor neurons. They begin in the cortex of one side of the
brain, descend through the internal capsule, cross to the opposite side in the brain stem,
descend through the corticospinal tract, and synapse with the lower motor neurons in the
cord. The lower motor neurons receive the impulse in the posterior part of the cord and run
to the myoneural junction located in the peripheral muscle. Upper Motor Neuron Lesions.
Upper motor neuron lesions can involve the motor cortex, the internal capsule, the spinal
cord, and other structures of the brain through which the corticospinal tract descends. If the
upper motor neurons are damaged or destroyed, as frequently occurs with stroke or spinal
cord injury, paralysis (loss of voluntary movement) results. However, because the inhibitory
influences of intact upper motor neurons are now impaired, reflex (involuntary) movements
are uninhibited, and hence hyperactive deep tendon reflexes, diminished or absent
superficial reflexes, and pathologic reflexes such as a Babinski response occur. Severe leg
spasms can occur as the result of an upper motor neuron lesion; the spasms result from the
preserved reflex arc, which lacks inhibition along the spinal cord below the level of injury.
There is little or no muscle atrophy, and muscles remain permanently tense, exhibiting
spastic paralysis or paresis (weakness). Paralysis associated with upper motor neuron lesions
usually affects a whole extremity, both extremities, and an entire half of the body.
Hemiplegia (paralysis of an arm and leg on the same side of the body) can be the result of an
upper motor neuron lesion.

19
If hemorrhage, an embolus, or a thrombus destroys the fibers from the motor area in the
internal capsule, the arm and the leg of the opposite side become stiff and very weak or
paralyzed, and the reflexes are hyperactive. When both legs are paralyzed, the condition is
called paraplegia; paralysis of all four extremities is quadriplegia Lower Motor Neuron
Lesions. A patient is considered to have lower motor neuron damage if a motor nerve is
severed between the muscle and the spinal cord. The result of lower motor neuron damage is
muscle paralysis. Reflexes are lost, and the muscle becomes flaccid (limp) and atrophied
from disuse. If the patient has injured the spinal trunk and it can heal, use of the muscles
connected to that section of the spinal cord may be regained. If the anterior horn motor cells
are destroyed, however, the nerves cannot regenerate and the muscles are never useful again.
Flaccid paralysis and atrophy of the affected muscles are the principal signs of lower motor
neuron disease. Lower motor neuron lesions can be the result of trauma, infection
(poliomyelitis), toxins, vascular disorders, congenital malformations, degenerative
processes, and neoplasms. Compression of nerve roots by herniated intervertebral disks is a
common cause of lower motor neuron dysfunction.
Coordination of Movement
The smoothness, accuracy, and strength that characterize the muscular movements of a
normal person are attributable to the influence of the cerebellum and the basal ganglia. The
cerebellum , is located beneath the occipital lobe of the cerebrum; it is responsible for the
coordination, balance, and timing of all muscular movements that originate in the motor
centers of the cerebral cortex. Through the action of the cerebellum, the contractions of
opposing muscle groups are adjusted in relation to each other to maximal mechanical
advantage; muscle contractions can be sustained evenly at the desired tension and without
significant fluctuation, and reciprocal movements can be reproduced at high and constant
speed, in stereotyped fashion and with relatively little effort. The basal ganglia, masses of
gray matter in the midbrain beneath the cerebral hemispheres, border the lateral ventricles
and lie in proximity to the internal capsule. The basal ganglia play an important role in
planning and coordinating motor movements and posture. Complex neural connections link
the basal ganglia with the cerebral cortex. The major effect of these structures is to inhibit
unwanted muscular activity; disorders of the basal ganglia result in exaggerated,
uncontrolled movements. Impaired cerebellar function, which may occur as a result of an

20
intracranial injury or some type of an expanding mass (eg, a hemorrhage, abscess, or tumor),
results in loss of muscle tone, weakness, and fatigue. Depending on the area of the brain
affected, the patient has different motor symptoms or responses. The patient may
demonstrate decorticate, decerebrate, or flaccid posturing, usually as a result of cerebral
trauma . Decortication (decorticate posturing) is the result of lesions of the internal capsule
or cerebral hemispheres; the patient has flexion and internal rotation of the arms and wrists
and extension, internal rotation, and plantar flexion of the feet. Decerebration (decerebrate
posturing), the result of lesions at the midbrain, is more ominous than decortication. The
patient has extension and external rotation of the arms and wrists and extension, plantar
flexion, and internal rotation of the feet. Flaccid posturing is usually the result of lower brain
stem dysfunction; the patient has no motor function, is limp, and lacks motor tone.
Flaccidity preceded by decerebration in a patient with cerebral injury indicates severe
neurologic impairment, which may herald brain death. However, before the declaration of
brain death, the patient must have spinal cord injury ruled out, the effects of all
neuromuscular paralyzing agents must have worn off, and any other possible treatable
causes of neurologic impairment must be investigated. Tumors, infection, or abscess and
increased intracranial pressure can all affect the cerebellum. Cerebellar signs, such as ataxia,
incoordination, and seizures, as well as CSF obstruction and compression of the brain stem
may be seen. Signs of increased intracranial pressure, including vomiting, headache, and
changes in vital signs and level of consciousness, are especially common when CSF flow is
obstructed. Destruction or dysfunction of the basal ganglia leads not to paralysis but to
muscle rigidity, with disturbances of posture and movement. Such patients tend to have
involuntary movements.These may take the form of coarse tremors, most often in the upper
extremities, particularly in the distal portions; athetosis, movement of a slow, squirming,
writhing, twisting type; or chorea, marked by spasmodic, purposeless, irregular,
uncoordinated motions of the trunk and the extremities, and facial grimacing. Disorders due
to lesions of the basal ganglia include Parkinson’s disease, Huntington’s disease , and
spasmodic torticollis.

21
SENSORY SYSTEM FUNCTION
Integrating Sensory Impulses.
The thalamus, a major receiving and transmitting center for the afferent sensory nerves, is a
large structure connected to the midbrain. It lies next to the third ventricle and forms the
floor of the lateral ventricle. The thalamus integrates all sensory impulses except olfaction. It
plays a role in the conscious awareness of pain and the recognition of variation in
temperature and touch. The thalamus is responsible for the sense of movement and position
and the ability to recognize the size, shape, and quality of objects.
Receiving Sensory Impulses
Afferent impulses travel from their points of origin to their destinations in the cerebral
cortex via the ascending pathways directly, or they may cross at the level of the spinal cord
or in the medulla, depending on the type of sensation that is registered. Sensory information
may be integrated at the level of the spinal cord or may be relayed to the brain. Knowledge
of these pathways is important for neurologic assessment and for understanding symptoms
and their relationship to various lesions.
Sensory impulses enter the spinal cord by way of the posterior root. These axons convey
sensations of heat, cold, and pain and enter the posterior gray column of the cord, where
they make connections with the cells of secondary neurons. Pain and temperature fibers
cross immediately to the opposite side of the cord and course upward to the thalamus. Fibers
carrying sensations of touch, light pressure, and localization do not connect immediately
with the second neuron but ascend the cord for a variable distance before entering the gray
matter and completing this connection. The axon of the secondary neuron crosses the cord
and proceeds upward to the thalamus. Position and vibratory sensation are produced by
stimuli arising from muscles, joints, and bones. These stimuli are conveyed, uncrossed, all
the way to the brain stem by the axon of the primary neuron. In the medulla, synaptic
connections are made with cells of the secondary neurons, whose axons cross to the opposite
side and then proceed to the thalamus.
Sensory Losses.
Destruction of a sensory nerve results in total loss of sensation in its area of distribution.
Transection of the spinal cord yields complete anesthesia below the level of injury.

22
Selective destruction or degeneration of the posterior columns of the spinal cord is
responsible for a loss of position and vibratory sense in segments distal to the lesion, without
loss of touch, pain, or temperature perception. A lesion, such as a cyst, in the center of the
spinal cord causes dissociation of sensation—loss of pain at the level of the lesion. This
occurs because the fibers carrying pain and temperature cross within the cord immediately
on entering; thus, any lesion that divides the cord longitudinally divides these fibers. Other
sensory fibers ascend the cord for variable distances, some even to the medulla, before
crossing, thereby bypassing the lesion and avoiding destruction. Lesions affecting the
posterior spinal nerve roots may cause impairment of tactile sensation, including intermittent
severe pain that is referred to their areas of distribution. Tingling of the fingers and the toes
can be a prominent symptom of spinal cord disease, presumably due to degenerative
changes in the sensory fibers that extend to the thalamus (ie, belonging to the spinothalamic
tract).

23
 SPINAL CORD INJURY
DEFINITION
The term ‘spinal cord injury’ refers to damage to the spinal cord resulting from trauma (e.g.
a car crash) or from disease or degeneration (e.g. cancer).
WHO
Spinal cord injury (SCI) is an insult to the spinal cord resulting in a change, either temporary
or permanent, in the cord’s normal motor, sensory, or autonomic function.
Medscape
Classification
Spinal cord injuries can be classified by mechanism, type of vertebral injury, or level of
injury.
The velocity and angle of impact, as well as the type of exaggerated mechanical movement
produced, influence the type of injury sustained. These factors are considered in the
classification of injuries. Patients who have anatomic abnormalities or disease processes of
the spinal column are much more vulnerable to SCI than those who do not. Chronic
conditions, such as cervical spondylosis, spinal stenosis, arthritis, and scoliosis, are
examples of conditions that increase the probability of injury.A basic classification of the
causes of injury to the vertebral column, spinal cord, and soft tissue includes the following
categories and their characteristics

Mechanism of Injury
Spinal cord injuries occur as a result of penetrating injury or blunt forces. Typical
mechanisms of blunt injury are shown in the given figure.
Hyperflexion injuries are caused by a sudden deceleration of the head and neck, and are
often seen in patients who have sustained trauma from a head-on MVC or diving accident.
The cervical region is most often involved, especially at the C5–C6 level. Because it is a
relatively stable fracture, it does not usually require surgery. Flexion extension imaging may
be ordered to rule out a fracture not seen on plain x-rays. If the posterior ligaments are torn,
the facets are usually disengaged and dislocated. Because this is an unstable fracture type,
surgical stabilization will most likely required.There is a high probability of cord damage
with fracture dislocations or bilateral jumped locked facet fractures. These injuries occur

24
most often in the cervical region and involve the greatest areas of stress, levels C-5 and C-6.
A lateral hyperflexion injury can result from extreme lateral flexion or rotation of the head
and neck.

Hyperextension injuries can be caused by a fall, a rear-end MVC (whiplash), or getting hit
in the head (eg, during a boxing match). Hyperextension of the head and neck may cause
contusion and ischemia of the spinal cord without vertebral column damage. In a
hyperextension injury, the spinal cord is stretched so that it lies against the ligamenta flava.
Despite a negative result on radiographic examination, there may be contusion and ischemia
to part of the spinal cord, and neurological deficits may appear. As a rule, ligaments remain
intact and no fractures or dislocations occur. The greatest area of stress in a hyperextension
injury is at the level of C-4 and C-5. Respiratory compromise, either from direct injury or
ascending edema, is a concern.Hyperextension injuries are commonly seen in elderly
persons who have fallen and struck their chin. A less severe form of hyperextension injury is
called a “whiplash” or acceleration injury, a stress and strain injury to the soft tissue
(muscles and ligaments), but with no vertebral or SCI
Axial loading (compression) injuries typically occur when a person lands on the feet,
buttocks,or head after falling, jumping, or diving from a height. Compression of the
vertebral column causes a burst fracture that can result in damage to the spinal cord.
Compression fractures are sometimes categorized as burst fracture, simple wedge fracture
and teardrop fracture, depending on the degree of compression or the fracture line noted
on x-ray or imaging films.
Rotational injuries result from forces that cause extreme twisting or lateral flexion of the
head and neck. Fracture or dislocation of vertebrae may also occur. One or two facets may
be involved. If one facet is dislocated or locked, usually no neurological deficits or
temporary
deficits result. In more than half the patients with two facets locked, neurological deficits
can be expected. Reduction of the fracture is achieved by traction (cervical traction or halo
with or without a jacket) or surgery to disengage the facets and stabilize the vertebral
column (Cotrel-Dubousset [CD] rods;

25
Penetrating Injuries
Penetrating injuries occur when missiles, such as bullets or shrapnel, or impalement
instruments (knives, ice picks) penetrate the spinal column or supporting soft tissue. The
object may shatter bone, create bone fragments, or transect a portion or complete plane of
the spinal cord or soft tissue.
SPECIFIC CATEGORIES OF INJURIES
Soft-Tissue Injuries
Whiplash
Whiplash is a lay term for an acceleration injury involving hyperextension of the head
during a rear-end vehicular collision. The ligaments and muscles of the neck sustain stress
and strain injury. The usual signs and symptoms, which include stiff neck, pain in the neck
and shoulder, limitation of movement, and muscle spasms, may not begin until 12 to 24
hours after injury. Other signs and symptoms may include headache, paresthesia, dizziness,
vertigo, and tinnitus. The findings on physical examination are normal except for the
previously listed signs and symptoms. The radiologic examination is negative. The diagnosis
is based on the history of injury and the presence of the characteristic signs and symptoms.
This is a common injury causing much pain and suffering to the patient, even though no
abnormalities are noted on radiographic examination. The pain caused by whiplash is
thought to be attributable to the tearing, stretching, microhemorrhage, and edema incurred
by the anterior neck muscles (sternocleidomastoid, scalenus,and longus colli muscles). The
muscles, and possibly the ligaments, are strained. Patients with pre-existing cervical
spondylosis and some with other conditions may have narrowing of the foramina and
osteophytes and also increased rigidity of the spinal column. These conditions put them at
greater risk of developing neurological problems if a whiplash injury occurs.
Treatment. Treatment of whiplash is directed toward makingthe patient comfortable. For
less serious injuries,ntreatment involves mild analgesics (e.g., nonsteroidal anti-
inflammatory drugs [NSAIDs], acetaminophen), local ice, and rest. More severe injuries are
treated with short-term use of a soft collar, heat and cold application, analgesics, muscle
relaxants, and anti-inflammatory agents.
Narcotic analgesics are reserved for severe pain and should be used sparingly to prevent
dependency. NSAIDs are commonly ordered both for their anti-inflammatory effect and for

26
their ability to inhibit prostaglandin synthesis, a substance known to be related to pain.
Muscle relaxants such as cyclobenzaprine hydrochloride (Flexeril) and methocarbamol
(Robaxin) are also used. Extended use of a cervical collar is controversial.Some physicians
believe that collars hinder recovery of involved muscles if worn for more than a few days.
Other Soft-Tissue Injuries
The vertebral column depends on soft tissue for its stability.Therefore, any significant soft-
tissue trauma that occurs with vertebral injury can compromise the vertebral column. The
other soft-tissue injuries with significance for vertebral stability are discussed in this chapter
in conjunction with vertebral injuries and SCI.
Type of Vertebral Injury
Mechanical forces can result in fracture or dislocation Of vertebrae, or both. A fracture may
be considered unstable if the longitudinal ligaments are torn. Although fractures can occur
singularly in any part of the vertebral arch, most injuries occur in combination with vertebral
body injuries. The “ends” of the vertebral column, the cervical and lumbar portions, have the
greatest built-in mobility, which predisposes them to injury. The thoracic region is less
prone to trauma because of the rigidity imparted to it by the rib cage. Vertebral injuries can
be classified based on various perspectives of the injury:

27
28
Types of Vertebral Fractures and Dislocations

Fractures
Simple fracture: single fracture; alignment of the vertebrae is intact
and neurological deficits do not occur
Compression fracture: fracture caused by axial loading and
hyperflexion
Wedge compression fracture: a stable fracture that involves
compression of the vertebral body in the cervical area
Teardrop fracture: an unstable fracture that involves a piece of bone
breaking off the vertebra; seen in wedge fractures
Comminuted fracture: the vertebra is shattered into several pieces;
bone fragments may be driven into spinal cord

Dislocations
Dislocation: one vertebra overrides another
Subluxation: partial or incomplete dislocation
Fracture–dislocation: fracture and dislocation
For the purposes of this discussion, vertebral fractures are subdivided into simple and
compression fractures
• Simple fractures appear as a singular break with the alignment of the vertebral parts
remaining intact. These types of fractures usually occur to the spinous or transverse process,
facets, pedicles, and vertebral body. There is usually no neural compression.
• Compression fractures are sometimes further subclassified as simple wedge fractures,
burst fractures, and teardrop fractures .They are caused by axial loading and hyperflexion.
• A simple (wedge) compression fracture is caused by vertical compression when the
cervical vertebral column is flexed. A burst fracture is caused by the same mechanical force,
but the vertebral column is straight. Because the posterior ligaments are intact, the simple
(wedge) compression fracture is stable. No surgery is required. These fractures heal well
with hard collar immobilization for about 2 months.4 A halo jacket may also be used.

29
• Burst fractures are explosive fractures caused by severe axial loading on a straight
cervical column. They shatter the vertebral body into several pieces. These fragments then
can be driven into the spinal cord, resulting in serious injury. If there is no neurological
damage and if the posterior ligaments are stable, wearing a hard collar for 2 months may be
adequate therapy.
However, burst fractures often require a combined neurosurgical- orthopedic procedure for
the removal of bone fragments, cord decompression, and vertebral column stabilization.
Stabilization is accomplished by insertion of instrumentation, such as CD rods, a type of
segmental rodding that can be accommodated to the individual’s level of injury. See section
on surgical management for further discussion.
• Teardrop fractures are caused by extreme flexion with axial loading. With this fracture a
vertebral body is crushed by the vertebral body superior to it, causing the anterior portion of
the compressed body to break away. These fractures, which are usually unstable (i.e.,
involving disruption of the posterior ligaments, resulting in forward dislocation), are
managed with anterior decompression and fusion with halo immobilization.
Fracture or Dislocation.
From another perspective, a vertebral injury can be a fracture without a dislocation, a
dislocation without a fracture, or a fracture combined with a dislocation.
Dislocation occurs when one vertebra overrides another, and there is unilateral or bilateral
facet dislocation. Radiographic studies reveal a disruption in the established alignment of the
vertebral column. Usually, the supporting ligaments are also injured, and the spinal cord
may or may not be involved.
Subluxation is a partial or incomplete dislocation of one vertebra over another. Damage to
the cord and supporting ligaments may or may not be present. With dislocation, re-
establishment of alignment is necessary. This may be accomplished by traction followed by
immobilization or by surgical stabilization (fusion or sometimes insertion of CD rods if the
posterior ligaments are injured).
Fracture-dislocation, as the name implies, denotes a combined injury of a fracture and a
dislocation that is usually accompanied by ligament and cord injury. As with simple
dislocation, realignment is necessary. The fracture must be allowed to heal, and any bone
fragments impinging on the cord must be removed. Therefore, surgery is indicated.

30
Stability or Instability of the Spinal Column.
The conceptof stability of the spinal column is addressed by White and Panjabi and
modified by Greenberg. Clinical stability is the ability of the spine under physiologic loads
to limit displacement so as to prevent injury or irritation of the spinal cord and nerve roots
(including cauda equina) and to prevent incapacitating deformity or pain due to structural
changes. When the spinal column fails to respond appropriately, the spinal column becomes
unstable, which results in injury and predisposes the spinal column, spinal cord, and soft
tissue to further injury. Therefore, nurses will hear much discussion about the clinical
stability or clinical instability of the spinal column, which influences the medical and
surgical managementof the patient. It is critical when considering vertebral fractures to
distinguish between stable and unstable fractures and dislocations. This distinction is often
based on the posterior ligaments. If the posterior ligaments are intact, the injury is
considered stable. If they have been torn, usually by a rotational force, they are considered
unstable. Stability of the vertebral-spinal elements is also addressed using a three-column
theoretical framework.
A stable fracture or dislocation is not apt to displace more than it was at the time of the
injury, whereas an unstable fracture or dislocation is highly likely to displace further with
extension of injury to the spinal cord. External immobilization or internal fixation
may be unnecessary for stable injuries, whereas it is essential for unstable injuries. In
addition, when ligaments heal, scar tissue forms. The scarred tissue, weaker than the
preinjury tissue, may result in chronic instability and lead to SCI.

31
The Three-Column Framework: Spinal Stability and Instability
Spinal stability refers to the ability of the vertebral support column to protect adequately the neural
elements from injury during inactivity and activity. This determination is critical in managing patients
because an unstable injury can result in extension of or new neurological deficits. Currently, criteria
for determining spinal stability or instability are controversial. Some physicians consider only the
condition of the posterior ligaments when determining stability. Another approach is the threecolumn
framework. The three-column approach provides an anatomic framework for considering stability.
The cross-section of the spine isorganized into three anatomic columns:

Three-Column Framework: Spinal Stability and Instability*

• The anterior column consists of the anterior longitudinal ligament, anterior half of the vertebral
body, annulus fibrosis, and disc.

• The middle column consists of the posterior half of the vertebral body, annulus, disc, and posterior
longitudinal ligament.
• The posterior column consists of the facet joints, ligamentum flavum, posterior elements, and
interconnecting ligaments. Applying this classification system to spinal injuries results in four
classification categories, which are determined by the specific column(s) injured

32
Level of Injury
Spinal cord injuries can also be classifi ed according to the segment of the spinal cord that is
affected:
• Upper cervical (C1–C2) injuries (atlas fractures, atlantoaxial subluxation, odontoid
fractures, hangman’s fractures)
• Lower cervical (C3–C8) injuries
• Thoracic (T1–T12) injuries
• Lumbar (L1–L5) injuries
• Sacral (S1–S5) injuries
The degree of functional recovery depends on the location and extent of the injury. The level
of spinal cord injury is determined by the effect of the injury on sensory and motor function.
The dermatome pathways are used to determine the level of sensory loss . Retention of all or
some of the motor or sensory function below the level of injury implies that the lesion is
incomplete, whereas total loss of voluntary muscle control and sensation below the level of
injury suggests that the lesion is complete
ETIOLOGY
Traumatic spinal cord injuries
The most common cause of spinal cord trauma in the UK is an incident involving sudden,
unexpected, impact, collision or deceleration. Speed at impact or height of fall are unreliable
in predicting the potential for spinal injury at the scene.
Non - traumatic spinal cord injuries
Not all spinal cord injuries are caused by trauma. Approximately 28% of all cases of spinal
cord paralysis are due to non - traumatic causes resulting in a similar non - progressive
neurological impairment . These include:
• Ischaemic vascular incidents such as a thrombosis or haemorrhage affecting the spinal cord
blood supply
• Viral and bacterial infections and abscesses such as those associated with tuberculosis and
meningitis
• Infammatory conditions such as transverse myelitis
• Non - malignant growths resulting in spinal cord compression
• Congenital defects such as spina bifida.

33
PATHOPHYSIOLOGY
The primary injury
This is the direct insult to the neural elements and occurs at the time of the initial injury.
The secondary injury
Haemorrhage, oedema and ischaemia results in a biochemical cascade that causes the
secondary injury. This may be accentuated by hypotension, hypoxia, spinal instability and/or
persistent compression of the neural elements. Management of a spinal cord injury must
focus on minimising secondary injury.
Injury to the spinal cord that occurs at the time of impact is referred to as the primary injury.
The more mobile areas of the vertebral column (eg, the cervical area) are most frequently
involved. Damage tothe spinal cord is most often associated with damage to the vertebral
column and ligaments. The vertebrae may be fractured, dislocated (subluxed), or
compressed. As a result of the injury to the vertebral column, the spinal cord itself may be
contused, compressed, or dislocated.
Equally destructive is the injury or damage to the spinal cord that continues for hours after
the trauma. Mechanisms of secondary injury include the following:
• During the inflammatory response, immune cells release harmful substances, causing
cellular damage.
• Hypoperfusion of the spinal cord from microscopic hemorrhage and edema leads to
ischemia.
• The release of catecholamines and vasoactive substances contributes to decreased
circulation and perfusion of the spinal cord.
• The release of excess neurotransmitters results in overexcitation of the nerve cells, which
allows high levels of calcium to enter the cells, causing cellular death.

34
35
CLINICAL MANIFESTATIONS
Spinal shock
Spinal shock is best described as the complete suppressionof all autonomic, somatic, and
reflex activity below the level of lesion. The term neurogenic shock refers specifcally to the
loss of sympathetic activity and the effects this has on the cardiovascular system. The effects
of spinal shock are most profound in complete lesions above the level of T6. On average,
spinal shock usually resolves within 2 – 14 days of onset but can persist for up to 6 weeks .
Although most patients with spinal shock will present at the scene of the accident with the
loss of all voluntary movement and sensation in addition to loss of autonomic and reflex
activity below the level of the injury, it is not uncommon for the onset of clinical symptoms
to be delayed by up to 72 hours after the original incident. Even when symptoms are present
immediately post trauma it is often difficult to be certain of the extent or permanence of the
functional loss. The presence of paralysis or paraesthesia does not imply any finality to the
process. In some instances, when spinal cord oedema and spinal shock resolve there can be a
subsequent improvement in neurological function. Further neurological deterioration,
resulting from lesion extension after the initial SCI, can occur naturally in about 5% of
trauma cases. A number of complications associated with the multisystem effects of SCI can
lead to respiratory, cardiovascular or other system compromise which can further
compromise the body ’ s attempts to limit nerve tissue death and can further reduce any
inherent potential for any degree of spinal cord recovery. Nursing and medical management
is directed at limiting these potential problems.
Complete and incomplete lesions
Spinal cord injuries will result in either complete or incomplete loss of function below the
level of the injury.A complete spinal cord lesion is when the cord is completely transected or
when the ischaemia affects the entire width of the spinal cord. There is complete loss of all
voluntary movement and sensation below the level of the injury. There is also a complete
loss of autonomic nerve function throughout the same area. The majority of patients will
have incomplete spinal cord lesions with varying degrees of impairment of sensory and/or
motor function consistent with the extent of their lesion. Tetraplegia (not quadriplegia) is the
preferred medical term for documenting any spinal cord lesion affecting all four limbs.

36
Paraplegia refers to a lesion affecting only the lower body and without any effect upon the
upper limbs.
Because of the dynamic nature of pathological processes that occur following the initial
incident, the medium and long - term outcomes of any spinal cord lesion cannot be
accurately predicted initially. However, detailed clinical assessments supported by
diagnostic imaging during the first few days and weeks can often help an experienced
clinician to predict what the most likely neurological and functional outcomes will be. MRI
of the spinal cord can inform the clinical prognosis, as the extent of cord compression,
swelling and bleeding are related to neurological outcome.
Complete and incomplete lesions
Spinal cord injuries will result in either complete or incomplete loss of function below the
level of the injury. A complete spinal cord lesion is when the cord is completely transected
or when the ischaemia affects the entire width of the spinal cord. There is complete loss of
all voluntary movement and sensation below the level of the injury. There is also a complete
loss of autonomic nerve function throughout the same area. The majority of patients will
have incomplete spinal cord lesions with varying degrees of impairment of sensory and/or
motor function consistent with the extent of their lesion.

37
Body system Impact of spinal shock
Respiratory Respirations compromised by flaccid skeletal muscles
Inability to cough and expectorate
Danger of vagal overstimulation during suctioning
Nasal passages blocked due to vasodilation
Cardiovascular Hypotension due to systemic vasodilation
Bradycardia due to vagal domination
Poikilothermia – adopting environmental temperature due to loss of
vasodilation, vasoconstriction, sweating, shivering and piloerection
(goose fl esh)

Poor renal perfusion due to hypotension

Genitourinary Loss of ureteric peristalsis
Atonic (flaccid) bladder and urethral sphincters
Pseudopriapism in males due to passive vasodilation
Amenorrhoea in females secondary to metabolic defi cits

Gastrointestinal Increased volume and concentration of gastric acid due to vagal

domination
Paralytic ileus due to loss of peristalsis (usually only for approximately
48
hours following injury)
Atonic (flaccid) ano - rectum and sphincters

38
Skin Increased pressure marking due to vasodilatation
Reduced tissue density over bony prominences and weight - bearing
areas due to redistribution of paralysed muscle bulk
Dry skin as unable to sweat or produce sebum

Incomplete spinal cord lesions

Anterior cord This is the most common form of incomplete lesion after a high - velocity

syndrome impact trauma. Flexion - rotation results in pressure against the

anterior grey horn (contains cell bodies of motor neurones) of the spinal

cord, the anterior spinal artery, and the anterior columns(contain the

spinothalamic and corticospinal tracts). The spinal cord lesion develops

through a combination of physical trauma, bony compression and

ischaemia. Anterior cord lesions result in loss of motor function and the

sensations of pain and temperature below the level of the lesion. The

senses of crude touch, position (proprioception) and vibration are

preserved below the level of the lesion

Posterior impact injuries or hyperextension forces compress or traumatise

Posterior cord
the posterior column and posterior grey horns (sensory) of the spinal cord.
syndrome
Posterior lesions present with the loss of deep touch, position and

vibration below the level of the lesion, with preservation of motor

function and sensations of pain and temperature. Unfortunately, the sense

of proprioception (the unconscious awareness of a limb ’ s position in

39
 space) is lost, which can limit the patient ’ s potential for developing a

functional gait

Brown - This lesion presents as a hemisection of the spinal cord. It is most

Sequard commonly associated with stabbing/penetration injuries, but it may also
syndrome occur from gross lateral fl exion injuries. Motor power is absent or
reduced on the same side as the lesion, but pain and temperature sensation
are preserved. This presentation is reversed on the uninjured side which
has good power but absent or reduced pain and temperature sensation.
This results from the fact that the spinothalamic tracts cross over within
the spinal cord, enabling sensory signals to travel up the side opposite to
that where the origin of the sensation is perceived to be.

Usually occurs in elderly or spondylotic patients after minor

hyperextension trauma to the neck. Vertebrae, discs and ligaments, which
Central cord have become stiffened or thickened with age, focus compression forces
syndrome and ischaemia towards the central portion of the cord, where the cervical
nerve tracts originate. Patients present with significant loss of function in
their upper limbs and hands, and partial preservation of function in their
lower limbs, usually with retained sacral sensation and partially preserved
bladder and bowel function

40
41
Tetraplegia (not quadriplegia) is the preferred medical term for documenting any spinal cord
lesion affecting all four limbs. Paraplegia refers to a lesion affecting only the lower body
and without any effect upon the upper limbs.
Because of the dynamic nature of pathological processes that occur following the initial
incident, the medium and long - term outcomes of any spinal cord lesion cannot be
accurately predicted initially. However, detailed clinical assessments supported by
diagnostic imaging during the first few days and weeks can often help an experienced
clinician to predict what the most likely neurological and functional outcomes will be. MRI
of the spinal cord can inform the clinical prognosis, as the extent of cord compression,
swelling and bleeding are related to neurological outcome.

42
43
Autonomic Dysfunction
The autonomic nervous system carries nerve impulses from the brain and spinal cord to
effector organs throughout the body. Sympathetic nerves exit the spinal cord between C7
and L1, and parasympathetic nerves exit between S2 and S4. Therefore, spinal cord injury
can result in autonomic nervous system dysfunction. Common manifestations of this
dysfunction include spinal shock, neurogenic shock, orthostatic hypotension, and autonomic
dysreflexia.

Spinal shock occurs immediately or within several hours of a spinal cord injury and is
caused by primary and secondary injury to the spinal cord. Clinically, the patient exhibits
the loss of motor, sensory, reflex, and autonomic function below the level of the injury, with
resultant flaccid paralysis. Loss of bowel and bladder function and the body’s ability to
control temperature (poikilothermia) occur. There is no treatment, and the duration of spinal
shock depends on the severity of the insult and the presence of other complications. The
return of perianal reflex activity signals the end of the period of spinal shock.
• Spasticity develops after recovery from the period of spinal shock. A physical therapy
consult is warranted to develop an exercise, stretching, and positioning program for the
patient. Pharmacotherapy (eg, baclofen, dantrolene sodium, diazepam, clonidine) may also
be indicated.
• Neurogenic shock, a form of distributive shock, is seen in patients with severe cervical
and upper thoracic injuries. It is caused by the loss of sympathetic control of the heart and
vasculature, resulting in vasodilation and bradycardia. Signs and symptoms include
hypotension, severe bradycardia, and loss of the ability to sweat below the level of injury.
The hypotension is managed with IV fl uid resuscitation. Symptomatic bradycardia may
require temporary external pacing.
• Orthostatic hypotension may occur in a patient with a spinal cord injury because the
body is unable to compensate for changes in position. The cord injury prevents the
vasoconstriction message from the medulla from reaching the blood vessels.
• Autonomic dysreflexia (hyperreflexia) is a medical emergency that can occur after the
resolution of spinal shock in patients with a spinal cord lesion at T7 or above. The syndrome

44
presents quickly and can precipitate hypertensive crisis and death. In autonomic dysreflexia,
a stimulus below the level of injury produces a sympathetic discharge that causes refl ex
vasoconstriction, leading to extreme hypertension and a throbbing headache.
The body attempts to reduce the hypertension through superficial vasodilation of vessels
above the spinal cord injury, leading to fl ushing, blurred vision, and nasal congestion. Other
signs and symptoms include bradycardia, profuse sweating above the level of the injury,
piloerection below the level of injury, pupil dilation, and nausea.
Precipitating Factors in Autonomic Dysreflexia
• Bladder distention, urinary tract infection, bladder or kidney stones
• Bowel distention
• Pressure areas or decubitus ulcers
• Thrombophlebitis
• Acute abdominal problems (eg, ulcers, gastritis)
• Pulmonary emboli
• Menstruation
• Second stage of labor
• Constrictive clothing
• Heterotopic bone
• Pain
• Sexual activity/ejaculation
• Manipulation or instrumentation of bladder or bowel
• Spasticity
• Exposure to hot or coldremoval of the stimulus.
Nursing Management of Autonomic Dysreflexia
Ideally, three members of the healthcare team are available to assist: one to check the blood
pressure, one to check the drainage system, and one to notify the physician.
1. Elevate the head of bed.
2. Quickly insert bladder catheter or check bladder drainage system in place to detect
possible obstruction.
• Check to make sure plug or clamp is not in catheter or on tubing.
• Check for kinks in catheter or drainage tubing.

45
• Check inlet to leg bag to make sure it is not corroded.
• Check to make sure leg bag is not overfull.
• If none of these are evident, proceed to step 3.
3. Determine whether catheter is plugged by irrigating the bladder slowly with no more than
30 mL of irrigation solution. If symptoms do not subside, proceed to step 4.
4. Change the catheter and empty the bladder.
5. If bladder overdistention does not seem to be the cause of the dysreflexia, rule out other
potential causes:
• Check for bowel impaction. Do not attempt to remove impaction, if present. Apply
Nupercainal ointment or Xylocaine jelly to the rectum and anal area. As the area is
anesthetized, the blood pressure should decrease. After the blood pressure stabilizes, using
generous amount of anesthetizing ointment or jelly, manually remove the impaction.
• Change the patient’s position to relieve pressure.
• Loosen tight clothing and shoes.
6. Continue monitoring the blood pressure (BP) during this time. If the BP remains elevated
and unable to find the source, call the physician immediately. The physician may order an
antihypertensive to lower the blood pressure.
PATIENT ASSESSMENT
Basic points Spinal immobilisation.
Advanced Trauma Life Support
(ATLS) principles apply in all cases .
The spine should initially be
immobilised on the assumption that
every trauma patient has a spinal
injury until proven otherwise . The
finding of a spinal injury makes it
more likely (not less) that there will
be a second injury at another level.
Spinal boards lead to skin breakdown
in insensate patients, and are very

46
uncomfortable for those with normal sensation. Therefore, they are for very short-term use
only
The unconscious patient
Definitive clearance of the spine may not be
possible in the initial stages and spinal
immobilisation should then be maintained, until
magnetic resonance imaging (MRI) or equivalent
can be used to rule out an unstable spinal injury
PHYSICAL EXAMINATION
Initial assessment
The primary survey always takes precedence,
followed by careful systems examination, paying
particular attention to the abdomen and chest.
Spinal cord injury may mask signs of
intraabdominal injury.
Identification of shock
Three categories of shock may occur in spinal
Spinal log roll
trauma:
1 Hypovolaemic shock. Hypotension with tachycardia and cold clammy peripheries. This is
most often due to haemorrhage. It should be treated with appropriate resuscitation.
2 Neurogenic shock. This presents with hypotension,
a normal heart rate or bradycardia and warm
The bulbocavernosus reflex (this
peripheries. This is due to unopposed vagal tone can be elicited in females by
traction on the Foley catheter).
resulting from cervical spinal cord injury above the
level of sympathetic outflow (C7/T1). It should be
treated with inotropicsupport, and care should
betaken to avoid fluid overload.
3 Spinal shock. There is initial loss of all
neurological function below the level of the injury. It
is characterised by paralysis hypotonia and areflexia.
It usually lasts 24 hours following

47
spinal cord injury. Once it has resolved the bulbocavernosusreflex returns.
Spinal examination The entire spine must be palpated and the overlying skin inspected. A
formal spinal log roll must be performed to achieve this . Significant swelling, tenderness,
palpable steps or gaps suggest a spinal injury. Wounds may be part of penetrating trauma.
Seat belt marks on the abdomen and chest mustbe noted, as these suggest a high energy
accident.

PERTINENT HISTORY
The mechanism and velocity of injury should be determined at an early stage. A check for
the presence of spinal pain should be made. The onset and duration of neurological
symptoms should also be recorded.
Neurological examination
The American Spinal Injury Association (ASIA) neurological evaluation system is an
internationally accepted method of neurological evaluation. Motor function is assessed using
the Medical Research Council (MRC) grading system (0–5) in key muscle groups. A motor
score can then be calculated (maximum100). Sensory function (light touch and pin prick) is
assessed using the dermatomal map . A total sensory score is then calculated. Rectal
examination is performed to assess anal tone, voluntary anal contraction and perianal
sensation.
Level of neurological injury
The level of neurological injury is simply the most caudal neurological level with normal
neurological function.
Complete versus incomplete spinal cord injury
A spinal cord injury is incomplete when there is preservation of perianal sensation.
Type of incomplete spinal cord injury
There are several types of incomplete spinal cord injuries. These include: central cord
syndrome, Brown-Séquard syndrome (hemisection), anterior spinal syndrome, posterior
cord syndrome and cauda equina syndrome.
Guidelines for transferring acute spinal cord injured patients
• The expected total journey time should usually not exceed 2.5 hours. If the journey is
likely to exceed 2.5 hours, consider aeromedical transfer or consult with the receiving SCI
centre regarding the possibility of delaying the transfer

48
• Inform the receiving SCI centre of the time that the patient left and their expected time of
arrival at the SCI centre
• All relevant medical, nursing and therapy notes, diagnostic imaging fi les and laboratory
reports must accompany the patient as either copies or originals
• An experienced and informed member of medical and/ or nursing staff, who is familiar
with the care that the patient has received before transfer to the SCI centre, is an essential
requirement as an escort. An anaesthetist must escort the SCI patient at risk of respiratory
difficulties
• It is possible for the SCI patient to vomit while being transferred, so their stomach should
be emptied before transfer. Other potential complications that may be encountered en route
are hypothermia, pressure ulcers, respiratory compromise, further neurological deterioration
and autonomic dysrefl exia. Additional patient distress may occur if the level of pain control
is inadequately maintained during transportation
• Transferring a SCI patient on a spinal board is not always required and the planned use of
any spinal protective devices during transfer should always be discussed in advance with SCI
centre staff
ASIA Impairment Scale (AIS)
ASIA score is the score developed by the American Spinal Injury Association for essential
minimal elements of neurologic assessment for all patients with a spinal injury. This is based
on scores as assessed by the examiner and is popularly called ASIA score.These minimal
elements are strength assessment of ten muscles on each side of the body and pin-prick
discrimination assessment at 28 specific sensory locations on each side.

Method of calculation

Sensory Examination

The sensory levels are scored on a 0 to 2 scale for each dermatome. If the body is divided
into two identical halves there are 28 key sensory points to be tested. Each dermatome is
tested for light touch and pinprick sensations and labeled as NT (not testable) if cannot be
tested. Otherwise, the following scores are given to each sensory point

49
  0 – The sensation is absent
 1 – The sensation is present but impaired
 2 – The sensation is normal

Scores are individually tested for both light touch and pinprick are normal. A maximum
possible score is 112 points for each of them for a patient with normal sensation. In addition,
presence or absence of anal sensation is noted.

Motor Examination

10 key muscles, 5 in the upper limb and 5 in the lower limb are tested. Five specific upper
extremity muscles, one from each respective segment of the cervical cord, are scored on a 5-
point muscle grading scale. Five specific lower extremity muscles are similarly
scored.Muscle strength is graded as

 0 Total paralysis
 1 – Palpable or visible contraction
 2 – Active movement, full range of motion, gravity eliminated
 3 – Active movement, full range of motion, against gravity
 4 – Active movement, full range of motion, against gravity and provides some
resistance
 5 – Active movement, full range of motion, against gravity and provides normal
resistance [Muscle able to exert, in examiner’s judgement, sufficient resistance
to be considered normal if identifiable inhibiting factors were not present]
 NT – not testable. Patient unable to reliably exert effort or muscle unavailable
for testing due to factors such as immobilization, pain on effort or contracture.

The sum of all 20 muscle yields a total motor score for each patient, with a maximum
possible score of 100 points for patients with no weakness. A different score, however, for
upper limbs and lower limbs can be calculated making it 50 maximum for both upper and
lower limb.

50
Voluntary anal contraction is also noted.

Determine Single Neurological Level

After motor and sensory levels have been determined, the information is assimilated for
determining a single neurological level. This is important because the sensory and motor
level may differ.The neurological level is the lowest segment where the motor and sensory
function is normal on both sides and is the most cephalad of the sensory and motor levels
determined in sensory and motor examination.

Complete or incomplete spinal cord injury

The injury is complete if there is

 No voluntary anal contraction

 S4-5 sensory scores = 0
 no anal sensation = No

Otherwise, the injury is incomplete.

A = Complete. No sensory or motor function is preserved in the sacral segments S4-5.

B = Sensory Incomplete. Sensory but not motor function is preserved below the
neurological level and includes the sacral segments S4-5 (light touch or pin prick at S4-5 or
deep anal pressure) AND no motor function is preserved more than three levels below the
motor level on either side of the body.
C = Motor Incomplete. Motor function is preserved at the most caudal sacral segments for
voluntary anal contraction (VAC) OR the patient meets the criteria for sensory incomplete
status (sensory function preserved at the most caudal sacral segments (S4-S5) by LT, PP or
DAP), and has some sparing of motor function more than three levels below the ipsilateral
motor level on either side of the body. (This includes key or non-key muscle functions to
determine motor incomplete status.) For AIS C – less than half of key muscle functions
below the single NLI have a muscle grade ≥ 3.

51
D = Motor Incomplete. Motor incomplete status as defined above, with at least half (half or
more) of key muscle functions below the single NLI having a muscle grade ≥ 3.
E = Normal. If sensation and motor function as tested with the ISNCSCI are graded as
normal in all segments, and the patient had prior deficits, then the AIS grade is E. Someone
without an initial SCI does not receive an AIS grade

When to Test Non-Key Muscles:

In a patient with an apparent AIS B classification, non-key muscle functions more than 3
levels below the motor level on each side should be tested to most accurately classify the
injury (differentiate between AIS B and C)

Movement Root level

Shoulder: Flexion, extension, C5
abduction,adduction, internal and external
rotation
Elbow: Supination C6
Elbow: Pronation Wrist: Flexion
Finger: Flexion at proximal joint, extension. C7
Thumb: Flexion, extension and abduction in
plane of thumb

Finger: Flexion at MCP joint Thumb: C8

Opposition, adduction and abduction
perpendicular to palm
T1
Finger: Abduction of the index finger T1
L2
Hip: Adduction L3

Hip: External rotation L4

Hip: Extension, abduction, internal rotation

52
Knee: Flexion Ankle: Inversion and eversion
Toe: MP and IP extension
Hallux and Toe: DIP and PIP flexion and L5
abduction
Hallux: Adduction S1

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54
DIAGNOSTIC IMAGING
Plain radiographs
A full cervical spine series includes anteroposterior and lateral views of the whole cervical
spine, and open mouth views. However, in many trauma centres computed tomography (CT)
scanning, with sagittal reformats, is considered more accurate.
This modality is particularly useful in visualising the cervicothoracic junction and in
surveying the entire spine.
Diagnostic imaging for potential spinal injury is directed by the accident history and clinical
examination. It usually begins with a series of plain x - rays to provide anteroposterior and
lateral views of the spinal column. Cervical views must include the odontoid peg and the C7
– T1 junction.However, because of the difficulty in adequately imaging the spine in this
way, many emergency departments now prefer to routinely CT the whole spine instead. CT
of the spine is essential for any patient who presents with a neurological deficit following
trauma. MRI of the spine should follow at the earliest opportunity, especially if surgical
stabilisation is being planned. When head injured or multi - trauma patients are sent for CT
scanning, every opportunity should be sought to extend the scan to include the whole spine
to avoid the need to return later after admission .

55
A system for evaluation of the lateral cervical spine x-
ray
1 Assessment of prevertebral soft tissue swelling

2 Assess sagittal alignment using three imaginary lines

3 Assess for instability.
a 3.5 mm of sagittal translation;
b Sagittal angulation of >11° (compared to adjacent level).

56
Computed tomography
CT scanning with two-dimensional reconstruction remains the most sensitive imaging
modality in spinal trauma.

Magnetic resonance imaging

MRI is indicated in cases with neurological deficit and where assessment of ligamentous
structures is important.

Steroid use
Evidence to support the administration of short - term, high - dose steroids such as
methylprednisolone as a defi native strategy for reducing the impact of a traumatic SCI is
extremely limited. The accumulated studies have been critically appraised within the
framework of evidence - based practice (Short, 2001 ) and the routine administration of high
- dose methylprednisolone can no longer be justified within current medical practice as a
standard treatment for acute spinal cord injury .High dose methylprednisolone can prove
hazardous for the patient and is associated with a significant increase in the incidence of
unexpected sepsis and pneumonia leading to ventilation and admission to intensive care .

57
CLASSIFICATION AND MANAGEMENT OF SPINAL AND SPINAL CORD
INJURIES
Medical management of acute spinal cord injury
Early recognition of actual or potential spinal cord injury utilizing:
• Accident history and mechanism of Injury
• Patient history and presenting symptoms
• Clinical survey including neurophysiological examination (including sacral nerve
pathways)
• Diagnostic Imaging Implement initial management of patient in accordance with local
trauma protocols:
• Prioritise interventions according to ATLS guidelines.
Ensure the judicious administration of fluid and pharmaceutical resuscitation protocols in
accordance with the diagnosis of actual or potential spinal cord injury as there is a signifi
cant potential for substantial over infusion and subsequent pulmonary oedema if neurogenic
hypotension is confused with hypovolaemia.
• Management of spinal shock may include the adaptation of local hospital early warning
score indicators to incorporate the physiological impact of spinal shock to avoid
inappropriate ‘ triggering ’ of unnecessary medical alerts or treatment interventions
Ensure accurate documentation of findings and actions undertaken:
Telephone referral of actual or suspected spinal cord injured patient to spinal cord injury
consultant at locally nominated spinal cord injury centre within 24 hours of diagnosis being
made. Additional information sent by fax and/or electronic data transfer as soon as possible
after referral. Maintain close collaboration with spinal cord injury consultant regarding the
options for surgical management of spinal trauma and the initial medical and multi -
professional management of spinal shock until transfer or further case discussion. This may
include seeking advice regarding the way in which the paralysis may mask the normal
symptoms of underlying soft tissue trauma or visceral complications.
Inform patient ’ s next - of - kin accurately of the diagnosis and tentative prognosis (if
appropriate) as advised by expert clinical peer. Where patient has been accepted for transfer,
include within this discussion the need to eventually transfer their relative to a tertiary
specialist centre which may be some distance away.

58
Prehospital Management
A spinal cord injury is suspected at the scene of an accident any time the patient has
decreased or absent movement or sensation. An unconscious patient or one with a head
injury is treated as though a spinal cord injury has occurred until proved otherwise. Airway
patency is assessed, and the cervical spine is immobilized and stabilized. A cervical collar
increases the level of stability but does not provide complete immobilization, especially in
the case of complete ligamentous disruption.
In-Hospital Management
Early Management
In the emergency department, the primary and secondary surveys are completed.
Management priorities include:
• Assessment and management of the patient’s airway and breathing.
Hypoventilation or respiratory failure from inadequate innervation of the respiratory
muscles and diaphragm is a common problem after spinal cord injury, particularly in
patients with high cervical injuries. In addition, spinal cord edema can act like an ascending
lesion and compromise function of the diaphragm. Preexisting pulmonary disease or
coexistent chest, laryngeal, tracheal, or esophageal injuries can further compromise
respiratory function. If the patient requires ventilator assistance, elective intubation and
mechanical ventilation are followed by a chest radiograph.
• Assessment and management of the patient’s circulatory status.
Hypotension may be due to neurogenic shock or hemorrhagic shock (secondary to
associated injuries). Fluid resuscitation is accomplished by the use of crystalloids or blood.
Early administration of blood enhances oxygenation and may minimize secondary ischemic
injury to the spinal cord.
• Completion of a thorough neurological assessment, including spine x-rays.
A digital rectal examination is performed to determine whether the injury is incomplete or
complete. The lesion is incomplete if the patient can feel the palpating finger or can contract
the perianal muscles around the finger voluntarily. Sensation usually accompanies voluntary
motor activity, and may be present in the absence of voluntary motor activity. In either case,
the prognosis for further motor and sensory return is good. Rectal tone by itself, without the

59
presence of voluntary perianal muscle contraction or rectal sensation, is not evidence of an
incomplete cord injury.
• Assessment for associated injuries.
TBI, intrathoracic injuries, intra-abdominal injuries, retroperitoneal injuries, and fractures
of the pelvis or long bones are often seen in association with spinal cord injury,When the
patient is stabilized, frequent assessment of neurological status is necessary to determine the
extent of the spinal cord injury and monitor for changes in level of consciousness that may
occur secondary to TBI. Most facilities use a specialized flow sheet. Classification of Spinal
Cord Injury flow sheet to assess and document the patient’s level of functioning.
Diagnostic studies may be ordered, including radiographs of the spine, chest, and other
structures as clinically indicated; CT and MRI (to evaluate soft tissue and ligament injuries).
Flexion–extension views are obtained to assess for ligament involvement in patients who are
conscious and can follow commands, even when plain radiographs and CT are negative for
bony injury. If the patient is unconscious or unable to tell the examiner if there is pain on
flexion, then an MRI is required to rule out ligament injuries. A cervical collar is kept on
until the MRI results are obtained or the patient regains consciousness and is able to
cooperate with the studies. The administration of high-dose steroids (eg,
methylprednisolone) in the emergency department to reduce swelling and minimize
secondary injury is controversial. Some studies have found improvement in function in
blunt, incomplete cord injuries. However, steroid use has also been associated with severe
pneumonia and sepsis.
Stabilization of the Spine
The goals of ongoing management are to stabilize and realign the spine to prevent further
neurological deterioration. This can be accomplished through closed reduction or surgical
techniques. Closed reduction of an unstable cervical fracture or subluxation often involves
skeletal traction. Short-term cervical traction can be achieved using Gardner– Wells, Vinke,
or Crutchfield tongs; long-term cervical traction entails the use of a halo vest. Stable
fractures can be immobilized using a Miami J or Aspen collar (cervical fractures), a Minerva
brace (cervicothoracic fractures), or a Jewett brace (thoracolumbosacral injuries). For some
patients, surgery may be necessary to stabilize and support the spine. The risks of surgery
must be balanced against the possible benefi ts. Rod placement, laminectomy and fusion,

60
and anterior fusion are techniques used for surgical stabilization. Bone for fusion usually
comes from the patient’s iliac crest, tibia, or ribs; alternatively, bone can be obtained from a
tissue bank. After surgery, the patient receives routine postoperative care. The nurse
monitors the patient’s motor and sensory status at least every hour for the first 24 hours, and
then every 4 hours after that. The physician is notifyed immediately if any deterioration in
neurological status occurs. The nurse also monitors for complications (eg, spinal fluid fi
stulas, infections, wound dehiscence). Older patients and those with preexisting
comorbidities who have open wounds, injuries to the thoracolumbar spine, or complete
injuries are at particularly high risk for postoperative infection.
Supportive Care
Supportive care focuses on preventing complications, and initiating prompt interventions to
treat any complications that do occur.
Basic management principles
Spinal realignment
In cases of cervical spine subluxation or dislocation, skeletal traction is necessary to achieve
anatomical realignment. This is done using skull tongs .
In many cases of spinal trauma, formal open reduction and stabilisation using internal
fixation is also required. A halo brace can be used to hold a closed realignment of cervical
fractures .
Stabilisation
The indication for operative intervention is influenced by the injury pattern, degree of
instability and the presence of a neurological deficit. The only absolute indication for
surgery in spinal trauma is deteriorating neurological function. Decompression of the neural
elements Decompression involves spinal realignment and/or direct decompression of the
neural elements. The timing of surgery in spinal cord trauma remains controversial.
Corticosteroids
Many spinal trauma centres no longer use steroids in cases of spinal cord injury due to lack
of evidence to support efficacy.

61
SURGICAL MANAGEMENT OF SPINAL CORD INJURY
Neurological assessment data and imaging studies provide the foundation for determining
the best approach to treatment. If surgery is indicated, selecting the best time for surgery
is critical. Early surgery (within the first 12 to 24 hours) can preserve or improve spinal cord
function. However, other clinicians prefer to have the patient well stabilized before
proceeding to surgery. The following are reasons for early surgery:
• Evidence of cord compression
• Progressive neurological deficit
• Compound fracture of the vertebra (potential for bony fragments to dislodge and penetrate
the cord)
• Penetrating wounds of the spinal cord or surrounding structures
• A bone fragment evident in the spinal canal
Early surgery is usually postponed in the following circumstances:
• When rapid and significant improvement in neurological function is demonstrated
• When staging is necessary, for instance, the need before surgery to first realign the
vertebral column or to reduce dislocations or fracture-dislocations through traction or
immobilization When a life-threatening injury or disease exists elsewhere in the body. With
severe trauma, the patient may have other injuries such as a brain injury, contused kidney,
cardiac contusion, intestinal rupture, or other problems in addition to SCI. Emergency
surgery for life-threatening injuries, such as a ruptured spleen, may be necessary. The
patient’s condition may not be stable enough to tolerate prolonged anesthesia and spinal
surgery.
Types of Procedures
For neural decompression, a posterior (most common), anterior, or lateral laminectomy is
performed. For stabilization, the most common procedure is a posterior laminectomy. An
open reduction and internal fixation with instrumentation is performed that utilizes plates,
screws, wires, and rods. A fusion, using autologous iliac bone graft, may also be performed.
It is beyond the scope of this text to summarize the selection criteria for surgical options or
surgical instrumentation.

62
All instrumentation systems have the same basic components that include a vertical device
and a fixation or anchoring device The vertical device is a rod or a plate that is attached
lengthwise to the vertebral column to provide stabilization.
Fixation or anchoring devices, which attach the vertical rod or plate to the vertebra, are
wires, screws, or hooks oriented at right angles to the vertical device. All systems pose
potential complications because of system failure as well as postoperative wound infection.
There are a number of available systems include Harrington rods, Luque rods, and the CD
system.
Harrington rods, developed in the early 1960s, were originally the cornerstone of spinal
surgery instrumentation. The Harrington rod system consists of a rod or rods and wires
affixed to the base of spinous processes and to the rod. This provides multiple fixation
points for stabilization. In some cases, loss of reduction with progressive kyphotic deformity
occurred in patients treated with Harrington instrumentation. Current instrumentation
systems are much more rigid and allow for segmental spinal fusion. CD rods, introduced in
the early 1990s, are an example. These rods, used in conjunction with lamina hooks or
pedicle screws, are the current approach for thoracic lumbar instrumentation.This system
provides for multiple points of fixation and greater stabilization. CD rod placement,
although technically more difficult, does not usually require postoperative immobility.
Ideally, use of CD instrumentation facilitates early mobility of the patient.

A halo, also known as a "halo ring" or "halo crown," is a piece of equipment that encircles
and is fixed to the head of a patient. This device is crucial for the
management of a variety of conditions that destabilize the cervical
spine.

Background
Although bed-based spinal traction has been used since the early
1930's for the stabilization or reduction of cervical spinal cord
injuries, the complications that occur with long-term confinement
to bed (pressure sores, muscle wasting, etc.) are considerable. In
the late 1950s, the concept of the "halo vest" was first described.
This technique is based on the attachment of the halo to a device

63
worn around the patient's torso, rather than equipment attached to a hospital bed, to provide
the needed force to immobilize the cervical spine.

The modern version of the halo vest attaches through adjustable metal bars to a rigid,
lightweight, fleece-lined vest that fits snugly about the patient's chest. This apparatus
provides continuous stability to the cervical spine while simultaneously allowing the patient
to be comfortable and mobile.

The advantages of the halo vest include precise positional control and solid external
stabilization of the cervical spine, ease of application, a low complication rate, minimal
patient discomfort, and early patient mobilization. The halo vest has been shown to be
extremely effective at preventing further neurological injury for patients who have sustained
cervical spinal injuries. Studies have demonstrated excellent rates of healing after three
months of halo vest use; however, in some cases there may be persistent instability from
bony or ligamentous damage to the cervical spine and surgery could be necessary to ensure
proper stabilization.At times a halo is needed to stabilize the cervical spine after surgery.
The role of the halo is to hold the spine immobile until the fusion matures.

Application of a Halo and Halo Vest

Fixation of the halo to a patient's head relies on a series of four titanium "pins" which are
equally spaced around the ring. After injection of a local anesthetic, the pins are placed in
tight connection with the head at two locations on each side (generally over the ridge of the
orbit and just behind the ear). The vast majority of patients do not experience significant
pain from the pins being too tight; in fact, loosening of the pins is by far the most common
cause of pain at the pin sites. Once the halo is in place, the physician may want to keep the
patient in bed-based traction for a few days before connecting the vest and getting the
patient up and around.

Once the halo vest is in place and appropriately positioned, a series of radiographs are
obtained to ensure adequate immobilization and positioning of the cervical spine. When this
has been verified, the patient is generally ready to go home. Accepted conservative
management of cervical spine instability requires the use of a halo vest for a period of three
months. Studies have shown that only a small minority of patients (~2%) find this three-

64
month period to be too long and will not tolerate the halo vest. During these three months,
the physician will want to see the patient back at regular intervals to verify the proper
positioning and tightness of the halo vest. These visits are usually more frequent early in the
course of the treatment. At these appointments, the patient will have the same series of
radiographs that were performed initially (again, to ensure adequate positioning and
stabilization of the cervical spine). In addition, the physician will do a complete neurological
assessment of the patient and tighten all of the hardware on the halo vest.

Side Effects/Complications

 Pin loosening is by far the most common of the potential complications. This
happens in about 60% of patients over the three-month course and, as mentioned
above, can result in some pain at the pin sites. However, this situation is very easily
remedied by ensuring tightness of the pins at each of the weekly follow-up visits.
 Infection at the pin sites is another potential complication that is much less common,
occurring in only 10-20% of patients. If a pin site does become infected, the pin will
most likely be removed and another pin placed in a new site.
 Serious side effects are extremely rare, and infection can be avoided by ensuring that
daily cleaning of the pin sites is performed. Adequate cleaning of the patient's skin
and fleece vest liner are crucial to prevent the possibility of localized skin breakdown
or the rare pressure sores that can be caused by the vest itself.
 Initially, the patient may have some difficulty with balance after having their cervical
spine fixed in place with a halo vest. This problem will rapidly improve as the
patient becomes more accustomed to the device.
 The patient may have some difficulty sleeping in the initial period after application
of the halo vest. After the vest is removed, some patients feel that their heads are
heavy or wobbly due to weakening of neck muscles, which have not been used for
some time. This resolves over the next few weeks. Occasionally physical therapy is
helpful in alleviating the problem.

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Cervical traction and halo devices
Cervical traction is a non - invasive method for the reduction and stabilisation of spinal
fractures and dislocations. It is the method of choice for patients unsuitable for surgery or
for whom surgery is not a priority. Guidelines for the appropriate application and
maintenance of cervical traction and halo brace systems are well established in most trauma
and critical care environments. Nursing management is orientated towards monitoring the
patient after application for any discernible change in neurology and maintaining the
condition and security of the traction cord, knots, weights and runners. The position of the
traction tongs or halo ring should be checked for any signs of slipping from the original
position. Pin – sites should be inspected daily for signs of excessive encrustation, pain,
bleeding, swelling or obvious infection.
Cleaning, dressing and swabbing of pin sites is undertaken in accordance with local policy,
but normal saline usually suffices for routine cleaning Gardner – Wells traction tongs have
an indicator pin situated within a pin head. Secure pressure is indicated whenever the pin
stands proud of its base and set on insertion. The traction should be tightened whenever the
pin is noted to be receding from this position. A compatible torque screwdriver is needed for
checking and tightening halo pins as required. A suitably sized spanner, key or wrench,
should always be available at the patient ’ s bedside in the event that the traction needs to be
removed in an emergency. During reduction of a cervical dislocation, traction weights are
applied under x - ray guidance. These are increased in stages and weight in excess of 60 lb
can be required before a successful reduction is achieved. During this time, the consultant
may manually adjust the angle of the patient ’ s neck between extension and flexion. He may
also request changes in the foot down angle of the patient ’ s bed to alter the amount of
counter traction provided by the patient ’ s body. With so many staff circulating around the
patient ’ s bed, care must be taken not to dislodge a traction weight onto a foot. After
reduction of the dislocation, the traction weight and bed angle will be reduced to support a
minimum maintenance weight of only a few pounds. This weight must never be removed
during turning unless it is first replaced by manual traction and/or a suitably prescribed
cervical collar. In addition, the consultant will indicate the degree of neck flexion/extension
required to maintain cervical alignment. This must be maintained during logrolling. Similar
precautions should be applied during transfers between fl at surfaces. When moving a

66
patient in bed between departments, ensure the traction weight does not pendulum too much.
If a halo jacket is being used, check to ensure that the jacket has been fitted with the hinged
access panel facing uppermost, for use in the event of cardiac arrest to provide chest
compressions. Check fastenings for security and wear and tear daily. Also ensure that an
appropriate wrench or hexagonal key to unfasten the frame struts is available (usually kept
taped to the jacket) in the event of an emergency. The cutaway panels in modern jackets
usually allow sufficient access for checking underlying skin condition. Skin under the jacket
can be washed with a damp cloth and dried. To maintain the underlying skin and jacket
lining in best condition, moisturising creams should be used sparingly and talcum powder
should not be used. If necessary, with the patient supine, the lining of most jackets can be
replaced or laundered as appropriate. Never use any part of the halo, jacket or framework as
a handhold during turning or transferring between surfaces.

Cervical collars

The management of cervical collars for patients with SCI during an extensive period of
supine bedrest continues to present nurses with many challenges . The decision to
discontinue spinal precautions is a medical decision and the clinical and radiological
investigations necessary to inform such a decision may take some time to complete.
Therefore, the decision to discontinue spinal precautions should not be unduly influenced by
the pressures and constraints that such a device places upon the delivery of nursing care
procedures. Nursing staff, as much as doctors, need to understand that radiological clearance
alone is insufficient to discontinue the use of spinal protective devices. The doctor
authorising removal of a cervical collar must document this decision in the patient ’ s
medical notes, citing the screening process which was followed before it is removed. The
two most commonly reported nursing concerns are the development of pressure ulcers

67
beneath the collar and the potential for increasing intracranial pressure (ICP) in patients with
accompanying or suspected traumatic brain injury (TBI)
Reducing pressure ulcer incidence in cervical collar use
It is important for nurses to know how to measure and size a cervical collar and to be aware
of the different types available. SCI patients are usually admitted wearing a rigid extraction
collar that was measured and fitted at the accident scene or in A & E. These collars are often
applied whilst a patient is sitting and need to be adjusted or replaced with a collar of a
different size or type to accommodate supine - lying pressures, for greater security and
patient comfort. Aspen and Philadelphia collars have been evaluated as having the lowest
potential for causing pressure ulcers in longer - term use and should replace the hard
extraction collars within 48 hours of admission. Most collars contain pre - cut access panels
for observation of the position of the trachea, accessing the blood vessels of the neck and
positioning tracheostomy tubes. Most pressure ulcers related to the wearing of cervical
collars during supine bed rest can be prevented through a programme of regular turning and
observation of the underlying skin, good skin hygiene and, where permitted, periods spent
without the collar in situ .
Strict attention must also be paid to collar hygiene. The inner surface of the collar should be
washed and dried, or its inner lining changed, every day.
Managing cervical collars in the presence of actual or suspected raised ICP
Collars should not be routinely discarded just because of the presence of actual brain injury.
Any new or problematic increase in ICP or symptomatic neurological deterioration must
first be identified as being related to the cervical collar in use. In such instances, close and
regular liaison with local specialists enables staff to adapt their care provision over time, and
to provide appropriate levels of spinal protection throughout the patient ’ s admission. First
establish that the collar has been sized and fi tted appropriately. If loosening or adjusting the
collar does not improve ICP within 15 minutes then the collar is not a contributing factor
and should be re - secured appropriately.If ICP does improve following loosening of the
collar then re - sizing the collar or changing it to a different type of collar may provide
cervical support without compromising ICP.

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Moving and handling patients with SCI
Wherever there is a reasonable suspicion of acute SCI, the aim is to maintain full spinal
alignment during any moving and handling activity. Careful handling, positioning and
turning, on every occasion, can reduce the potential for secondary spinal cord trauma during
patient transfers and movements. Maintaining full spinal protection during logrolling
involves at least four members of staff to maintain spinal alignment throughout the
procedure. Additional staff will be required to undertake examination or care associated with
the logroll such as washing and checking of skin, placement of pillows, insertion or removal
of transfer devices, etc. Nurses required to undertake the turning or transferring of actual or
potential SCI patients during the acute period must have supreme confidence in their ability
to work as a team, especially when other health service staff are involved. It is essential that
all moving and handling is coordinated by a nominated team leader.
Routine two - hourly turning and repositioning of SCI patients during the initial period of
spinal shock can reduce the incidence of multi - system complications of acute bedrest by
reducing the extent and duration of pressure on weight - bearing areas and also the duration
of fluid stasis in the body . As spinal shock resolves and the patient ’ s systemic condition
improves, a three to four hourly turning regime can be implemented until transfer to a SCI
centre or specialist rehabilitation unit.
Logrolling
Four nurses are needed to log - roll an acute tetraplegic patient and this does not vary in the
acute SCI patient even following surgery. Three nurses suffi ce for paraplegic patients as the
head does not need to be held. All commands will come from the team leader who is always
the nurse holding or nearest to, the patient ’ s head.

Logrolling patients with cervical SCI

After explaining how the turn is to be accomplished, the team leader positions their hands to
support the patient ’ s head and cervical spine. Hands should be positioned to support the
whole of the patient ’ s neck. The left hand of the second nurse is positioned at the patient ’ s
shoulder and the right hand on the upper pelvis. The left hand of the of the logroll . When
the next turn is due it is imperative that staff members occupy a different position in the
turning team to avoid repetitive strain injury. This is particularly so for the nurse holding the

69
head. After full examination of the underlying skin for signs of pressure damage, pillows or
foam wedges can now be placed in situ , suffi cient to maintain the patient in a 30 ° lateral
position. Lateral positioning can vary between 30 ° and 90 ° dependent upon skin condition,
comfort and clinical need, although a position between 20 ° and 30 ° is preferred in order to
prevent excessive pressure being exerted upon the lower (right) trochanter of the hip. Where
staffing numbers make manual turning difficult, or where a patient presents with injuries to
both the cervical and thoracolumbar spine, or with multiple injuries, which make lateral
positioning difficult or painful, an electric turning bed such as Huntleigh ’ s Atlas can be
used.

SPECIFIC SPINAL INJURIES

Upper cervical spine (skull–C2)
Craniocervical dislocation
This injury is usually caused by high energy trauma and is often fatal. The dislocation may
be anterior, posterior or vertical Power’s ratio is used to assess skull translation.
Atlantoaxial instability
This is uncommon and either resolves spontaneously or with traction. Isolated, traumatic
transverse ligament rupture leading to C1/2 instability is uncommon and is treated with
posterior C1/2 fusion .
Occipital condyle fracture
This is a stable injury often associated with head injuries, and is best treated in a hard collar
for 8 weeks.
Jefferson fractures (C1 ring)
These injuries are associated with axial loading of the cervical spine and may be stable or
unstable . transverse ligament rupture may occur . Most are treated non-operatively in a
collar or halo brace.
Odontoid fractures
There are three types of Odontoid peg fracture . Neurological injury is rare. The majority of
acute injuries are treated non-operatively in a halo jacket or hard collar for three months.
Internal fixation with an anterior compression screw is indicated in displaced fractures .
Posterior C1/2 fusion is required in cases of non-union.

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Hangman’s fracture
The Hangman’s fracture is a traumatic spondylolisthesis of C2 on C3. There are four types
with varying degrees of instability. Those with significant displacement or associated facet
dislocation are treated operatively, usually with posterior stabilisation.
Subaxial cervical spine (C3–C7)
The pattern of lower cervical spine injury depends on the mechanism of trauma. These
include wedge (hyperflexion), burst (axial compression), tear-drop fractures
(hyperextension) and facet subluxation/dislocation (rotation and hyperflexion). The more
severe injuries are accompanied by spinal cord injury. Operative intervention may be
required to decompress the spinal cord and stabilize the spine with internal fixation .Facet
subluxation/dislocation ranges in severity from minor instability to complete dislocation
with spinal cord injury
Thoracic and thoracolumbar fractures
The system developed by the AO (Arbeitsgemeinschaft fu˝rOsteosynthesefragen) can be
used to classify these fractures. There are three main injury types (A, B and C) with
increasing instability and risk of neurological injury. Type A fractures involve the vertebral
body. Type B injuries have additional distraction/ disruption of the posterior elements and
type C injuries are AO (Arbeitsgemeinschaft fu˝r Osteosynthesefragen) which may be
translated from the German as ‘Working Party on Problems of Bone Repair’. rotational.
The majority of type B and type C injuries require surgical stabilization.
Thoracic spine (T1–T10)
Osteoporotic wedge compression fractures in the elderly are the most common injury in this
group. Symptomatic fractures can be treated with percutaneous bone cement augmentation,
known as vertebroplasty or kyphoplasty . In trauma cases, unstable fractures are associated
with significant energy transfer to the patient and may be associated with major internal
injuries, such as pulmonary contusion and spinal cord injury. The combination of thoracic
spine disruption and a sternal fracture also carries a significant risk of aortic rupture.
Multiple posterior rib fractures and rib dislocations above and below a thoracic spinal injury
signify a major rotational injury to the chest and are associated with vascular injury and
significant pulmonary contusion . Multimodality diagnostic imaging is recommended.
Surgery is appropriate in almost all unstable thoracic injuries.

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Thoracolumbar spinal fractures (T11–S1) The thoracolumbar junction is especially prone to
injury. This can vary from a minor wedge fracture to spinal dislocation. Burst fractures are
comminuted fractures of the vertebral body. Usually the distance between the pedicles is
widened and bone fragments are retropulsed into the spinal canal . The surgical approach
can be anterior, posterior or combined. For burst fractures with neurological compromise, an
anterior approach with vertebral corpectomy, canal clearance and anterior reconstruction is
often used. Chance fractures are flexion–distraction injuries of the thoracolumbar junction
and are classically associated with the use of lap belts . Duodenal, pancreatic and/or aortic
rupture, are also associated with these injuries.

REHABILITATION AND PATIENT OUTCOME

The goal of spinal cord injury rehabilitation focuses on maximizing the remaining
neurological function. The level of neurological impairment determines functional outcome .
Prognosis of spinal cord injury
Despite continuing improvements in patient care, life expectancy remains reduced .The
prognosis for neurological recovery is strongly influenced by the pattern of initial injury, the
completeness of the cord injury and the age at the time of injury.

Complications associated with spinal cord injury

Pain and spasticity
Neurogenic pain is common. Once reflex activity returns following cord injury, spasticity
may occur and can be problematic. Intrathecal infusion of baclofen may be required in
resistant cases.
Autonomic dysreflexia
This is a paroxysmal syndrome of hypertension, hypohydrosis (above level of injury),
bradycardia, flushing and headache in response to noxious visceral and other stimuli. It is
most commonly triggered by bladder distension or rectal loading from faecal impaction.
Neurological deterioration
Post-traumatic syringomyelia may cause late (>3 months postinjury) neurological
deterioration and occurs in 3–5 per cent of spinal cord injury cases. Increase in pain and/or

72
spasticity, ascending loss of sensation and deep tendon reflexes are suspicious and warrant
early MRI assessment. Expanding cavities require neurosurgical intervention.
Thromboembolic events
Deep vein thrombosis (DVT) occurs in 30 per cent of spinal cord-injured patients. Fatal
pulmonary embolus is reported in 1–2 per cent of cases. Therefore, prophylaxis with low
molecular heparin is recommended.
Osteoporosis, heterotopic ossification and contaractures
Disuse osteoporosis is an inevitable consequence of spinal cord injury, and fragility fractures
may occur. Heterotopic ossification may affect hips, knees, shoulders and elbows. It occurs
in 25 per cent of spinal cord-injured patients. Surgery is appropriate in selected cases. Soft
tissue contractures around joints may occur due to spasticity, but can be avoided by
appropriate physical therapy, positioning and splinting.

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COLLABORATIVE CARE GUIDE for the Patient With Spinal Cord Injury
OUTCOMES INTERVENTIONS
Oxygenation/Ventilation Monitor respiratory rate, arterial oxygen
ABGs are within normal limits. saturation, and pulmonary function test
Airway patency is maintained. results, and auscultate breath sounds.
The patient does not aspirate. • Assess need for mechanical ventilation.
The patient does not develop pulmonary • Provide for deep breathing, assistive
complications (eg, infection, atelectasis) coughing, and incentive spirometer
exercises.
• Turn frequently; mobilize out of bed to
chair when able.
• Apply abdominal binder when out of bed.
• Consult pulmonology as needed

Circulation/Perfusion
There is no evidence of neurogenic (spinal) • Monitor for bradycardia, vasodilation, and
shock (T10 injuries and higher). hypotension.
Blood pressure is adequate to maintain vital • Assess for dysrhythmias.
organ function. • Prepare to administer intravascular volume,
There is no development of DVT or vasopressors, and positive chronotropic
pulmonary embolism. agents.
• Begin DVT prophylaxis on admission (eg,
external compression device, low-dose
heparin or LMWH).
• Measure calf and thigh circumference daily
and at same location; report increase.
• Apply compression hose to lower
extremities before mobilizing out of bed.
• Monitor for orthostatic hypotension when
raising head of bed and getting out of bed.
• Allow patient to “dangle” before

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 mobilizing out of bed.
• Consult cardiology as needed.

Neurological Perform neurological checks and spinal cord

There is no evidence of deterioration in
function checks q2–4h.
neurological status.
• Monitor for deterioration in neurological
The vertebral column is maintained in a
status and report to the physician.
neutral position and in proper alignment
For patients with cervical traction: check the
orthopedic frame, traction, and tongs daily to
be sure that they are secure. Ensure that
traction weights hang freely.
• For patients with a halo vest: Ensure that
the pins on the halo ring are secure and tight

Fluids/Electrolytes
• Monitor laboratory studies as indicated by
Serum electrolytes are within normal limits.
patient’s condition.
Fluid balance is maintained as evidenced by
• Assess for dehydration.
stable weight, absence of edema, normal
• Administer mineral/electrolyte replacement
skin turgor.
as ordered.
• Monitor gastrointestinal and insensible
fluid loss.
• Make accurate daily fluid intake and output
measurements.
• Weigh weekly.
• Monitor results of laboratory studies,
particularly albumin and electrolyte levels.

Mobility/Safety
Joint range of motion is maintained and
Position in correct alignment.
contractures prevented. Muscle tone is
• Begin range-of-motion exercises early after
maintained. The patient ambulates in a safe
admission.

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manner to the best of his or her ability. • Maintain splint, brace, and adaptive device
schedule; check for pressure ulcers q4h or
more often if indicated.
• Consult with physical and occupational
therapy.

Skin Integrity Consult with wound care specialist to

Patient is without evidence of skin determine correct type of bed.

breakdown. • Reposition patient at least q2h while in

Skin integrity is maintained under or around bed.

stabilization devices (eg, cervical collar, halo • Position patient to prevent pressure on
vest). bony prominences.
• Use upright, straight-backed chair when
patient is out of bed (not a reclining
chair). Use felt pad on chair seat.
• Reposition/shift weight q1h when sitting
upright.
• Use Braden scale to monitor risk for skin
breakdown.
• Monitor skin underneath stabilization
devices and around pins.
• Use meticulous skin care underneath
stabilization devices and around pins.
• Ensure proper fit of vest-like stabilization
devices by sliding a finger between the vest
and skin.

Nutrition • Consult dietitian.

Protein, carbohydrate, fat, and calorie intake • Encourage fluids, high-fiber diet.
meet minimal daily requirements. • Monitor fluid I&O, calorie count.

The patient has a fluid intake of up to 3000 • Administer parenteral and enteral nutrition

76
mL daily. Aspiration is prevented. as appropriate.
• Assist with feeding/feed as needed.
Encourage the patient to take small bites and
chew well.

Elimination • Institute bowel and bladder training

programs.
Post void residuals < 100 mL.
• Record the frequency and consistency of
Pattern of bowel evacuation every 1–2 d
stool.
is established
• If the patient is voiding independently,
monitor post void residuals

• Assess and differentiate pain from anxiety

Comfort/Pain or stress response.
Pain < “4” on visual analog scale • Administer appropriate analgesic or
sedative to relieve pain and monitor patient
response.
• Use nonpharmacological pain relief
techniques (eg, distraction, music, relaxation
therapies).

Provide emotional support by encouraging

Psychosocial expression of concerns, arranging for
Patient adapts to loss of motor and support services (eg, social services, clergy,
sensory function, and maintains a neuropsychologist, support groups), and so
positive body image on.
Integration is made into prior social • Provide patient/family counseling
role. regarding stages of grief, sexual function and

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 management techniques, social services and
community resources

Teaching/Discharge Planning • Teach patient/family:

Complications associated with loss of bowel • Bowel program and training
or bladder control are prevented. • Dietary habits to maintain bowel function
Complications of immobility are prevented. •Bladder training/intermittent catheterization
Patient is discharged to appropriate postacute • Prevention of, and signs/symptoms of
setting. autonomic dysreflexia

• Teach patient/family:
• Positioning to prevent skin breakdown
• Physical therapy exercises
• Consult rehabilitation/discharge
planner/social services early after admission
to initiate placement arrangements

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NURSING DIAGNOSES
Based on the assessment data, the patient’s major nursing diagnoses may include the
following:
• Ineffective breathing patterns related to weakness or paralysis of abdominal and intercostal
muscles and inability to clear secretions
• Ineffective airway clearance related to weakness of intercostals muscles
• Impaired physical mobility related to motor and sensory impairment
• Disturbed sensory perception related to motor and sensory impairment
• Risk for impaired skin integrity related to immobility and sensory loss
• Urinary retention related to inability to void spontaneously
• Constipation related to presence of atonic bowel as a result of autonomic disruption
• Acute pain and discomfort related to treatment and prolonged Immobility
Planning and Goals
The goals for the patient may include improved breathing pattern and airway clearance,
improved mobility, improved sensory and perceptual awareness, maintenance of skin
integrity, relief of urinary retention, improved bowel function, promotion of comfort, and
absence of complications.
Nursing Interventions
PROMOTING ADEQUATE BREATHING AND AIRWAY CLEARANCE
Possible impending respiratory failure is detected by observing the patient, measuring vital
capacity, monitoring oxygen saturation through pulse oximetry, and monitoring arterial
blood gas values. Early and vigorous attention to clearing bronchial and pharyngeal
secretions can prevent retention of secretions and atelectasis.Suctioning may be indicated,
but caution must be used during suctioning because this procedure can stimulate thevagus
nerve, producing bradycardia, which can result in cardiac arrest.
If the patient cannot cough effectively because of decreased inspiratory volume and inability
to generate sufficient expiratory pressure, chest physical therapy and assisted coughing may
be indicated.Specific breathing exercises are supervised by the nurse to increase the strength
and endurance of the inspiratory muscles, particularly the diaphragm. Assisted coughing
promotes clearing of secretions from the upper respiratory tract and is similar to using
abdominal thrusts to clear an airway . It is important to ensure proper humidification and

79
hydration to prevent secretions from becoming thick and difficult to remove even with
coughing. The patient is assessed for signs of respiratory infection (cough, fever, dyspnea).
Smoking is discouraged because it increases bronchial and pulmonary secretions and
impairs ciliary action.
Ascending edema of the spinal cord in the acute phase may cause respiratory difficulty that
requires immediate intervention. Therefore, the patient’s respiratory status must be
monitored frequently.
IMPROVING MOBILITY
Proper body alignment is maintained at all times. The patient is repositioned frequently and
is assisted out of bed as soon as the spinal column is stabilized. The feet are prone to
footdrop;
therefore, various types of splints are used to prevent footdrop. When used, the splints are
removed and reapplied every 2 hours. Trochanter rolls, applied from the crest of the ilium to
the midthigh of both legs, help prevent external rotation of the hip joints. Patients with
lesions above the midthoracic level have loss of sympathetic control of peripheral
vasoconstrictor activity, leading to hypotension. These patients may tolerate changes in
position poorly and require monitoring of blood pressure when positions are changed.
Usually the patient is turned every 2 hours. If not on a rotating bed, the patient should not be
turned unless the spine is stable and the physician has indicated that it is safe to do so.
Contractures develop rapidly with immobility and muscle paralysis. A joint that is
immobilized too long becomes fixed as a result of contractures of the tendon and joint
capsule. Atrophy of the extremities results from disuse. Contractures and other
complications may be prevented by range-of-motion exercises that help preserve joint
motion and stimulate circulation. Passive range-of motion exercises should be implemented
as soon as possible after injury. Toes, metatarsals, ankles, knees, and hips should be put
through a full range of motion at least four, and ideally five, times daily.
For most patients with a cervical fracture without neurologic deficit, reduction in traction
followed by rigid immobilization for about 6 to 8 weeks restores skeletal integrity. These
patients are allowed to move gradually to an erect position. A four-poster neck brace or
molded collar is applied when the patient is mobilized after traction is removed .

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PROMOTING ADAPTATION TO SENSORY AND PERCEPTUAL ALTERATIONS
The nurse assists the patient to compensate for sensory and perceptual alterations that occur
with SCI. The intact senses above the level of the injury are stimulated through touch,
aromas, flavorful food and beverages, conversation, and music. Additional strategies include
the following:
• Providing prism glasses to enable the patient to see from the supine position
• Encouraging use of hearing aids, if indicated, to enable the patient to hear conversations
and environmental sounds
• Providing emotional support to the patient
• Teaching the patient strategies to compensate for or cope with these deficits
MAINTAINING SKIN INTEGRITY
Because the patient with SCI is immobilized and has loss of sensation below the level of the
lesion, there is an ever-present, lifethreatening risk of pressure ulcers. In areas of local tissue
ischemia, where there is continuous pressure and where the peripheral circulation is
inadequate as a result of the spinal shock and recumbent position, pressure ulcers have
developed within 6 hours. Prolonged immobilization of the patient on a transfer board
increases the risk of pressure ulcers. The most common sites are over the ischial tuberosity,
the greater trochanter, and the sacrum. In addition, patients who wear cervical collars for
prolonged periods may develop breakdown from the pressure of the collar under the chin, on
the shoulders, and at the occiput.
The patient’s position is changed at least every 2 hours. Turning not only assists in the
prevention of pressure ulcers but also prevents the pooling of blood and tissue fluid in the
dependent areas. Careful inspection of the skin is made each time the patient is turned. The
skin over the pressure points is assessed for redness or breaks; the perineum is checked for
soilage and the catheter is observed for adequate drainage. The patient’s general body
alignment and comfort are assessed. Special attention should be given to pressure areas in
contact with the transfer board The patient’s skin should be kept clean by washing with a
mild soap, rinsed well, and blotted dry. Pressure-sensitive areas should be kept well
lubricated and soft with bland cream or lotion. The patient is informed about the danger of
pressure ulcers to encourage understanding of the reason for preventive measures.

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MAINTAINING URINARY ELIMINATION
Immediately after SCI, the urinary bladder becomes atonic and cannot contract by reflex
activity. Urinary retention is the immediate result. Because the patient has no sensation of
bladder distention, overstretching of the bladder and detrusor muscle may occur, delaying
the return of bladder function. Intermittent catheterization is carried out to avoid
overdistention of the bladder and UTI. If this is not feasible, an indwelling catheter is
inserted temporarily. At an early stage, family members are shown how to carry out
intermittent catheterization and are encouraged to participate in this facet of care, because
they will be involved in long-term follow-up and must be able to recognize complications so
that treatment can be instituted.
The patient is taught to record fluid intake, voiding pattern, amounts of residual urine after
catheterization, characteristics of urine, and any unusual sensations that may occur.
IMPROVING BOWEL FUNCTION
Immediately after SCI, a paralytic ileus usually develops due to neurogenic paralysis of the
bowel; therefore, a nasogastric tube is often required to relieve distention and prevent
aspiration. Bowel activity usually returns within the first week. As soon as bowel sounds are
heard on auscultation, the patient is given a high-calorie, high-protein, high-fiber diet, with
the amount of food gradually increased. The nurse administers prescribed stool softeners to
counteract the effects of immobility and pain medications. A bowel program is instituted as
early as possible.

PROVIDING COMFORT MEASURES

After cervical injury, if pins, tongs, or calipers are in place, the skull is assessed for signs of
infection, including drainage. The back of the head is checked periodically for signs of
pressure, with care taken not to move the neck. The hair around the tongs usually is shaved
to facilitate inspection. Probing under encrusted areas is avoided.
The Patient in Halo Traction
Patients who have been placed in a halo device after cervical stabilization may have a slight
headache or discomfort around the skull pins for several days after the pins are inserted. The
patient initially may be bothered by the rather startling appearance of this apparatus but
usually readily adapts to it because the device provides comfort for the unstable neck. The

82
patient may complain of being caged in and of noise created by any object coming in contact
with the steel frame, but he or she can be reassured that adaptation to such annoyances will
occur.
The areas around the pin sites are cleansed daily and observed for redness, drainage, and
pain. The pins are observed for loosening, which may contribute to infection. If one of the
pins becomes detached, the head is stabilized in a neutral position by one person while
another notifies the neurosurgeon. A torque screwdriver should be readily available should
the screws on the frame need tightening.The skin under the halo vest is inspected for
excessive perspiration, redness, and skin blistering, especially on the bony prominences. The
vest is opened at the sides to allow the torso to be washed. The liner of the vest should not
become wet, because dampness causes skin excoriation. Powder is not used inside the vest,
because it may contribute to the development of pressure ulcers. The liner should be
changed periodically to promote hygiene and good skin care. If the patient is to be
discharged with the vest, detailed instructions must be given to the family and time allowed
for them to return demonstrate the necessary skills
Evaluation
EXPECTED PATIENT OUTCOMES
Expected patient outcomes may include:
1. Demonstrates improvement in gas exchange and clearance of secretions, as evidenced by
normal breath sounds on auscultation
a. Breathes easily without shortness of breath
b. Performs hourly deep-breathing exercises, coughs effectively,
and clears pulmonary secretions c. Is free of respiratory infection (ie, has normal
temperature, respiratory rate, and pulse, normal breath sounds, absence of purulent sputum)
2. Moves within limits of the dysfunction and demonstrates completion of exercises within
functional limitations
3. Demonstrates adaptation to sensory and perceptual alterations
a. Uses assistive devices (eg, prism glasses, hearing aids, computers) as indicated
b. Describes sensory and perceptual alterations as a consequence of injury
4. Demonstrates optimal skin integrity
a. Exhibits normal skin turgor; skin is free of reddened areas or breaks

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b. Participates in skin care and monitoring procedures within functional limitations
5. Regains urinary bladder function
a. Exhibits no signs of UTI (ie, has normal temperature; voids clear, dilute urine)
b. Has adequate fluid intake
c. Participates in bladder training program within functional limitations
6. Regains bowel function
a. Reports regular pattern of bowel movement
b. Consumes adequate dietary fiber and oral fluids
c. Participates in bowel training program within functional limitations
7. Reports absence of pain and discomfort
8. Is free of complications
a. Demonstrates no signs of thrombophlebitis, DVT, or PE
b. Exhibits no manifestations of pulmonary embolism
(eg, no chest pain or shortness of breath; arterial blood gas values are normal)
c. Maintains blood pressure within normal limits
d. Has no lightheadedness with position changes
e. Exhibits no manifestations of autonomic dysreflexia (ie, no headache, diaphoresis, nasal
congestion, bradycardia, or diaphoresis

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NURSING ROLE AND RESPONSIBILITIES WITHIN SCI REHABILITATION
PROGRAMMES
Inpatient rehabilitation and education following SCI involves a lot more than simply re -
learning new skills.People with newly acquired SCI will experience a series of challenges
during their initial coping and adjustment phase. Aside from addressing the acute
psychological dimension, life skills such as empowerment, self – efficacy and problem
solving abilities are crucial if the patient is to be autonomous, confident and capable of
dealing with day to day minor issues, or prepared to tackle major life issues such as further
education, returning to work, managing finances and exploring personal and social
relationships. The development of appropriate coping skills is known to contribute to
positive mood, social integration and life satisfaction.Individuals who are able to adjust to
their new disability status, will have less dependency behavior and this correlates positively
with quality of life, while individuals with poor emotional adjustment tend to demonstrate
negative coping style.
Elliott et al. (2006) suggest that individuals with poor problem solving abilities are more at
risk of developing additional health problems and complications. Since the incidence of
health problems increases with the ageing process, the more information and advice
available to the individual, the better prepared they will be to cope with them.
During the initial rehabilitation phase, information needs to be delivered in a format that is
relevant and appropriate to the individual. The nurse should always bear in mind the volume
of information that the patient needs to digest at this time, and so information regarding
changes to their status or disability as a consequence of ageing may not be appropriate or a
priority. Expanding the individual ’ s knowledge base in such a direction should be saved for
a more appropriate time. Whilst health care professionals would like to explore with the
patient the potential for future complications and problems and to some degree these are
touched upon, the initial focus is much more on immediate concerns and initial post -
discharge care issues and not what will happen as they age. As an organisation
predominantly run by people with SCI, the Spinal Injuries Association shares a commitment
with other SCI service providers to deliver continuous and long term support, and their peer
support scheme bears testament to this. Peer support officers are positive role models, whose
unique insight enables newly paralysed individuals to acquire a more informed opinion of

85
their future potential in the world after discharge. Unlike health care professionals, peer
support officers are in a unique position to engage in facilitating problem – solving
approaches with other spinal cord injured individuals and, because their role and relationship
with them extends beyond the initial hospital experience, they can continue to provide their
peer support ‘ lifeline ’ to the individual after hospital discharge. Community Peer Support
can include introducing the newly discharged individual to a more extensive peer network
that can enable wider access to a range of vocational and non - vocational opportunities.
Peer networks are an excellent source of post - discharge support and community
integration, all of which are known to contribute to positive well - being .
Bladder management following SCI
The change to bladder function after SCI is caused by the disruption of nerve supply and is
therefore termed neurogenic bladder dysfunction. Some patients with incomplete lesions
(e.g. Brown - S é quard), may have normal or near normal bladder function. If the sacral
segments of the spinal cord have been destroyed the bladder is totally disconnected from
nervous control. People with complete sacral SCI effectively have an areflexic bladder,
although the bladder muscle may recover some tone and therefore fail to relax during filling
which results in high bladder pressures, kidney damage and infection. The urethral sphincter
is weak, causing stress incontinence (leakage on coughing, straining, etc).
A typical patient with an areflexic bladder will have a lesion below T12/L1 level. If the
sacral segments survive, the bladder detrusor muscle and urethral sphincter maintain a nerve
supply from the sacral micturition centre, but their actions are not coordinated by the pontine
micturition centre because of the disruption in communication caused by the intervening
SCI. If the bladder emptying process is not perfectly coordinated,detrusor – sphincter
dyssynergia (DSD) can occur. This is where the detrusor may contract against a tight
sphincter resulting in abnormally high bladder pressures which damage the upper tract. A
further consequence of DSD is incomplete emptying of the bladder which can lead to
retention of ‘ stale ’ urine and urinary tract infection (UTI) . A typical patient with a reflex
bladder potential will have a lesion above T12/L1 .
There are a number of other patterns of bladder dysfunction. Many people with incomplete
SCI may have some degree of sensory sparing or even voluntary control of the urethral
sphincter. Urge incontinence is common in central cord syndrome .

86
Others may have a degree of voluntary control over voiding but be unable to use a toilet or
urinal independently because of a lack of hand function or reduced mobility. Yet others may
experience unpleasant or painful sensations as the bladder fills. Those with partial damage
to the sacral spinal cord may have a reflex bladder but a weak urethral sphincter causing
both urge and stress incontinence .
The primary aims of bladder management after SCI are to:
• Achieve a system of management that is safe and acceptable,arising from a process of
negotiation with thepatient
• Protect the upper tract by preserving a low – pressure system and ensuring adequate
emptying
• Minimise the risk of renal and ureteric stone formation and chronic infection
• Preserve the capacity of the bladder.
Catheters (intermittent or indwelling) may cause urethral stricture. Erosion of the penile
urethra is possible if indwelling catheters or external urinary collection devices are poorly
managed. Bladder stones are common in patients with indwelling catheters .
Methods for managing the neurogenic bladder
Intermittent self - catheterisation
• Preferred method for areflexic bladder
• Allows the bladder to fi ll and completely empty periodically
• Reduces risk of UTI
• May need to take anticholinergic drugs (oxybutynin, tolterodine, propantheline) to stay dry
between catheterisations
• May lead to urethral stricture formation
Indwelling urethral catheters
• Least satisfactory option
• Increased risk of infection, trauma, encrustation and autonomic dysrefl exia
Suprapubic catheterisation (SPC)
• Advantages over indwelling urethral catheters, e.g.
_ Improved quality of life
_ Easier to manage for wheelchair users
_ Easier if sexually active

87
_ More comfortable and reduced urethral trauma
• Patient may still void urethrally – this can be reduced by anticholinergics
External urinary collection devices (e.g. penile sheath, bioderm)
• Take advantage of the return of detrusor voiding Reflexes in suitable SCI males
• May need to try range of products to identify most suitable equipment for the individual
• May still be at risk of kidney damage due to the dysfunctional bladder
• Regular monitoring of renal function is required
Voiding with voluntary control
• Some neurologically incomplete patients may achieve voluntary control
• Monitor long - term for upper tract damage

Bowel management following SCI

As voluntary control is mainly conferred via the sacral nerves (S2 – S4), any SCI is likely to
affect neurological communication between the brain and the anorectal structures .Lesions
above T12/LI principally affect upper motor neurones, leaving the reflex pathways that
utilise the lower motor neurones intact. In this type of dysfunction, the reflex functions of
the anorectum are preserved, but sensation and voluntary control are abolished .
Areflexic dysfunction typically affects patients with neurologically complete lesions at L1
and below. As with reflex dysfunction, voluntary control and sensation are disrupted, but in
addition, there is an absence of refl ex function. This restricts the options for management .
Some individuals with incomplete lesions may have a degree of preserved sensation or
residual voluntary control. However this may not be sufficient to enable reliable bowel
control.
The primary aims of bowel management after SCI are to:
• Achieve a system or programme of management that is both safe and acceptable to the
individual
• Prevent incontinence in order to enable social and recreational activities including
employment and educational opportunities
• Enable sexual activity and other intimate human Behaviours
• Protect skin integrity

88
• Enable the patient to complete a routine bowel management episode within a maximum of
one hour from commencement
Involvement of community nurses is best avoided wherever possible because of the
restrictions this places on the lifestyle of the individual. The capacity of local community
nursing services to assist with bowel care in accordance with an established programme
should always be confirmed beforehand and the alternative option of employing personal
carers explored where available. The components of a bowel management programme
are as follows:
• Maintain continence, avoid constipation, and facilitate regularity of evacuation, by
maintaining an appropriate consistency of stool through careful attention to diet, fluid intake
and physical activity as well as the use of oral laxatives and rectal stimulant.
• Gentle abdominal massage can be used as a precursor to the insertion of rectal stimulants,
and before and after digital stimulation, in order to aid evacuation.
• Most individuals with reflex bowel dysfunction can be established on an alternate day
routine, while those with areflexic bowel dysfunction usually need, or prefer, to evacuate at
least once a day.
Evacuation techniques for managing the neurogenic bowel
Areflexic bowel management
Because the bowel will not respond to rectal stimulants, as there is no refl ex activity, the
principal evacuation technique in areflexic bowel dysfunction is digital removal of faeces
(DRF) This is an established form of bowel management and there is no evidence that it is
harmful if performed properly. For most patients there is no satisfactory alternative
• Place patient in a left lateral position on the bed and undertake digital rectal examination
(DRE) by inserting a single gloved and lubricated finger into the rectum
• Any faeces present in the rectum can be digitally removed using a circling and ‘ beckoning
’ motion with the finger. This action is repeated until the rectum is empty.
• Since areflexic dysfunction mainly occurs in lesions below T12/L1, the patient will often
have reasonable hand function and during rehabilitation will learn how to perform DRF
independently on the toilet.

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Reflex bowel management
The nursing care strategy for long – term reflex bowel management is to achieve complete
and timely evacuation by using the mildest form of a proprietary chemical stimulant initially
(usually suppositories or microenemas), reserving stronger stimulants for future occasions
when problems may arise
• Place patient in a left lateral position on the bed and undertake DRE as above
• If faeces already present in the rectum, digitally remove some of this until sufficient space
is created to accommodate the rectal stimulant and to achieve maximum contact with the
rectal wall for best effect
• Insert the prescribed rectal stimulant and leave in situ for an appropriate period of time to
deliver effective stimulation
• Following refl ex bowel evacuation, undertake DRE to confirm that the rectum is
completely empty
• In the event of incomplete emptying, perform DRS by circling a finger within the rectum
two or three times maintaining gentle contact with the rectal wall throughout. Do not repeat
DRS more than three times within each bowel management episode, allowing five minutes
rest between stimulations

Sexual issues and sexual dysfunction after SCI

Sexual function is highly complex, involving a continuous combination of psychological,
hormonal, vascular and neurological factors . The neurological changes following injury
undoubtedly have the most profound and permanent effect on sexual function for individuals
with a SCI.Addressing the totality of the impact of SCI on the sexual function and sexuality
of individuals is challenging, as many of the effects emerge relatively slowly as individuals
readjust and reintegrate after initial hospitalisation. It is difficult to prepare a newly
paralysed individual for what to expect, especially as the focus for professionals and SCI
people alike is frequently on the more basic functional aspects of SCI rehabilitation (bowel
and bladder care, self - care skills, etc.). In addition, many professionals feel that they do not
have sufficient interpersonal skills or specialist knowledge to deal with such intimate and
complex issues.

90
Initiating discussions about sexual issues, should, as far as is possible, be directed by the
SCI person who should be enabled to choose someone they trust, at a time they feel
appropriate and in a setting they feel suitable. For their part, professionals should be able
and willing to respond to direct or indirect cues that the patient is ready to talk, and should
find ways to let them know that it is acceptable to start talking about these intimate
concerns.Most SCI males have some degree of erectile dysfunction and in addition, any SCI
is likely to disrupt ejaculatory function. However, there have been many advances in
treatment over the past 20 years and it is now possible to treat most erectile and ejaculatory
dysfunction in SCI men. Specialist clinics
now exist in many hospitals to supplement the services provided by SCI centres. Skilled
patient education and follow - up is essential for all of these treatments and can have a
marked impact upon effectiveness. After an initial period of amenorrhoea, which is a normal
reaction to the severe metabolic disturbance that occurs immediately post injury, women
with SCI usually regain their full reproductive abilities within their first post - injury year
although there is a slight chance that in some vulnerable mature women, the trauma of SCI
may induce an early menopause. The same neurological pathways (both refl exogenic and
psychogenic) that govern erectile function in men produce clitoral and vulval engorgement
and vaginal lubrication in women in response to arousal (psychogenic) or cutaneous genital
stimulation (reflex). The degree of dysfunction will depend on the level and degree of
completeness of the SCI.
This emphasis on dysfunctions and their treatment may give SCI people and their partners
the impression that sexual activity is no longer about having fun or sharing sensual pleasure,
and can no longer be spontaneous. On the other hand, once the initial psychological and
emotional impact of SCI subsides, arousal and desire are often fully restored. Though genital
sensation is often absent, greatly diminished or altered, most spinal cord injured people
report a magnification of the pleasurable sensations in erogenous zones above the level of
injury. Individuals should be encouraged to explore the possibilities of such changes in
sensation. Most spinal cord injured people also discover that a huge part of the pleasure of
sexual activity comes from giving pleasure to their partner, and that this does not necessarily
require penetrative sex or genital sensation.

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The prevention and management of pressure ulcers
The risk of pressure ulcer development increases with age and 80% of people with a chronic
SCI will experience at least one pressure ulcer of significance within their lifetime. Pressure
ulcers form at least 30% of SCI centre readmissions and up to 8% of spinal cord injured
individuals will die as a direct consequence of developing a pressure ulcer.
For this reason, the education of patients and their carers in the care and protection of those
areas of skin presenting with lost or reduced sensation is a fundamental and heavily
promoted component of SCI rehabilitation programmes. Pre - discharge education
programmes within SCI centres benefit from their ability to utilise peer support to enable
patients to develop a more realistic appreciation of the true impact of developing a pressure
ulcer. The true potential for pressure ulcer development after discharge is based upon the
individual ’ s self - perception of risk . Those who are able to establish and maintain a
responsible attitude towards active living cannot avoid pressure ulcers but, by acting
appropriately when one does occur, will experience fewer days adversely affected by them.
In the initial period following discharge, compliance with precautionary skin care
procedures is usually high as the perceptible risk increases with the return of the patient to a
new environment.
However, following discharge the routine monitoring of skin using a hand mirror may soon
become perceived as an avoidable chore. To sustain this task over time requires a level of
belief, motivation and discipline that may prove difficult to maintain in the face of the
distractions which present after discharge.
In the community, the development of a pressure ulcer means that a previously independent
paraplegic may find himself reliant upon family, friends, community professionals and home
care services for a wide range of personal care tasks. It may be no different for tetraplegic
individuals being nursed in bed at home with subsequent disruption of established care
packages and family routines. Many SCI people express a distinct lack of confidence in
community services and local general hospitals. This is because they need to be convinced
that nurses outside of specialist centres can demonstrate an appropriate knowledge of SCI in
general and of the management of pressure ulcers in people with SCI in particular.
As a consequence, most spinal cord injured people expect their pressure sore to be managed
by SCI centre community liaison teams and to be readmitted to a SCI centre if

92
hospitalisation is necessary. This additional reliance upon the SCI centre is in fact proving
detrimental, resulting in an increased workload which should be the remit of community
services.

JOURNAL ARTICLES
 Optical Assessment of Spinal Cord Tissue Oxygenation Using a Miniaturized Near
Infrared Spectroscopy Sensor
Despite advances in the treatment of acute spinal cord injury (SCI), measures to
mitigate permanent neurological deficits in affected patients are limited. Immediate
post-trauma hemodynamic management of patients, to maintain blood supply and
improve oxygenation to the injured spinal cord, is currently one aspect of critical
care which clinicians can utilize to improve neurological outcomes. However,
without a way to monitor the response of spinal cord hemodynamics and
oxygenation in real time, optimizing hemodynamic management is challenging and
limited in scope. This study aims to investigate the feasibility and validity of using a
miniaturized multi-wavelength near-infrared spectroscopy (NIRS) sensor for direct
transdural monitoring of spinal cord oxygenation in an animal model of acute SCI.
Nine Yorkshire pigs underwent a weight-drop T10 contusion-compression injury and
received episodes of ventilatory hypoxia and alterations in mean arterial pressure
(MAP). Spinal cord hemodynamics and oxygenation were monitored throughout by
a non-invasive transdural NIRS sensor, as well as an invasive intraparenchymal
sensor as a comparison. NIRS parameters of tissue oxygenation were highly
correlated with intraparenchymal measures of tissue oxygenation. In particular,
during periods of hypoxia and MAP alterations, changes of NIRS-derived spinal
cord oxygenated hemoglobin and tissue oxygenation percentage corresponded well
with the changes in spinal cord oxygen partial pressures measured by the
intraparenchymal sensor. Their data confirm that during hypoxic episodes and as
changes occur in the MAP, non-invasive NIRS can detect and measure real-time
changes in spinal cord oxygenation with a high degree of sensitivity and specificity.
 Neurointensive Care for Spinal Injuries; Perspective on Its Role in Early Stage

93
 Multimodal approach to the patient is essential in neurocritical care for spinal cord
injury (SCI) patients. This study highlights the issues regarding early stage
neurointensive care for SCI. Although there are still some debate regarding the
optimal neurointensive care in SCI patients, it is clear by previous literature that
proper medical and surgical management play important role for neurocritical care
in SCI patients. Not only neurological problems but also several life threatening
medical issues such as DVT, PE, respiration problems or pressure sores should also
be considered during the early neurointensive care in order to optimize treatment
for SCI patients. By understanding the early role of neurointensive care in SCI, we
believe we can better treat these patients.

CONCLUSION
Spinal cord injury (SCI) is a devastating state following high energy trauma, which results
in devastating burden to the patient and to the society as well, and the prevalence is known
to be more than 700 per million. As SCIs mostly lead to irreversible sequalae and
neurologic deficits, it finally results in great social costs as well as heart-aching personal
loss. The functional impairment and the socioeconomic burden induced by SCI is already
well documented1. On the papyrus from ancient Egypt 4000 years ago, the Egyptians state
SCI as “The disease that cannot be cured”. In the modern era, SCI is not considered as a
disease that cannot be cured, but it is true that it is still a disease that is difficult to deal
with for both the clinicians and the patients themselves. Although many studies have been
taken to the field regarding the treatment for spinal cord injury, many of SCI patients still
finally remain with remnant neurologic deficits. Considering the impact of this injury on
each patients, and also considering its socioeconomic burden, proper approach to the SCI
patients and good selection of treatment modalities are of great interest. Especiall y, the
early stage of treatment is of importance. During last several decades, there have been
dramatic development and evolutionary improvement in the treatment for SCI with or
without spinal vertebral injuries.

94
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