Sabtu, 25 Oktober 2008

Acute Management Of Spinal Cord Injury

Acute Management of Spinal Cord Injury

Dr Harry Sunaryo SpOT

Each year in the United States,
between 7,600 and 10,000 individuals
sustain and survive a spinal
cord injury. A complex interplay
of regulatory developments and
social issues has influenced trends
in spinal injury. Improvements in
emergency medical services systems,
the development of safer
automobiles, more occupational
safety standards, and better regulation
of contact sports have had a
positive impact on demographic
trends. However, while the overall
incidence of traumatic spinal cord
injury is decreasing nationally, the
percentage due to acts of domestic
violence is sharply on the rise. In
general, more patients are surviving
the initial traumatic injury, and
trends over time indicate an increase
in the proportion of persons
with incomplete paraplegia and a
decrease in the proportion of persons
with complete tetraplegia.1
A number of postinjury trends
have developed: Advances in the
rehabilitation of patients with
spinal cord injuries have resulted
in shorter hospital stays. Between
1974 and 1994, average acute and
rehabilitation hospital stays following
injury declined from 122 days
to 53 days for paraplegic patients
and from 150 days to 75 days for
quadriplegic patients.1 According
to a 1996 study,1 92% of patients
with spinal cord injury are discharged
to independent living or
residential living situations with
assistance. The average life expectancy
for an individual with a
spinal cord injury remains below
normal, but continues to increase.
These positive trends notwithstanding,
the overall impact of
spinal cord injury on society and
on the individual patients and their
families is staggering. It has been
estimated that there are between
183,000 and 203,000 persons living
with spinal cord injuries in the
United States. Estimates of lifetime
costs for health care and living
expenses vary depending on severity
of injury and age at the time of
injury. For example, lifetime costs
for a 25-year-old individual with
high quadriplegia are estimated to
be $1,350,000, whereas costs for a
50-year-old paraplegic patient are
estimated to be $326,000.1
Moreover, each person who sustains
a spinal cord injury undergoes
a devastating transformation
in quality of life, with a loss of
independence and a profound
impact on lifestyle, personal goals,
economic security, and interpersonal
relationships. For example,
in a study from the National Spinal
Cord Injury Statistical Center,1 only


Demographic trends in the occurrence of injury and improvements in the early
management of spinal trauma are changing the long-term profile of patients
with spinal cord injuries. More patients are surviving the initial injury, and
proportionately fewer patients are sustaining complete injuries. While preventive
efforts to reduce the overall incidence of spinal cord injury are important, a
number of steps can be taken to minimize secondary injury once the initial trauma
has occurred. Recent efforts have focused on understanding the biochemical
basis of secondary injury and developing pharmacologic agents to intervene in
the progression of neurologic deterioration. The Third National Acute Spinal
Cord Injury Study investigators concluded that methylprednisolone improves
neurologic recovery after acute spinal cord injury and recommended that
patients who receive methylprednisolone within 3 hours of injury should be
maintained on the treatment regimen for 24 hours. When methylprednisolone
therapy is initiated 3 to 8 hours after injury, it should continue for 48 hours. In
addition to the adoption of the guidelines of that study, rapid reduction and stabilization
of injuries causing spinal cord compression are critical steps in optimizing
patientsÔ long-term neurologic and functional outcomes.
about a third of persons with paraplegia
and about a fourth of those
with quadriplegia were employed
at postinjury year 8. The likelihood
of a marriage remaining intact or of
getting married is far lower than in
the noninjured population.
Most recent successes have been
the result of efforts to decrease the
incidence of primary spinal cord
injury and advances in the rehabilitation
phase of care. This article
focuses on measures to reduce the
potential for secondary mechanical
injury and to address the physiologic
process that ensues once the
primary spinal cord injury has
occurred.
Pathophysiology of Spinal
Cord Injury
Mechanism of Injury
The initial traumatic injury typically
involves impact, compression
and contusion of the spinal cord,
and resultant immediate damage to
nerve cells, axonal tracts, and blood
vessels. Complete severance of the
spinal cord following cervical trauma
is rare; however, as a
result of the primary mechanical
insult, the secondary physiologic
processes, including hemorrhage,
edema, and ischemia, rapidly extend
to contiguous areas in the
cord. Residual pressure on the
cord from bone, ligaments, and
disk material can also exacerbate
the mechanical damage to the cord
after the primary injury.
The secondary injury process is a
complex cascade of biochemical
events, the exact mechanism and
sequence of which are only partially
understood. After the initial impact,
hemorrhage and inflammation
occur in the central gray matter of
the cord. On a systemic level, autonomic
nervous system dysfunction,
hypotension, and bradycardia contribute
to impaired spinal cord perfusion,
which further compounds
the ischemia. Experimental studies
in animal models of spinal cord
injury have shown increases in tissue
water content and sodium and
lactate levels, along with decreases
in extracellular calcium levels, tissue
oxygenation, and pyruvate and
adenosine triphosphate concentrations.
2 Taken together, these observations
are consistent with an overall
scenario of ischemia, hypoxia,
uncoupling of oxidative phosphorylation,
and aerobic glycolysis.
A number of theories have been
proposed to explain the pathophysiology
of secondary injury. Each
theory provides a piece of this complex
puzzle, and there is evidence
of close synergism between the various
mechanisms of secondary
injury. The free-radical theory suggests
that due to rapid depletion of
antioxidants, oxygen free radicals
accumulate in injured central nervous
system tissue and attack membrane
lipids, proteins, and nucleic
acids. As a result, lipid peroxides
are produced, causing the cell
membrane to fail.
The calcium theory implicates
the influx of extracellular calcium
ions into nerve cells in the propagation
of secondary injury. Calcium
ions activate phospholipases,
proteases, and phosphatases, resulting
in both interruption of
mitochondrial activity and disruption
of the cell membrane.
The opiate receptor theory is
based on evidence that endogenous
opioids may be involved in the
propagation of secondary spinal
cord injury. There is evidence that
opiate antagonists, such as naloxone,
may improve neurologic recovery
in experimental models of
spinal cord injury. However, different
studies have reported conflicting
results, and it may be that
the beneficial effect of opiate antagonists
is dose-responsive.
The inflammatory theory is based
on the hypothesis that inflammatory
substances (e.g., prostaglandins,
leukotrienes, platelet-activating factor,
and serotonin) accumulate in
acutely injured spinal cord tissue
and are mediators of secondary tissue
damage.3 Anti-inflammatory
agents have been tested extensively
in spinal cord injury.
Histologic manifestations of
acute spinal cord injury include
necrosis of central cord gray matter
in the first hours after injury, followed
by cystic degeneration. Over
the ensuing several weeks, the
development of scar tissue extends
into the axonal long tracts, with disruption
of axonal continuity.
Effect of Timing of
Decompression
In a 1995 in vivo animal study,
Delamarter et al4 evaluated the
Fig. 1 Complete severance of the spinal
cord after a severe C6 fracture-subluxation.
The 18-year-old male patient sustained a
diving injury and immediate C6 quadriplegia.
This magnetic resonance image obtained
90 minutes after the injury depicts
complete severance of the cord at the base
of the C6 vertebra and hemorrhage into the
cord cephalad to the C6 level (arrow).
Acute Management of Spinal Cord Injury
168 Journal of the American Academy of Orthopaedic Surgeons
effect of timing of decompression of
the spinal cord after acute experimental
spinal cord compression
injury . In their canine
model, 50% spinal cord compression
was surgically obtained with a
constriction band. Decompression
was then performed immediately in
6 dogs and at 1 hour, 6 hours, 24
hours, and 1 week, respectively, in
the other four groups of 6 dogs
each. Data from somatosensory
evoked potential monitoring, daily
neurologic examinations, and histologic
and electron-microscopic studies
performed at autopsy were
available for all animals. Initially,
all 30 dogs were paraplegic. The
dogs that underwent immediate
decompression or decompression
after 1 hour recovered the ability to
walk as well as control of the bowels
and bladder. When compression
lasted 6 hours or more, there was no
neurologic recovery, and progressive
necrosis of the spinal cord was
noted on histologic examination
This research suggests that
not all damage to the spinal cord
occurs at the time of initial trauma
and that the extent and persistence
of damage depend in part on the
duration of compression.
Pharmacologic
Intervention
The development of pharmacologic
agents to halt progression of secondary
neurologic damage after a
primary injury has been based on a
growing understanding of the
sequence of biochemical events.
There are ongoing research efforts
at the basic and preclinical levels,
as well as several major clinical
studies. A number of agents,
including corticosteroids, 21-
aminosteroids, free-radical scavengers,
opiate antagonists, calciumchannel
blockers, and neurotrophic
factors, are being investigated.
Table 1 lists a number of these
agents by class. Methylprednisolone,
tirilazad, and GM1 ganglioside
are each currently being evaluated
in ongoing clinical trials.
Methylprednisolone
The initial rationale for use of glucocorticoids
in the treatment of acute
spinal cord injury was based on
their efficacy in treatment of cerebral
edema in patients with closed head
injury and brain tumors. Subsequently,
additional mechanisms
have been proposed for the beneficial
effects of methylprednisolone,
including reduction of excitatory
amino acid neurotoxicity, inhibition
of lipid peroxidation, increases in
spinal-tissue blood perfusion, and
slowing of traumatic ion shifts.5
The Second National Acute Spinal
Cord Injury Study (NASCIS-II),
which was a prospective, randomized,
placebo-controlled, doubleblinded
clinical trial, demonstrated
that intravenous administration of
high-dose methylprednisolone improved
clinical outcomes.6 Completed
in January 1990, NASCIS-II
was the first clinical trial to demonstrate
statistically significant neurologic
recovery from, or reversal of,
neurologic injury. The NASCIS-II investigators
evaluated the efficacy
and safety of methylprednisolone
and naloxone in a placebo-controlled
multicenter study of 487 patients
with acute spinal cord injury.
Ninety-five percent of the patients
were treated within 14 hours of
injury. Methylprednisolone was
given to 162 patients in a bolus dose
of 30 mg per kilogram of body
weight, followed by an infusion at
the rate of 5.4 mg/kg per hour for 23
hours. Naloxone was given to 154
patients as a 5.4-mg/kg bolus injection,
followed by an infusion at the
Preoperative
SEP
SEP After
Compression
SEP
6 Weeks After
Decompression
% of Tibial Amplitude
20
10
0
30
40
50
60
70
80
90
100
Time of Decompression
Zero
1 Hour
6 Hours
24 Hours
1 Week
Fig. 2 Somatosensory evoked potential (SEP) recovery after decompression of experimental
spinal cord injury in 30 dogs. Note the mean deterioration of the amplitude of posterior
tibial SEPs, compared with preoperative values, after compression of the spinal cord and
the subsequent recovery in amplitude 6 weeks after decompression. Six weeks after
decompression, only the dogs in group 1 (immediate decompression) and group 2 (decompression
at 1 hour) showed significant improvement (P<0.05) in amplitude. (Reproduced
with permission from Delamarter RB, Sherman J, Carr JB: Pathophysiology of spinal cord
injury: Recovery after immediate and delayed compression. rate of 4.0 mg/kg per hour for 23
hours. Placebo was given to 171
patients.
The NASCIS-II data demonstrated
that patients who received a
high-dose methylprednisolone
infusion within 8 hours of spinal
cord injury had better recovery of
neurologic function at 6 weeks, 6
months, and 1 year after injury,
compared with patients treated
with placebo or naloxone.6 Although
the degree of neurologic
recovery was strongly related to
the completeness of injury, patients
with complete injuries as well as
those with incomplete injuries
improved more after treatment
with methylprednisolone than after
placebo administration.
There were no statistically significant
differences in mortality and
morbidity in the methylprednisolone
group in comparison to
the placebo group. However, patients
with incomplete spinal cord
injuries treated with methylprednisolone
beyond 8 hours postinjury
had significantly less neurologic
recovery than similar patients treated
with placebo, indicating that
there may be a detrimental effect to
late administration of methylprednisolone.
Treatment with naloxone
in the doses used in NASCIS-II did
not significantly improve neurologic
recovery in comparison to placebo.
6
The NASCIS-II study has been
criticized for deficiencies in experimental
design and incomplete data.
Detailed medical and surgical protocols,
as well as radiologic descriptions
of the injuries, were not
reported. Description of the initial
severity of neurologic injuries within
each of the treatment groups was
not provided in detail. The scheme
for grading neurologic improvement
in NASCIS-II did not employ
functional measures of outcome;
therefore, it was not possible to
assess clinically useful degrees of
recovery.7,8
The Third National Acute Spinal
Cord Injury Study (NASCIS-III)
was a multicenter, randomized,
double-blinded prospective study
reported in May 1997.9 Because
NASCIS-II showed greater neurologic
recovery with methylprednisolone,
the investigators felt an
obligation to include methylprednisolone
in the treatment of all
A B
C D
Fig. 3 Histologic findings in an experimental model of spinal cord injury in dogs. A,
Section of spinal cord approximately 1 cm cephalad to spinal cord injury after immediate
decompression. Note the mild deformity of the spinal cord but only minimal histologic
damage (hematoxylin-eosin staining). B, Higher-power view of a similar section from a
dog after 1 hour of constriction. Note the mild to moderate cord deformity, the early
degeneration in the central cord, and mild peripheral destructive changes. C, Spinal cord
section from a dog with decompression after 6 hours of compression (hematoxylin-eosin,
original magnification ´6. Note the severe degeneration in the central cord (arrows) and
the posterior columns. Spinal cord damage was significantly related to the duration of
compression. D, Electron-microscopic view showing neural tissue and exiting dendrite.
Section was taken 5 mm caudad to the level of compression from a dog after 6 hours of
compression. Note the severe degenerative changes in the mitochondria (arrows) and disorganization
on both sides of the exiting dendrite (arrowheads) (original magnification
´6,000). (Parts C and D reproduced with permission from Delamarter RB, Sherman J, Carr
JB: Pathophysiology of spinal cord injury: Recovery after immediate and delayed compression.
patients in NASCIS-III and all subsequent
clinical trials. Therefore,
the three groups of patients in
NASCIS-III all received an initial
30-mg/kg bolus dose of methylprednisolone
before randomization.
The first group of NASCIS-III
patients (n = 166) received an infusion
of methylprednisolone at a
rate of 5.4 mg/kg per hour for 23
hours after the bolus dose. The
second group (n = 166) received the
methylprednisolone infusion for a
total of 48 hours after the bolus
dose. The third group (n = 167)
received a bolus dose of methylprednisolone,
followed by a 2.5-
mg/kg bolus of tirilazad every 6
hours for 48 hours.
Neurologic function was assessed
at the time of initial presentation
and at 6 weeks and 6 months
after spinal cord injury. At the time
of the 6-month follow-up, 94.7% of
surviving patients were available
for evaluation. Examinations were
conducted by NASCIS-trained
physicians and nurses and included
quantitative scoring of motor and
sensory function, as well as functional
independence measures.
In patients who were treated less
than 3 hours after injury, essentially
identical rates of motor recovery
were observed in all three treatment
groups. In patients in whom
treatment was initiated between 3
and 8 hours after injury, the 48-
hour methylprednisolone group
recovered significantly more motor
function than the 24-hour methylprednisolone
group. The 48-hour
tirilazad group recovered at a rate
slightly faster than the 24-hour
methylprednisolone group, but the
difference was not statistically significant.
Patterns of recovery of
sensory function paralleled those
for recovery of motor function.
However, differences in sensory
function improvement between the
groups were smaller. Greater improvement
in functional independence
measures at 6 months was
observed in the 48-hour methylprednisolone
group than in the 24-
hour group. The 48-hour tirilazad
group improved at rates between
those for the two methylprednisolone
groups.
Small differences in complication
rates were noted between the
groups, with higher rates of severe
sepsis and severe pneumonia in the
48-hour methylprednisolone group.
These complications did not affect
overall mortality. Although the
NASCIS-II investigators did not
report a statistically significant difference
in mortality and morbidity
between treatment and control
groups, the first NASCIS study
demonstrated that 10 days of glucocorticoid
treatment was associated
with an increased risk of complications.
7 Other authors have associated
the use of high-dose glucocorticoids
in the treatment of acute
spinal cord injury with increased
risk of pneumonia and wound infections
and prolongation of hospital
stay.10
On the basis of the results of the
NASCIS-III trial, the investigators
recommended that patients with
acute spinal cord injury who receive
methylprednisolone within 3
hours of injury should be maintained
on the treatment regimen for
24 hours. They further recommended
that when methylprednisolone
therapy is initiated 3 to 8
hours after injury, it should be continued
for 48 hours.9
Tirilazad
Tirilazad is a lazeroid (synthetic
21-aminosteroid). Lazeroids are
extremely potent antioxidants and
exhibit neuroprotective effects by a
variety of other mechanisms as
well, such as improving spinal cord
blood flow and membrane stabilization.
Because lazeroids have
none of the glucocorticoid properties
of methylprednisolone, tirilazad
may have fewer side effects.
GM1 Ganglioside
Gangliosides are complex acidic
glycolipids found in high concentrations
in central nervous system
tissue as a major component of the
cell membrane. In animal studies,
gangliosides have been shown to
stimulate the growth of nerve cells
in damaged tissue.11 Their mechanism
of action involves enhancing
survival of residual axonal tracts
passing through the site of injury,
thereby facilitating the recovery of
useful motor function distally.
Gangliosides also act to limit cell
destruction by excitatory amino
acids.
In a 1991 randomized, prospective
clinical trial, Geisler et al12
demonstrated statistically significant
neurologic improvement in
patients given a parenteral GM1
Table 1
Pharmacologic Agents Under Investigation for Use in Treatment of Acute
Spinal Cord Injury
Agent Class
Naloxone m-Opiate receptor antagonist
Methylprednisolone Corticosteroid
Nimodipine Calcium-channel blocker
4-Aminopyridine Potassium-channel blocker
GM1 Ganglioside Glycolipid (neurotrophic factor)
Tirilazad (lazeroid) Lipid peroxidase inhibitor
Vitamin E Free-radical scavenger
ganglioside sodium salt, compared
with patients given placebo. At
follow-up 1 year after injury, significant
improvement was noted
on the basis of both the American
Spinal Injury Association motor
score and the Frankel classification
grade. Analysis of the data indicated
that improved function in
patients treated with GM1 ganglioside
occurred in initially paralyzed,
rather than paretic, muscles.
Currently, a large multicenter
study is in progress to validate the
initial clinical results seen with
GM1 ganglioside treatment.13 The
study also seeks to establish the
safety and efficacy of two dose regimens
of GM1 ganglioside.
4-Aminopyridine
4-Aminopyridine is a fast potassium-
channel blocker, which has
been shown in experimental models
of spinal cord injury to enhance
nerve conduction through demyelinated
nerve fibers by prolonging
the duration of action potentials.
When 4-aminopyridine was given
in limited clinical trials to patients
with incomplete injuries, it produced
temporary neurologic improvements,
which persisted for as
long as several days after administration
of the drug.14
Spinal Cord Regeneration
A number of studies to investigate
the regeneration of axonal tracts
after traumatic spinal cord injury
are currently underway. For example,
researchers at the University of
Zurich administered antibodies to
neutralize myelin-associated neurite
growth inhibitory factor to
young adult rats that had undergone
partial transection of the
midthoracic spinal cord. The treatment
resulted in growth of corticospinal
axons around the site of
injury and into spinal cord levels
caudal to the injury.15
Recently, Cheng et al16 reported
on a study in which they completely
transected a 5-mm section of
spinal cord at the T8 level in adult
rats. This was followed by grafting
of peripheral nerve implants from
individual axonal tracts to areas of
neuronal cell bodies to bridge the
gap. Acidic fibroblast growth factor,
a constituent of normal spinal
cord tissue, was mixed with fibrin
glue and then used to stabilize the
grafts. Rat hind-limb function
improved progressively over a 6-
month period, compared with controls.
Although this study is far
removed from clinical application
to traumatic spinal cord injury in
humans, it represents the first evidence
that regeneration can occur
in a completely transected spinal
cord of an adult animal and suggests
that therapies will eventually
be discovered for regeneration of
the spinal cord after traumatic
injury.
Management of Acute
Spinal Cord Injury
Evaluation and Medical
Management
Although current understanding
of the pathophysiology of acute
spinal cord injury is limited, the
recommended treatment protocol
is based on three major
objectives. First is prevention of
secondary injury by pharmacologic
intervention, such as administration
of methylprednisolone within
8 hours after injury, in accordance
with the guidelines established in
NASCIS-III. Patients should be
given a 30-mg/kg bolus dose of
methylprednisolone, followed by
either a 23-hour or a 48-hour infusion
at the rate of 5.4 mg/kg per
hour.6
Second, hypoxia and ischemia at
the local site of spinal cord injury
should be minimized by controlling
hemodynamic status and oxygenation.
All patients should receive
supplemental oxygen sufficient to
achieve an oxygen saturation approaching
100%. This should be
initiated as soon as the diagnosis of
spinal cord injury is made. Patients
with high cervical injuries may
require intubation to reach this
level.
Neurogenic shock results from
the disruption of sympathetic outflow
by cord injury. It is clinically
manifested by hypotension due to
vasodilatation and bradycardia
secondary to unopposed vagal
influence on the heart. Patients in
neurogenic shock typically have a
heart rate between 50 and 70 beats
per minute and a systolic pressure
30 to 50 mm Hg below normal.
Neurogenic shock must be differentiated
from hypovolemic shock,
Table 2
Acute Management of Cervical Spinal Cord Injury
1. Maintenance of perfusion systolic blood pressure >90 mm Hg
2. 100% O2 saturation via nasal cannula
3. Early diagnosis by plain radiography
4. Methylprednisolone therapy (loading dose of 30 mg/kg followed by
infusion at rate of 5.4 mg/kg per hour for 23 or 48 hours)
5. Immediate traction reduction for cervical fracture and dislocation
6. Spinal imaging (MR imaging and/or computed tomography)
7. Surgery if indicated for residual cord compression or fracture instability
Acute Management of Spinal Cord Injury
172 Journal of the American Academy of Orthopaedic Surgeons
which presents with a combination
of tachycardia and hypotension,
generally due to blood loss
from abdominal or pelvic injury.17
Treatment of neurogenic shock
includes an initial fluid challenge,
Trendelenburg positioning (10 to
20 degrees), vasopressors (e.g.,
dopamine and phenylephrine hydrochloride)
after central line
placement, and atropine for treatment
of bradyarrhythmias. Systolic
blood pressure should be
restored to normal as quickly as
possible.
Third, once a spinal cord injury
is suspected, the spine should be
immobilized to prevent further
neurologic injury. Currently, most
spinal cord injury patients are
transported to trauma centers by
emergency medical services personnel
and arrive immobilized on a
trauma board with a collar. Effective
management requires the assumption
that every polytraumatized
or unconscious patient has a
spinal cord injury until proven otherwise.
Early recognition and appropriate
acute management of spinal
cord injuries is critical to improving
overall patient outcome. For
example, the incidence of complete
neurologic injury in patients with
traumatic spinal insults admitted to
one regional spinal cord injury system
in 1972 was 81%; by 1992, this
had dropped to 57%.18 In another
study,19 the proportion of complete
spinal cord injuries decreased from
64% to 46% after the establishment
of a regional spinal cord injury
unit.
Spinal cord injury is frequently
accompanied by other injuries,
many of which can be life-threatening.
For example, of patients with
spinal cord injury secondary to
motor-vehicle accidents, 40% have
associated fractures, 42.5% experience
loss of consciousness, and
16.6% have a traumatic pneumothorax
or hemothorax.20 The initiation
of evaluation and treatment of
acute spinal cord injuries may be
delayed by the need to treat more
life-threatening injuries. Nevertheless,
during the acute resuscitation
and evaluation of the polytrauma
patient, the spine should be stabilized
and protected from further
injury at all times.
Accurate radiologic (Fig. 4) and
neurologic assessment of the patient
with a spinal cord injury
should be part of the secondary
trauma survey. When feasible,
malaligned vertebral fractures or
dislocations should be reduced concurrently
with ongoing trauma
resuscitation measures. Early intervention
is essential to limit the secondary
spinal cord injury. If the
patient survives the life-threatening
injuries, the outcome of the spinal
injury will be a predominant factor
influencing the future quality of
life.
Patients presenting with either a
neurologic deficit or evidence of
cervical spine instability should be
placed in cervical traction with
tongs or a halo ring. Contraindications
to cervical traction include
distraction injuries at any level in
the cervical spine and type IIA
hangmanÕs fractures. The objectives
of application of halo or tong
traction are spinal stabilization
and, when possible, rapid decompression
through realignment of
the spinal canal.
A lateral cervical spine film
showing C1 to T1 should be available
before the application of traction
and should be repeated after
the initial application of 10 to 15 lb.
Weight can then be added in 5- and
10-lb increments, followed by serial
neurologic evaluations and repeat
radiographs until evidence of
alignment is seen. Intravenous
administration of 1 to 4 mg of
midazolam hydrochloride as an
adjunct to achieve muscle relaxation
and use of fluoroscopy can
facilitate a more rapid, controlled
reduction of cervical facet dislocations.
Contraindications to continued
attempts at reduction using
traction include worsening neurologic
deficits and evidence of distraction
by more than 1.0 cm in a
disk space. Reduction is typically
obtained with 40 to 70 lb of traction,
although use of more than 100
lb has been reported.21
For initial immobilization, cervical
tongs and the halo ring each
have advantages. In some centers,
cervical tongs are preferred because
of the rapidity and ease with which
they can be applied by one person
in an emergency room. Halo application
takes somewhat longer and
generally requires two persons, but
has the advantage of control of
alignment in three planes and can
facilitate the reduction of unilateral
and bilateral facet dislocations.
Availability of traction equipment
is important; delays in application
of traction are common due to the
necessity of obtaining a halo from
another location or due to ongoing
radiologic or trauma evaluation.
Ideally, the halo or tongs should be
compatible with magnetic resonance
(MR) imaging. However, the
application of cervical traction
should not be delayed in order to
first obtain a diagnostic study, such
as MR imaging or computed tomography/
myelography.
Slucky and Eismont19 recommend
MR imaging for assessment
of the degree of spinal cord compression
in patients with complete
or incomplete neurologic deficit, as
well as in patients whose neurologic
status has deteriorated and
those in whom disk retropulsion
with canal compromise or posterior
ligament injury is suspected. The
MR images should be obtained
after application of traction; reduction
of a dislocation in a patient
with a severe incomplete or complete
neurologic deficit should not
be delayed for completion of an
MR study.
A B C
D E
F G
Images of a 26-year-old woman who fell while
rollerblading and sustained a severe C5 fracture-subluxation
(teardrop fracture). Twenty minutes after the
injury she was urgently transported to the emergency
room, and complete C5 quadriplegia was identified.
A, Initial MR image shows severe spinal cord compression
by the C5 vertebral body, illustrated by the marked
signal change in the cord directly above the fractured
vertebra. B, The initial computed tomographic (CT)
reconstruction illustrates the severe fracture-subluxation
of the C5 vertebral body. The initial MR imaging and
CT studies were obtained within 1 hour after injury.
C, Axial MR image demonstrates severe damage to the
spinal cord (arrows) with what appears to be midline
separation of the cord, probably representing hematoma
into both sides of the cord. D, Axial CT scan depicts a
midline fracture through the C5 vertebral body as well
as posterior laminar fractures bilaterally and severe
spinal canal compression. E, Lateral cervical spine radiograph
taken after application of Gardner-Wells tongs
and 30 lb of traction demonstrates restoration of the normal
cervical alignment and partial reduction of the C5
vertebral fracture-subluxation. F, Approximately 2
hours after the injury, the patient underwent a C5 vertebrectomy
with spinal cord decompression and anterior
fusion with an iliac-crest strut graft and anterior plate
fixation. A Philadelphia collar was worn for 6 weeks.
The patient was transferred to a spinal cord rehabilitation
unit 4 days after surgery. G, At the 6-month followup
examination, the patient demonstrated complete root
recovery to the C7 level on the right side and single-root
recovery to the C6 level on the left side. An MR image
obtained at that time depicts significant signal changes
in the spinal canal at the level of the cord injury.
Serial Examinations
The objectives of the initial neurologic
examination conducted
during the secondary trauma survey
are to establish the level and
type of neurologic deficit and to
determine whether there is any
motor or sensory sparing distal to
the level of injury. The initial evaluation
is the most valuable from a
prognostic standpoint, as it guides
treatment decisions and serves as a
baseline for subsequent evaluations.
Follow-up examinations
should be performed at regular
intervals and also whenever the
patient is transferred or undergoes
traction adjustments or surgical
procedures. In a multicenter study
of deterioration of neurologic status
after spinal cord injury, Marshall
et al22 prospectively evaluated
283 patients admitted to five trauma
centers. Fourteen of these patients
deteriorated neurologically
during acute hospital management.
In 12 of the patients, deterioration
could be specifically associated
with a management intervention,
such as traction or halo-vest application,
surgery, or Stryker frame or
rotating bed rotation.
The use of the American Spinal
Injury Association scoring diagram
for spinal cord injury helps examiners
obtain accurate, complete,
and reproducible neurologic assessments.
If examinations are
recorded each time in the same format
and with use of the same data
points, they can be easily compared
with one another.
Timing of Operative Treatment
The timing of surgery remains a
controversial issue. There is little
debate that emergency surgical
decompression is indicated for a
progressive neurologic deficit in the
presence of persistent spinal cord
compression. Operative intervention
in other clinical circumstances
can be done on an acute or urgent
basis or can be delayed. Ducker et
al23 advocated acute operative
intervention for patients with cervical
spinal cord injury who require
open reduction or decompression
for persistent spinal cord compression,
instability at the occipital cervical
junction, or atlantoaxial instability.
Other authors recommend
treating nonprogressive neurologic
deficits on a semiurgent basis,
when the patient is medically stable.
24
In a multicenter study, Marshall
et al22 had three patients with cervical
spinal cord injuries whose
neurologic condition deteriorated
after surgery. Each patient had
been operated on within 5 days of
injury. No such deterioration was
noted when surgery was performed
after 5 days. On the basis
of these observations in a very
small sample of patients, they recommended
that early surgical
intervention should be performed
only to avoid further deterioration
in neurologic function.
There have been other reports of
marked neurologic recovery in
patients who presented initially
with complete deficits and canal
compromise and were treated with
rapid closed reduction and restoration
of alignment. In one of the
earliest retrospective reviews,
Frankel et al25 evaluated the data
on 682 patients who underwent
postural reduction at the National
Spinal Injuries Centre in England
between 1951 and 1968. On detailed
analysis of the neurologic
results, the authors noted that a
small number of patients with complete
neurologic lesions initially
and a larger number of patients
with incomplete lesions improved.
No mention was made of a correlation
between timing of the reduction
and degree of recovery. Furthermore,
the authors could not
correlate the severity of the neurologic
lesion or the degree of reduction
achieved with the neurologic
recovery.
Hadley et al26 presented the data
on a series of 68 patients with acute
traumatic cervical-facet fracturedislocations.
One patient, who presented
initially with a unilateral
dislocation and a complete deficit,
improved neurologically after reduction
to the point that he could
ambulate with arm braces. Another
patient, who presented with
a complete neurologic deficit due
to a bilateral facet dislocation,
underwent closed reduction with
cervical traction within 4 hours of
injury and was neurologically
intact at last follow-up (54 months
after injury).
In patients with incomplete neurologic
function, the results of very
rapid reduction are more promising.
In a series of 100 surgically
treated cervical spine injuries, Aebi
et al27 noted neurologic improvement
after manual or surgical
reduction in 31 patients. Of these
patients, 75% underwent reduction
within 6 hours of the injury. In
contrast, 85% of the 69 patients
who had no neurologic recovery
underwent reduction more than 6
hours after injury.
These clinical observations are
consistent with the previously cited
experimental conclusions drawn by
Delamarter et al4 regarding the
effect of timing of decompression
of the spinal cord after acute experimental
spinal cord compression
injury. The findings in that study
suggest that not all damage to the
spinal cord occurs at the time of
initial trauma and that the extent
and persistence of damage depend
in part on the duration of compression.
It therefore appears that a
window of opportunity may exist
in many spinal cord injuries. Although
the time available for intervention
is short, there is a period
when complete injury may be partially
reversible.
Other authors have considered
both the force of the initial injury
and the timing of decompression in
the prognosis for recovery.28 Although
the force of the initial injury
may be the predominant factor, the
timing of decompression or reduction
and medical management are
the only factors over which the
spine surgeon has control.
Summary
Recent advances in understanding
of the pathogenesis of spinal cord
injury hold promise for future
improvement in clinical outcomes.
In the meantime, early management
in accordance with the
NASCIS-III protocol, along with
rapid reduction and stabilization,
affords the best opportunity for
optimization of the long-term outcome
in patients with spinal cord
injuries.
References
1. National Spinal Cord Injury Statistical
Center: Spinal Cord Injury Facts and
Figures at a Glance. Birmingham, Ala:
University of Alabama, 1999.
2. Janssen L, Hansebout RR: Pathogenesis
of spinal cord injury and newer treatments:
A review. Spine 1989;14:23-32.
3. Young W, Huang P, Kume-Kick J:
Cellular ionic and biomolecular mechanisms
of the injury process, in Benzel
EC, Tator CH (eds): Contemporary
Management of Spinal Cord Injury. Park
Ridge, Ill: American Association of
Neurological Surgeons, 1995, pp 28-31.
4. Delamarter RB, Sherman J, Carr JB:
Pathophysiology of spinal cord injury:
Recovery after immediate and delayed
compression. J Bone Joint Surg Am
1995;77:1042-1049.
5. Greene KA, Marciano FF, Sonntag VK:
Pharmacological management of
spinal cord injury: Current status of
drugs designed to augment functional
recovery of the injured human spinal
cord. J Spinal Disord 1996;9:355-366.
6. Bracken MB, Shepard MJ, Collins WF,
et al: A randomized, controlled trial of
methylprednisolone or naloxone in the
treatment of acute spinal-cord injury:
Results of the Second National Acute
Spinal Cord Injury Study. N Engl J
Med 1990;322:1405-1411.
7. Zeidman SM, Ling GS, Ducker TB,
Ellenbogen RG: Clinical applications of
pharmacologic therapies for spinal cord
injury. J Spinal Disord 1996;9:367-380.
8. Geisler F: Prevention of spinal cord
injury, in Benzel EC, Tator CH (eds):
Contemporary Management of Spinal
Cord Injury. Park Ridge, Ill: American
Association of Neurological Surgeons,
1995, p 262.
9. Bracken MB, Shepard MJ, Holford TR,
et al: Administration of methylprednisolone
for 24 or 48 hours or tirilazad
mesylate for 48 hours in the treatment
of acute spinal cord injury: Results of
the Third National Acute Spinal Cord
Injury Randomized Controlled TrialÑ
National Acute Spinal Cord Injury
Study. JAMA 1997;277:1597-1604.
10. Galandiuk S, Raque G, Appel S, Polk
HC Jr: The two-edged sword of largedose
steroids for spinal cord trauma.
Ann Surg 1993;218:419-425.
11. Rengachary S, Alton S: Resuscitation
and early medical management of the
spinal cord injury patient, in Benzel
EC, Tator CH (eds): Contemporary
Management of Spinal Cord Injury. Park
Ridge, Ill: American Association of
Neurological Surgeons, 1995, pp 60-61.
12. Geisler FH, Dorsey FC, Coleman WP:
Recovery of motor function after
spinal-cord injury: A randomized,
placebo-controlled trial with GM-1
ganglioside. N Engl J Med 1991;324:
1829-1838.
13. Geisler FH, Dorsey FC, Coleman WP:
Past and current clinical studies with
GM-1 ganglioside in acute spinal cord injury.
Ann Emerg Med 1993;22:1041-1047.
14. Hansebout RR, Blight AR, Fawcett S,
Reddy K: 4-Aminopyridine in chronic
spinal cord injury: A controlled,
double-blind, crossover study in eight
patients. J Neurotrauma 1993;10:1-18.
15. Bregman BS, Kunkel-Bagden E, Schnell
L, Dai HN, Gao D, Schwab ME: Recovery
from spinal cord injury mediated
by antibodies to neurite growth
inhibitors. Nature 1995;378:498-501.
16. Cheng H, Cao Y, Olson L: Spinal cord
repair in adult paraplegic rats: Partial
restoration of hind limb function.
Science 1996;273:510-513.
17. Soderstrom CA, McArdle DQ, Ducker
TB, Militello PR: The diagnosis of
intra-abdominal injury in patients
with cervical cord trauma. J Trauma
1983;23:1061-1065.
18. Waters RL, Apple DF Jr, Meyer PR Jr,
Cotler JM, Adkins RH: Emergency and
acute management of spine trauma, in
Stover SL, DeLisa JA, Whiteneck GG
(eds): Spinal Cord Injury: Clinical Outcomes
From the Model Systems. Gaithersburg,
Md: Aspen Publishers, 1995, p 57.
19. Slucky AV, Eismont FJ: Treatment of
acute injury of the cervical spine. Instr
Course Lect 1995;44:67-80.
20. Go BK, DeVivo MJ, Richards JS: The
epidemiology of spinal cord injury, in
Stover SL, DeLisa JA, Whiteneck GG
(eds): Spinal Cord Injury: Clinical
Outcomes From the Model Systems.
Gaithersburg, Md: Aspen Publishers,
1995, pp 44-45.
21. Cotler JM, Herbison GJ, Nasuti JF,
Ditunno JF Jr, An H, Wolff BE: Closed
reduction of traumatic cervical spine
dislocation using traction weights up
to 140 pounds. Spine 1993;18:386-390.
22. Marshall LF, Knowlton S, Garfin SR, et
al: Deterioration following spinal cord
injury: A multicenter study. J Neurosurg
1987;66:400-404.
23. Ducker TB, Bellegarrigue R, Salcman
M, Walleck C: Timing of operative
care in cervical spinal cord injury.
Spine 1984;9:525-531.
24. Connolly PJ, Abitbol JJ, Martin RJ,
Yuan HA: Spine: Trauma, in Garfin
SR, Vaccaro AR (eds): Orthopaedic
Knowledge Update: Spine. Rosemont,
Ill: American Academy of Orthopaedic
Surgeons, 1997, p 202.
25. Frankel HL, Hancock DO, Hyslop G,
et al: The value of postural reduction
in the initial management of closed
injuries of the spine with paraplegia
and tetraplegia: I. Paraplegia 1969;7:
179-192.
26. Hadley MN, Fitzpatrick BC, Sonntag
VK, Browner CM: Facet fracturedislocation
injuries of the cervical
spine. Neurosurgery 1992;30:661-666.
27. Aebi M, Mohler J, Zach GA, Morscher E:
Indication, surgical technique, and
results of 100 surgically-treated fractures
and fracture-dislocations of the cervical
spine. Clin Orthop 1986;203:244-257.
28. Guha A, Tator CH, Endrenyi L, Piper
I: Decompression of the spinal cord
improves recovery after acute experimental
spinal cord compression injury.
Paraplegia 1987;25:324-339.
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