TEXTBOOK READING

August 2018

Spinal Cord Injury

Presented by :
Myzard Arief
Muhammad Farid
Virginia Lestari R
Siti Nurul Magfirah
Elma Nur

Resident Advisors :
dr. Asri Abidin
dr. Ricky M Tambunan
dr. William Limoa

Advisors :
DR. dr. Karya Triko Biakto Sp. OT (K) Spine

ORTHOPAEDIC AND TRAUMATOLOGY DEPARTMENT

FACULTY OF MEDICINE
UNIVERSITY HASANUDDIN
MAKASSAR

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 LEMBAR PENGESAHAN
Yang bertanda tangan di bawah ini menyatakan bahwa :

Nama : Myzard Arief

Muhammad Farid
Virginia Lestari R
Siti Nurul Magfirah
Elma Nur

Judul Texbook reading : Spinal Cord Injury

Telah menyelesaikan tugas dalam rangka kepaniteraan klinik pada bagian Orthopaedic dan
Traumatology Fakultas Kedokteran Universitas Hasanuddin.

Makassar, Agustus 2018

Pembimbing 2 Pembimbing 1

dr. Ricky M Tambunan dr. Asri Abidin

Supervisor Pembimbing 3

DR. dr. Karya Triko Biakto Sp. OT (K) Spine dr. William Limoa

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 SPINAL CORD INJURY

There is still no cure for spinal cord injury (SCI). Recovery in the spinal cord is thwarted by
two fundamental obstacles: the inherently weak regenerative ability of central nervous system
(CNS) axons and a powerfully inhibitive—and often deleterious—postinjury milieu of physical
and chemical factors. These factors are intertwined in a so-called secondary response of
tremendous complexity that ironically does more to injure the spinal cord further than to heal
it. Years of research have slowly elucidated the pathophysiologic processes that follow a
traumatic insult to the spinal cord. This chapter reviews the biochemical and physiologic
features of the SCI response and establishes a foundation on which the latest therapeutic
strategies can be understood. The first section discusses the inlammatory cascade that occurs
in the moments after an assault to the spinal cord. The second section reviews current
understanding of the inhibitory extracellular environment that results from the injury response
and that ultimately prevents axonal regeneration. the chapter concludes with a review of the
biochemical processes that can be targeted by candidate therapies.

Pathophysiologic Response to Spinal Cord Injury

The acutely traumatized spinal cord is subjected to multiple physical and chemical mediators
that cause additional (secondary) injury. This concept of secondary injury has been validated
in both animal and clinical studies, and secondary injury mechanisms have been the target of
the bulk of pharmacologic interventions to date. hese processes begin immediately following
the injury and continue for weeks.

Hemorrhage and Circulatory Collapse

Upon injury, the blood–spinal cord barrier is disrupted and intraparenchymal hemorrhage
occurs, the extent of which depends on the force of the initial trauma. Microcirculatory
insuiciency follows. Vascular hypoperfusion due to capillary loss, capillary spasm, thrombosis,
systemic hypotension, and autonomic regulatory interruption lead to cellular ischemia at the
epicenter of cord injury. he neuronal cell bodies in the gray matter are highly vulnerable to
ischemia. The resultant shit in pH renders neuronal cell body and axonal membranes highly
vulnerable to subsequent injury.

Oxidative Damage

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Reperfusion and oxidative stress follow the transient period of hypoperfusion. he introduction
of oxygen to the compromised cell membranes produces a highly toxic environment in which
the membrane lipid fatty acids undergo oxidation. This membrane lipid peroxidation produces
several varieties of free radicals that, in turn, drive even further lipid peroxidation and free
radical production. Some of the free radicals accumulate within the cell and denature
deoxyribonucleic acid, mitochondrial proteins, and eventually bring energy production to a
halt, resulting in irreversible damage and cell death.

Excitotoxicity
Disruption of the neuronal cellular membrane undermines one of the crucial features of cellular
equilibrium—ionic regulation. The destabilized neurons undergo an inlux of sodium ions that
eventually alters cellular pH and leads to cytotoxicity. The ionic balance is perturbed by, and
will cause neuronal destruction via, an additional important mechanism: the cellular release of
the ubiquitous neurotransmitter glutamate changes the extracellular space into a hostile
extracellular milieu. Glutamate activates various cell surface receptors that, in turn, mediate a
large variety of intracellular processes. Excessive glutamate will drive these processes to the
point of fatal overload to the cell. he most studied of the glutamic receptors is the N-methyl-
D-aspartate receptor, which mediates entry of Ca2+ into cellular cytoplasm from both
extracellular and intracellular stores. While calcium in physiologic amounts is the necessary
component for many important enzyme-mediated cellular processes, pathophysiologic
quantities of calcium lead to the persistent activity of destructive enzymes, including
lipoxygenases and phospholipases. These enzymes will target the beleaguered cell membrane
again to generate free radicals from lipid oxidation. he radicals will disrupt cellular proteins, in
particular, those that mediate the ability of mitochondria, the chief source of cellular energy, to
drive oxidative phosphorylation.

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Mitochondrial Collapse and Cytotoxicity
The aforementioned free radical formation and glut of Ca2+ ions abolish mitochondrial
integrity by activating mitochondrial permeability transition pores. The opening of these pores
leads to a massive increase in mitochondrial membrane permeability. he organelle loses its
electrochemical gradient, adenosine triphosphate production ceases, and the outer membrane
swells until it ruptures. he damage is far-reaching. Calcium ions, free radicals, and cytochrome
c, once sequestered within the mitochondria, are now free to escape into the neuronal cytoplasm
where they immediately activate necrosis and apoptosis.

Neuroimmunologic Response
The cells of the immune system are eventually attracted to the neuronal self-destruction. Over
the next hours to weeks, they will lay the foundations for an extracellular environment that will
inhibit axonal regeneration. he irst of these cells to appear at the site of injury are circulating
neutrophils. Once active, neutrophils will secrete cytokines that stimulate production of
phospholipases and cyclooxygenase. The former will consume neural membranes to produce
arachidonic acid, which the latter (cyclooxygenase) uses to produce prostaglandins and
thromboxanes. Prostaglandins (PGE2, PGD2, PGF2α, PGI2) serve (1) to amplify the
inlammatory response by increasing capillary permeability to allow additional inlammatory
cell inlux; (2) to increase neuronal calcium concentration, thus promoting excitotoxicity; and
(3) to activate other inlammatory cells. Thromboxanes promote platelet aggregation within
capillaries and thus worsen local tissue ischemia. Macrophages, local microglia, and astrocytes
eventually appear and begin secreting the two most important factors of the cytotoxic

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inlammatory response: interleukin-1 and tumor necrosis factor α. Interleukin-1 stimulates the
expression of adhesion factors on endothelial cells, which will allow circulating lymphocytes
to penetrate the blood–brain barrier. Tumor necrosis factor α serves to recruit activated
cytotoxic lymphocytes to irst adhere to endothelial cells and then to the site of injury. he
recruited lymphocytes, which target myelin basic protein, are particularly adept at causing
disruption of the all-important myelin sheath—a critical component of nerve conductivity and
axonal regeneration. The epicenter of traumatic injury thus becomes an inlammatory tangle of
necrosis, apoptosis, and demyelination. Over the coming weeks, the cellular debris will first
liquefy into a posttraumatic cyst and then organize into the notorious astroglial scar, which will
inhibit axonal regeneration.

PATHOPHYSIOLOGY OF SPINE INJURIES

Stable and unstable injuries
Spinal injuries carry a double threat: damage to the vertebral column and damage to the neural
tissues. While the full extent of the damage may be apparent from the moment of injury, there
is always the fear that movement may cause or aggravate the neural lesion; hence the
importance of establishing whether the injury is stable or unstable and treating it as unstable
until proven otherwise.
A stable injury is one in which the vertebral components will not be displaced by normal
movements; in a stable injury, if the neural elements are undamaged there is little risk of them
becoming damaged.
An unstable injury is one in which there is a
significant risk of displacement and consequent
damage – or further damage – to the neural tissues.
In assessing spinal stability, three structural
elements must be considered: the posterior
osseoligamentous complex (or posterior column)
consisting of the pedicles, facet joints, posterior
bony arch, interspinous and supraspinous
ligaments; the middle column comprising the
27.1 Structural elements of the spine The posterior half of the vertebral body, the posterior
vertical lines show Denis’ classification of the
structural elements of the spine. The three part of the intervertebral disc and the posterior
elements are: the posterior complex, the
middle component and the anterior column. longitudinal ligament; and the anterior column
This concept is particularly useful in assessing
the stability of lumbar injuries. composed of the anterior half of the vertebral body,

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the anterior part of the intervertebral disc and the anterior longitudinal ligament (Denis, 1983).
All fractures involving the middle column and at least one other column should be regarded as
unstable. Fortunately, only 10 per cent of spinal fractures are unstable and less than 5 per cent
are associated with cord damage.

Mechanism of injury
There are three basic mechanisms of injury: traction (avulsion), direct injury and indirect
injury.
Traction injury In the lumbar spine resisted muscle effort may avulse transverse processes; in
the cervical spine the seventh spinous process can be avulsed (‘clayshoveller’s fracture’).
Direct injury Penetrating injuries to the spine, particularly from firearms and knives, are
becoming increasingly common.
Indirect injury This is the most common cause of significant spinal damage; it occurs most
typically in a fall from a height when the spinal column collapses in its vertical axis, or else
during violent free movements of the neck or trunk. A variety of forces may be applied to the
spine (often simultaneously): axial compression, flexion, lateral compression, flexion-rotation,
shear, flexion-distraction and extension.

Assessment of the Spine-Injured Patient

Initial Evaluation
Patients sustaining blunt trauma should be assumed to have a potential spinal column injury.
During transport, patients are placed on a backboard and immobilized in a hard extraction
collar. he immediate primary care is to evaluate airway, breathing, and cardiovascular
functions, and begin resuscitation. The secondary exam includes visual examination of the
spinal column by log rolling the patient and palpation to determine tenderness, crepitus, and
gaps or step-ofs between spinous processes. Hemorrhage, contusion, and abrasion on the face,
head, or dorsal spine should raise suspicion of spinal injury. The goal of spinal evaluation is to
identify patients who require further imaging and to critically measure neurologic function.

Clearing the Cervical Spine

The goal of this evaluation is to identify patients who have significant cervical injury after
trauma. Patients can be divided into four categories: asymptomatic, temporarily not evaluable,
symptomatic, and obtunded. Asymptomatic patients are those who have no pain, tenderness to
palpation, normal cognitive function, and no distracting injuries. Distracting injuries are other

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sources of trauma that may decrease or eliminate cervical spine signs or symptoms. Examples
of distracting injuries are fracture-dislocations, long-bone fractures, burns, shock, chest trauma,
and craniofacial trauma.

Asymptomatic Patients
Asymptomatic adult patients can be cleared of cervical spine injury without any radiologic
imaging. he National Emergency X-Radiography Utilization Study (NEXUS) screened 34,068
patients using the criteria and identiied 99.8% of all injuries. Six of the eight missed cases were
trivial fractures and two were signiicant (odontoid fractures) that did not develop a neurologic
injury. he speciicity was low (12.8%), indicating that many patients still required imaging,
which was negative. A simple modification is the Canadian Cervical Spine Rule (CCR), which
adds 45 degrees of pain-free rotation of the head to the examination. Stiell reported a 100%
sensitivity using this method and improved specificity over the NEXUS method. Both of these
protocols are not applicable to children and are less accurate in geriatric patients.

Temporarily Not Evaluable

These patients are less well deined. However, they could be cleared using the asymptomatic
criteria, but have distractinginjuries or impaired cognitive function, such as intoxication, that
will clear or be corrected within 24 to 48 hours. Initially, they are immobilized in an orthosis,
then later reevaluated based on NEXUS or CCR criteria. If negative at that time, they may be
cleared with further imaging. If clearance is required immediately, then they should be
evaluated as described later for obtunded patients.

Symptomatic Patients
All symptomatic patients following blunt trauma are at high risk for cervical spine injury, thus
require radiologic imaging. Computed tomography (CT) in adults is highly sensitive and
preferred over plain radiography. Magnetic resonance imaging (MRI) is not recommended as
a screening examination due to its cost and high rate of false positives. MRI is indicated in
patients who have unexplained neurologic deicits (such as central cord syndrome), for patients
for whom there is suspected ligamentous injury, in patients with signiicant degenerative or
postsurgical changes, as well as to aid surgical decision making. A negative MRI, however,
does accurately exclude the presence of a cervical spine injury.

Obtunded Patients
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The clearance of obtunded patients remains controversial. Maintaining spine precautions and
cervical immobilization in this patient population is associated with reduced pulmonary
function, increased intracranial pressure, and risk of skin decubitus. hus, timely clearance is
important. Two options are available in obtunded patients: utilize results of CT or include MRI.
Modern helical CT is highly sensitive and rarely have signiicant injuries been reported
following CT.
Most cases are results of misreading by radiologists. MRI, however, has been shown to identify
more injuries than CT and, in some studies, resulted in need for surgical treatment. Like
investigations regarding CT, these studies are small retrospective studies without adequate
statistical power. I recommend that each institution utilize its own protocol and continue to
monitor efectiveness.

Neurologic Examination
A complete neurologic examination is performed, including cognitive function, cranial nerve,
motor sensory function in the extremities, relexes, and pathologic relexes. In addition, in
patients with any neurologic deicits, careful evaluation of perineal function is performed.
Patients’ neurologic function should be reported per American Spinal Injury Association
(ASIA) standards. The ASIA motor score is the summation of motor function of 10 key muscle
groups, five in the upper and five in the lower extremities, bilaterally; each is graded from 0 to
5. Summation of these scores deines the ASIA motor score and the total ranges from 0 to 100.
Sensory examination of each dermatome is recorded as intact, hypoesthesia, or absent. Perianal
examination is essential, as patients may have only sacral root sparing, which can dramatically
change the prognosis.
Perianal rectal function is determined by digital rectal examination, assessing the initial tone
and asking the patient to perform voluntary rectal contractions. he bulbocavernosus relex and
the anal wink are spinal cord–mediated relexes at the level of the conus medullaris. he anal
wink is obtained by brushing the paraspinal area with a pin and observing for an anal
contraction. he bulbocavernosus relex is best obtained during digital rectal examination by
placing tension on a Foley catheter and observing for a rectal contraction. These reflexes are
present in intact patients. Although they are typically absent in acute spinal cord–injured
patients, they may return early (within 7 to 10 days ater spinal cord injury).
Intact perianal function in injuries at the conus medullaris, such as L1 or T12 fractures, or for
cauda equina injuries is a good prognostic sign, as it indicates that the aferent and eferent
neurons and the conus are functional. Deep tendon relexes, including biceps, triceps, patella,

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and Achilles, are assessed. In acute spinal cord injuries, the reflexes below the level of injury
are usually absent due to spinal shock, but will return in 10 to 21 days when they will become
hyperrelexic. In addition, pathologic relexes—such as Hofman, Babinski, and clonus—should
be recorded. Priapism, if present, is a sign of acute spinal cord injury.

Spinal Cord Injury Classiication

Spinal cord injuries are classiied at the level and extent of injury. ASIA deines the level as the
lowest segment with at least antigravity (grade _3) motor function. The extent of spinal cord
injuries is how much of the cross-sectional area of the cord is injured. Complete cord injuries
are deined as complete loss of motor and sensory function; incomplete cord injuries have some
retained motor and/or sensory function below the zone of injury. Special attention needs to be
focused in the perineal area, as this may be the only area distinguishing complete from
incomplete injuries. Incomplete cord injuries are important to recognize and have a much better
prognosis.
The anterior cord syndrome represents loss of the anterior two-thirds of the spinal cord, where
there is paralysis of distal motor function and loss of pain and temperature sensation. These
patients have retained dorsal column function, so that they may experience light touch,
proprioception, and vibratory sensation, but no pinprick or motor function.
Central cord syndrome is a common cord injury in which there is loss of gray matter and central
white matter. he white matter tracts are laminated, with cervical tracts positioned more centrally
and lumbar and sacral tracts located toward the periphery. Because of the relative sparing of
these laterally located tracts, the central cord syndrome is manifested by greater loss of upper
than lower extremity function. The prognosis for central cord syndrome is good, with an
expectation for ambulation, but hand function may be chronically impaired.
The posterior cord syndrome is the loss of the posterior column with sparing of the anterior
cord. These injuries produce loss of vibration, light touch, and position sense, but maintain
pain, temperature, and motor functions.
Brown-Sequard syndrome is a hemicord injury with ipsilateral motor paralysis and loss of
dorsal column function as well ascontralateral loss of pain and temperature. he prognosis for
Brown-Sequard syndrome is excellent.
The ASIA Impairment Scale (AIS) assesses the extent of injury and is highly predictive of
outcomes. Complete cord injuries with absence of distal and sensory motor function are ASIA
A. The ASIA B patient has some sensation, but no motor function below the zone of injury.
ASIA C patients have both motor and sensory function below the zone of injury, but the motor

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function is less than grade 3. ASIA D patients, like ASIA C patients, have both motor and
sensory function, but motor function is grade 4 or 5. ASIA E patients are intact. Patients with
neurologic deicits should have neurologic exams at least every 2 hours, which are documented
in the record. Neurologic function may change in the initial stages after spinal cord injury,
which will be an important determinant of treatment. herefore, accurate reporting of the
neurologic exams is essential. The ASIA classiication is useful for a comprehensive report of
the neurologic examination.

General Approach to Treatment of Injuries

Each patient is assessed clinically for signs of injury by palpation, checking for tenderness, and
by a detailed neurologic examination. A patient with tenderness or signs and symptoms of
neurologic injury should have a CT to identify injury patterns. If any ligamentous injury is
suspected or unexplained neurologic deicits are present, an MRI scan is indicated. At this point,
the injury is classiied morphologically using the AO system. he severity is then graded using
CSISS or SLIC. Patients who have a score greater than 5 SLIC or greater than 7 CSISS are
treated surgically. In patients with less severe injuries, nonoperative treatment in orthosis is
attempted.

Nonoperative Care of Subaxial Cervical Injuries

Nonoperative care is indicated for those with stable fractures or those who are not otherwise
surgical candidates. For most lower cervical spine injuries, patients are managed in an orthosis.
Choices include sot collar, hard collar (e.g., Miami J [Ossur]; Aspen collar [Aspen Medical
Products], or CervMax [PMT Corporation]), cervicothoracic brace, and halo vest.
The general approach in all orthotic management is similar. The orthosis is fitted by a trained
orthotist. Pads that wick luids away from the skin can help to prevent skin breakdown. he brace
needs to control head-mandible motion relative to the thorax. No brace, including the halo vest,
will completely prevent segmental motion in a fractured cervical spine, as the spinal column
can easily assume snakelike intervertebral motions. Twice-daily skin checks are ordered while
the patient is hospitalized or in a rehabilitation facility.
Training of patients and family is essential to ensure proper use and to avoid complications of
the orthosis. In patientsolder than 65 years, a swallow consult is obtained to assess aspiration
risk prior to institution of diet. Occupational therapy trains patients to use the brace and in the
activities of daily living while immobilized. Upright radiographs are obtained ater brace
placement and scrutinized for increasing kyphosis and/or subluxation. Any change in these, or

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new or worsening neurologic symptoms indicates instability, and surgery is recommended.
Follow-up radiographs are obtained at 2, 6, and 10 weeks. In most subaxial injuries, healing
will occur by 10 to 12 weeks or earlier. Patients are initially informed that their orthosis is a
test of stability and that about 5% to 10% of patients will fail and may require surgery. In
patients without clear surgical indication (such as SLIC scores of 4 or 5 and CSISS scores of 5
to 7), either approach can be chosen. In general, I recommend a trial of nonoperative therapy
with orthosis in these cases. In such cases, shared decision making should occur, taking into
account the patient’s preferences.

Soft Collar
Sot collars provide little stability and are used for comfort but also to alert medical personnel
that injury is present. hese are indicated for frail elderly patients with minimal or stable
fractures or in patients who cannot tolerate even a hard collar.

Hard Collar
Many forms of hard collar are available. Use of extraction collars and Philadelphia collars
should be avoided, as these it poorly and can lead to skin breakdown. It does not appear that
the stabilization efect among well-fitting hard collars varies by manufacturer. It is best that the
orthotist use a single brand so that personnel can become familiar with their use and
maintenance. Hard collars do not provide sufficient stability for unstable fractures, but are
efective, in my experience, in stable SLIC score less than 3 and CSISS score less than 5.

Cervicothoracic Orthosis
The cervicothoracic orthosis (CTO) has anterior and posterior chest pads that are connected by
straps under the axilla and over the shoulder. Vertically, they are connected to occipital and
mandibular pads rigidly. The CTO brace provides greater stability than hard collars, especially
at the cervicothoracic junction. The CTO places increasing pressure on the occiput and chin,
and should be used with caution. I do not recommend its use in spinal cord–injury patients who
lack body control or any patient with cognitive impairment due to the risk of skin ulcerations.
I recommend the CTO for patients with injuries at the cervicothoracic junction, those with
multilevel spine fractures where multilevel fusions might be otherwise utilized, and cervical
spine injuries combined with upper thoracic injuries. An alternative treatment for this injury
pattern is the thoracolumbosacral orthosis with chin piece (cervical-thoraco-lumbosacral
orthosis). I have abandoned its use due to risk for skin ulceration and poor patient acceptance.

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Halo Vest
The halo vest is the most rigid external orthosis, although segmental motion can still occur at
the fracture site. Anderson reported in patients with unstable fractures treated in the halo vest
that 1.8 mm of translation and 7 degrees of angulation fracture site motion occur during
position change from supine to upright.20 he use of the halo vest has declined and is rarely
used today in my experience for subaxial injuries. It is indicated for unstable fractures in which
fusion is a poor alternative, such as young patients who are neurologically intact or those with
multilevel injuries. For these cases, the halo vest may provide the best nonoperative approach,
thereby avoiding multilevel fusions.

Treatment of Acute Spinal Cord Injury

The goals of treatment of spinal cord–injury patients are to protect the neural tissues from
further injury, reduce and stabilize fracture-dislocations, and provide a stable long-termpainless
spine.

Transport
Patients presumed to have spinal cord injuries should betransferred to institutions that are
experienced in their management, have advanced imaging available, and can provide intensive
care and urgent surgical services. Treatment of spinal cord injuries in Level 1 trauma centers
is shown to reduce rates of complication as well as shorten the length of hospitalization and
rehabilitation time. Spinal cord–injury patients require intensive care to monitor neurologic
state and provide hemodynamic support, assess pulmonary function (which often deteriorates
over time), and prevent adverse events, such as skin breakdown.

Immediate Care of the Spinal-Injured Patient

Once a subaxial fracture is diagnosed, consideration of immediate treatment is entertained. All
patients with spinal cord and nerve root injury as well as those with unstable fractures are
candidates for immediate intervention. his includes hemodynamic support, further diagnostic
testing, administration of neuroprotective agents, reduction using tong traction, and urgent
surgery. While the decision-making process for resuscitation is taking place, patients with
subaxial fractures should be immobilized in a hard collar and maintained lat on a bed or
stretcher. Although the backboard is an excellent aid for transport to and within the hospital, it
should be removed as soon as possible to reduce the risk of skin breakdown. In addition,

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backboards can be associated with fracture displacement, especially in children or in patients
with thoracic kyphosis.

Hemodynamic Support
The injured or compressed spinal cord is ischemic, which can further exacerbate the spinal cord
injury. If spinal cord injuryis present, there is a loss of vasomotor tone, with resultant
hypotension and bradycardia, causing a condition known as neurogenic shock. In addition, the
spinal cord, like the traumatized brain, loses its ability to autoregulate blood low.
Therefore, intramedullary blood low becomes related to the systemic arterial pressure. Any
hypotension, either from loss of vasomotor control or from blood loss, can worsen or
exacerbate the spinal cord injury. Guidelines recommend resuscitation of a spinal cord–injured
patient to a systolic blood pressure greater than 120 mm Hg (usually with pressor agents) and
maintaining the mean arterial pressure at 85 mm Hg. A high FiO2 should be administered to
maintain O2 saturation greater than 95%. Ventilatory failure may be present or develop over
time and requires intubation and mechanical support. Intubation needs to be performed
carefully so that fracture displacement is minimized. It is best that the surgical team assist in
this task by holding the head while maintaining traction.

Magnetic Resonance Imaging in Acute Spinal Cord Injuries

Early treatment decisions may require further imaging by MRI. Urgent MRI is indicated for
unexplained neurologic deicits, neurologic deterioration, to evaluate ligamentous structures, or
in patients with no or minimal deicits who have facet dislocations to determine the presence of
a traumatic disc herniation. In these cases, neurologic worsening has been reported ater open
reduction when the disc lies behind the vertebral body compressing the spinal cord ater
reduction. Several case reports have documented that disc herniation behind the vertebral body
remains in that location ater reduction, causing signiicant neurologic deicits. In addition, MRI
is useful for preoperative planning.

Neuroprotection
To address the secondary spinal cord injury caused by vascular, molecular, biochemical, and/or
inlammatory changes, early treatment using neuroprotective agents has been proposed. Many
pharmacologic and cellular agents show promise in laboratory animals. However, only
methylprednisolone is approved for current use. Methylprednisolone, when given within 8

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hours of injury, has an antioxidant efect by reducing lipid peroxidation that occurs as part of
the secondary injury pathophysiology.
The clinical evidence for use of methylprednisolone is based on the National Acute Spinal Cord
Injury Study 2 (NACISC2). In this randomized control trial, 454 patients with blunt traumatic
spinal cord injuries were randomized to naloxone, methylprednisolone, and placebo. All
patients had randomization and administration of drugs within 8 hours of injury.
Naloxone was thought to have neuroprotective properties at the time. Patients receiving
methylprednisolone had a statistically signiicant improvement of 5 points of ASIA motor level.
The impact of the NACISC2 study was signiicant; subsequently, almost all spinal cord injuries
were treated using the NACISC2 protocols. However, critical analysis of the statistical
methodology, identification of potential harms, including death, and the minimal perceived
benefits have led many to abandon orlimit the use of methylprednisolone for spinal cord injury.
Recent guidelines by the American Academy of Neurological
Surgeons and the Congress of Neurological Surgeons recommend against the use of
methylprednisolone in acute spinal cord injury. Unfortunately, the data from the NACISC2
study included mostly patients who did not have surgery or even reduction of fracture
dislocations within 24 hours. Further, hemodynamic support was not utilized routinely at the
time of the original study. Thus, there is a knowledge gap as to whether methylprednisolone
may have a beneicial efect when combined with other current standard practices in care. My
current recommendations are to administer methylprednisolone in select patients with cervical
cord injuries, both complete and incomplete, and in incomplete thoracic cord injuries.
Methylprednisolone is recommended only in patients without other significant traumatic
injuries or comorbidities. I do not recommend its use in geriatric patients with spinal cord
injuries. When used, methylprednisolone is administered as a 30-mg/kg loading bolus over 1
hour and a continuous infusion of 5.4 mg/kg per hour for 23 hours.

Fracture-Dislocation Reduction
Early fracture-dislocation reduction is important to remove neural compression and reestablish
blood low to ischemic tissue to prevent deterioration and maximize the chance of neurologic
recovery. This can be achieved by two methods:
cranial tong traction and surgery. Cranial tong traction is a useful and generally safe method to
stabilize the spine and to achieve realignments of fractures and dislocations.26 Indications for
cranial tong traction vary and are being supplanted by immediate surgery where reduction by
traction is avoided.

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In a study to evaluate the timing of surgery on the outcomes of spinal cord injury, the authors
found that only one-third of patients were ever treated with tong traction before surgery. Cranial
tong traction is a fast method to reestablish spinal cord blood low through reduction. In low-
energy facet dislocations, such as from sporting accidents, early reduction within 4 hours of
injury in patients with quadriplegia was shown to have a reversible efect in 80% of cases.

Timing of Surgery
The timing of surgery in humans remains controversial, despite a large volume of animal data
that demonstrates early surgery correlates with greater neurologic recovery. Because of
diiculties with study design, heterogeneity, and severity of injury, these beneits of early surgery
have not been proven in humans. A recent observational study, Surgical Timing in Acute Spinal
Cord Injury Study (STASCIS), compared neurologic improvement at 6 months based on ASIA
impairment scale between early (_24 hours) and late (>24 hours). Patients were stratiied
according to whether surgery was performed before or ater 24 hours. here was no diference for
the chance of improving one ASIA level; however, there was a statistically signiicant and better
chance of improving 2 ASIA levels if surgery was performed within 24 hours. In patients with
spinal cord injuries, the potential for neurologic deterioration caused by early surgery has been
a concern. he mechanics of this are unclear, but likely are due to hemodynamic changes that
occur during surgery. In the STASCIS study, only one patient deteriorated neurologically; the
authors believe that early surgery was feasible and safe in patients treated at centers with
experience in managing spinal cord injuries.

Cranial Tong Technique

Cranial tongs have a metal or carbon iber arc, two pins which are inserted into the skull, and a
hook for traction rope. The pins are disposable, and one pin has a compression spring that acts
to measure the applied force of the pins into the skull. Both MRI-compatible and non–MRI-
compatible devices are available. Unless heavy weights are anticipated, I recommend the use
of MRI-compatible devices. Guidelines for Initial Closed Reduction of Subaxial Cervical
Fractures Gelb reported guidelines based on a systematic review of the use of closed reduction
with tong traction in subaxial fractures and dislocations. Based on a retrospective case series,
the recommends early reduction with cranial tong traction for subaxial injuries in awake
patients without more rostral injuries. Prereduction MRI should be obtained in patients who
cannot be examined during closed reduction or if closed reduction fails. MRI will identify disc

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disruptions in up to 50% of cases, but does not appear to inluence outcomes in awake patients;
therefore, their utility is questioned.

Cranial Tong Insertion

The location of tong insertion is 1 cm above the pin and in line with the external auditory
meatus. Placement more anteriorly or posteriorly can change the force vectors, which may
theoretically aid reduction. For consistency, I recommend placement in line with the exterior
auditory meatus. The skin is prepared with chlorhexidine and the subcutaneous tissue and
periosteum is iniltrated with local anesthetic. No shaving of the scalp is required. he surgeon
holds the tongs with pins located just above the correct starting point, which are then
symmetrically tightened into the skin and skull. The pin containing the compression spring is
scrutinized until it protrudes 1 mm out from the surface of the pin. Jam nuts along the side of
the pins are tightened to prevent inadvertent further tightening of the pins. If the traction is to
be continued (unusual today), the pins may be retightened one time at 24 hours. The rope is
attached to the tongs and connected to weights by a pulley at the head of the bed. I prefer to
raise the head of the bed 20 to 30 degrees while keeping the angle of the rope at the same slope.

Reduction Technique
Reduction of fractures and dislocations requires a rigid protocol to maintain safety. he initial
weight is selected dependingon many factors, including body weight, level of injury, age, and
fracture pattern. For midcervical and lower cervical spine injuries, it is recommended starting
with 10 kg (20–25 lb). Ater the weight has been attached (and ater any increase or decrease of
weight), a radiograph is obtained and a neurologic examination is performed and documented
in the medical record. The radiograph is assessed to determine if reduction has been achieved
and for signs of overdistraction. Overdistraction is assessed by examination of the disc space
and facet joints. Overdistraction may cause excess traction on the spinal cord and vertebral
arteries, which could result in neurologic deterioration. However, to reduce a facet dislocation
in the absence of fractures, overdistraction of 3 to 5 mm may be required. he neurologic
examination assesses any change in perceived sensations, increasing pain, or paresthesia in the
extremities, or deterioration of sensory or motor function. If reduction is not achieved, 5 to 7
kg of additional weight is added as long as no neurologic deicits or radiologic signs of
overdistraction occur. A C-arm with the patient on a stretcher or Jackson-type table can reduce
the time required to obtain the reduction. In general, once the reduction is achieved, weights
may be decreased. However, for unstable fractures, reducing weight can result in displacement

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and neurologic injury. herefore, if weights are decreased, it is essential to repeat the neurologic
examination and examine new radiographs. Some manipulation may be required to achieve
reduction, which should only be done by experienced surgeons. In facet dislocations, slight
lexion may be required to unlock the impacted dislocated facets. his is accomplished by adding
bolsters underneath the occiput to create neck lexion. Another method is to manually
manipulate the spine while in traction. For bilateral facet dislocations, an attempt to reduce
each facet independently is preferred. The tongs are grasped and a lateral bending movement
and forward lexion is applied, ideally reducing one facet. he same movements are performed
on the contralateral side.
In several conditions, cranial tong traction reduction may lead to neurologic deicits. Distractive
lesions, although uncommon in the subaxial cervical spine, lack any longitudinal running
ligaments, which provide the potential for ligamentotaxis that controls reductions. Facet
dislocations have a disrupted disc complex in almost all cases. In a few cases, however, the
intervertebral disc may be herniated behind the cranial vertebral body. he disc may not reduce
when the spinal column is realigned and the disc behind the vertebral body may increase
compression on the spinal cord, resulting in neurologic deicit. his appears to be a rare condition
and almost exclusively occurs during closed reductions with patients under general anesthesia.
Most surgeons agree that cervical tong traction in awake patients using the method described
earlier is much safer. In patients with signiicant neurologic deicits, I believe that the beneit of
immediate reduction exceeds the potential for worsening due to disc herniation, and I proceed
with rapid reduction when indicated.
In patients who are intact or have mild deicits, it is usually possible to obtain an MRI scan prior
to reduction. If a traumatic disc herniation behind the body of the cranial vertebra is present,
the patient should undergo anterior discectomy and then reduction using direct vertebral
manipulation or intraoperative tong traction. If reduction is achieved, then anterior interbody
fusion with a plate is performed. If reduction is not achieved, the patient is turned prone on a
turning frame and open posterior reduction is performed. Lateral mass ixation and bone grat is
applied. The wound is closed and the patient is repositioned supine and anterior body fusion
performed with or without addition of an anterior plate.
Another contraindication to traction reduction is ankylosing spondylitis. hese are highly
unstable injuries in which the ALL and PLL are absent and thus do not provide ligamentotaxis.
Traction in these cases can lead to loss of alignment, overdistraction, and neurologic deficits.

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 DAFTAR PUSTAKA
Simeone, R, (2018) Spine Trauma in Basic Science of Spinal Cord injury : Rasouli, Alexander.
Rothamn-Simeone and Herkowitz The Spine, seventh ed. United of State. Philadelpia. Elsevier

Blom, Ashley, David Warwick, Michael RW (2018) Section 3 in Injuries of The Spine :Dunn,
Robert, Nicholas Krugger . Apley & Solomon’s System of Orthopaedics and Trauma, tenth ed.
United of State. CRC press.

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