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© 2013 Neurocritical Care Society Practice Update
Traumatic Spinal Cord Injury
William M. Coplin, MD, FCCM
St. Anthony Hospital / Centura Health
Denver, CO
CLINICAL CASE
A 73-year old man slipped while practicing Tai Chi in the park. At the scene, he was awake, had
never lost consciousness, and complained of pain in his neck. He was said to not have any
movement or sensation in his arms or his legs. His blood pressure (BP) was 148 mm
Hg/palpable, and his heart rate was 92 beats per minute (bpm). In the Emergency Department,
he was awake and breathing comfortably, and his BP was 130/75 mm Hg. Within an hour, his
BP had fallen to 100/60 mm Hg, while his heart rate remained relatively steady at 82 bpm. His
neurological examination demonstrated that he could shrug his right shoulder, and that he
barely had antigravity strength in his left biceps; he had minimal sensation on the lateral aspect
of his forearms. In the spinal cord levels below these findings, he was insensate and flaccid.
Computed tomography of the cervical spine demonstrated degenerative joint disease and
ossification of the posterior longitudinal ligament.
Magnetic resonance imaging showed increased T2 signal in the mid- cervical spinal cord.
His American Spinal Injury Association (ASIA) scale grade was B with a C5 injury level (motor
incomplete but less than anti-gravity; some sensation)
© 2013 Neurocritical Care Society Practice Update
He received a 24-hour infusion of methylprednisolone, in accordance with prevailing
management guidelines at the time. He underwent posterior surgical decompression via C4 and
C5 laminectomies in the seventh hour after injury. His post-operative care included: monitoring
with subclavian central venous and radial arterial catheters, hemodynamic augmentation with
two liters of 0.9% NaCl and a phenylephrine infusion titrated to a mean arterial pressure (MAP)
of 85-90 mm Hg, venous thromboembolism prophylaxis with sequential compression devices
on his legs and subcutaneous heparin through the first day and low molecular weight heparin
starting 24 hours after surgery. He was liberated from the ventilator the morning after surgery,
and, with assisted externally applied abdominal pressure (with a pillow) in synchrony with his
coughing efforts, he was safely extubated that morning. He started eating with assistance later
that day. He received a bowel regimen with scheduled senna tablets twice daily and a rectal
laxative suppository every other day as needed. An initially placed Foley catheter was removed
the day after surgery and he received intermittent bladder catheterization as needed. His
nurses repositioned him every two hours, and his skin was kept clean and dry. Temperature >
37.5oC was controlled with an external water-circulating gelpad device after he developed mild
fevers to 37.9oC; all cultures across the first 72 hours were unremarkable, and a first-generation
cephalosporin was discontinued in accordance with SCIP guidelines 24 hours after surgery.
Physical Medicine & Rehabilitation and physical and occupational therapy consultations were
obtained the day after admission, and he was assisted to a chair the second day after injury
with 2/5 strength below his initial spinal injury level, competent sacral innervation with nearnormal bowel and bladder function, and return of most sensation below his initial level of injury
(ASIA C). He was discharged from the ICU on post-injury day 5 to rehabilitation
OVERVIEW/EPIDEMIOLOGY
Traumatic spinal cord injury (SCI) has an incidence of about 12,000 per year in the Unites
States, according to a 2009 report from the National Spinal Cord Injury Statistics Center and
from the SCI Model Systems project of the National Institute of Disability and Rehabilitation
Research (NIDRR, part of the US Department of Education). The majority of these injuries occur
to the cervical cord, resulting in incomplete tetraparesis in about 30% and complete
tetraparesis in about 20% of all patients with SCI. As to thoracic SCI, about 25% of patients are
left completely paraparetic, and 18.5% are incompletely paraparetic. The average age at injury
has increased from 29 to 40 years, in line with ageing of the population in general. Eight in 10 of
those injured are male; this figure has remained unchanged for well over the past 30 years. The
most common mechanisms of injury are motor vehicle accidents (42.1%), falls, assaults
(including penetrating injuries, e.g., gunshot wounds), and sports-related injuries. Far more
injuries occur during the summer months and around holidays.
Survival from Spinal Cord Injury
Mean survival for patients after SCI has steadily continued to increase over the years from 52.8
months in 1955 [1] to 110.5 months by 1976 to 126 months by 1982 and is now upwards of 12
years after injury. The largest gains over this secular time period have been in survival during
© 2013 Neurocritical Care Society Practice Update
the first two years after SCI [2]. These figures do not include suicide, which remains a leading
cause of patient demise after SCI, after cardiovascular and cardiopulmonary system illnesses.
Urinary tract disease is also a leading cause of death after SCI [3]. Nearly 88% of those surviving
from the time of injury through hospital discharge return to private noninstitutional domiciles.
PATHOPHYSIOLOGY
Primary non-penetrating injury occurs primarily as a result of disc herniation, fracture, and/or
subluxation compressing upon the cord in the bony spinal canal. Complete transection of the
cord (often from missile or other penetrating injuries) is rare. The series of concomitant events
include hemorrhage into the cord, release of excitatory amino acids, accumulation of
endogenous opiates, lipid hydrolysis, free radical release, ischemia and reperfusion injury.
Inflammation, free radicals, excitotoxicity [4], and vascular disruption and ischemia ultimately
lead to necrotic and apoptotic cell death within the cord. These various components have been
the putative targets, along with edema formation, for various therapeutic trials to medically
manage secondary cord injury from these processes [5]. Pressure injury from compromise of
the spinal canal also contributes to impedance of blood flow through the single anterior artery
and paired dorsal arteries centripetally into the cord; this can lead to further oligemia and
ischemia to the already injured areas of the cord. Other causes of secondary injury to the cord,
in addition to hypoperfusion, inflammation, and edema, include, but are not limited to:
hyperthermia/fever and apoptosis. Apoptosis is a current target of clinical trials (e.g.,
minocycline), but this is currently under research and not ready for recommended clinical
practice.
CLINICAL FEATURES
Airway Issues in SCI
As with any post-traumatic assessment and resuscitation, first maintaining or secondarily
otherwise securing the airway is of primary concern. There are two issues in particular that are
peculiar to patients with traumatic SCI: preventing further cord damage from manipulating an
unstable cervical spine and that the patient may be already somatically paralyzed and
traumatized. As to the latter issue, this author cannot remember the last time he used a
depolarizing agent (i.e., succinylcholine) to intubate such patient. Nasotracheal intubation, with
proper topical mucosal anesthesia, allows the patient to remain spontaneously breathing and
receive ventilatory support. Fiberoptic intubation has an added benefit of not having to risk
moving the neck and potentially exacerbating the SCI. Short-acting sedation with a non-muscle
relaxing agent (e.g., etomidate) can be useful when these forms of awake intubation are not
practically possible. A short-acting non-depolarizing agent (i.e., rocuronium) may be preferred,
if muscle relaxation is truly needed; this would obviate the potential for excessive muscular
potassium release in a paralyzed patient who may also have sustained muscular crush injury.
There are no randomized studies of these various techniques. Manual in-line stabilization it is
recommended with the recognition that it may not always protect against cervical spine motion
© 2013 Neurocritical Care Society Practice Update
[6]. Additionally, there are concerns regarding traction causing distracting injury in patients
with ligamentous injury, so care must be taken when using in-line stabilization not to distract or
extend the neck.
Ventilatory Dysfunction In SCI
As the phrenic nerve originates from the third through fifth cervical cord level, there is
necessarily complete ventilatory paralysis with injuries above this level; if these patients are to
survive, they require immediate ventilatory support. Patients with injuries to the C3-5 area of
the cord may maintain varying degrees of ventilatory function; these patients usually require
ventilatory support at least initially, when, from the time of injury, they will have substantial
reductions in airflow and vital capacity (VC) [7]. Similarly, patients with lower cervical and high
thoracic SCI may also have reduced VC early after injury. Paralysis of the intercostal and other
non-diaphragmatic ventilatory musculature whose innervation derives from below the C5 cord
level may result from an initial period of spinal shock or from permanent injury. Loss of
strength, tone, and proprioception in these muscles compounds weakness-induced ventilatory
dysfunction by changing the shape of the thoracic cavity, furthering ventilatory inefficiency.
Similar weakness and loss of abdominal tone can hamper the effectiveness of coughing to clear
airway secretions. Patients may become relatively hypoxemic when supine, as the abdominal
contents may press on the lower lung fields, interfering with normal basal expansion. This may
produce mismatch, as the blood flow, particularly in the setting of the reduced vascular tone of
neurogenic shock, tends to follow gravity into these lower relatively less-ventilated lung fields.
When spasticity has developed, often by the middle of the second week after injury,
paradoxical abdominal ventilatory movements decrease, the thoracic cavity resumes a more
normal shape and capacity, and cough can improve [8]. With assisted pulmonary toilet and
strengthening of cervical accessory musculature of breathing, up to 80% of those with C3-5
lesions can be liberated from mechanical ventilation. Those with functioning diaphragms
(lesions below C5) infrequently need mechanical ventilatory support after the above
physiological changes finish their sequence.
Cardiovascular Changes in SCI
Most notable changes in cardiac performance are related to sympathetic denervation. Cardiac
innervation occurs above the T5 level, so below this level, cardiac manifestations of acute SCI
are rare. Electrographic changes include diffuse ST segment and T-wave depression. Also seen
are large upright T-waves with ST elevation, QT interval prolongation and prominent U-waves.
Bradycardia, from unopposed vagal innervation, may occur episodically with vagal stimulation
(e.g., oral suctioning). Occurring as a manifestation of neurogenic shock, this usually peaks
about post-injury day 4 and usually resolves within 2-6 weeks after injury [9].
Spinal Shock and Neurogenic Shock
These forms of shock are discussed elsewhere in this manuscript as well. Spinal shock is the
temporary loss of spinal cord neural function above the level of the more lasting, if not
© 2013 Neurocritical Care Society Practice Update
permanent, lesion. As such, a person may appear to neurologically have less remaining function
than will ultimately be the case. This effect may last several hours up to a few days. Neurogenic
shock is so-called “warm shock”. It is a form of distributive shock that may lead to
hypoperfusion (including the spinal cord) from associated bradycardia (from unopposed vagal
tone) and hypotension (from loss of sympathetically-mediated vascular tone/decreased
systemic vascular resistance). This is usually seen with lesions at T4 (the lowest takeoff of
cardiac sympathetic innervation) and above. The presence and severity both depend on the
spinal level affected: ubiquitous to varying severity with cervical injuries and variable with
thoracic injuries. It is uncommon with injuries in the region of the conus medullaris. Varying
degrees of neurogenic shock may last for weeks. Treatment includes maintenance of euvolemia
and substitution of α sympathetic agonists such as phenylephrine, ephedrine, or midodrine (the
latter two following the acute phase of injury) if needed. While fludrocortisone, a
mineralicorticoid, encourages fluid retention, it does not clearly benefit the clinical syndrome of
neurogenic shock.
Associated Cervical Spinal Column Injuries
The spectrum of neck and thoracic injuries associated with SCI include multiple pathologies.
Fractures can be stable or unstable. Those involving posterior elements alone (e.g., spinous
processes, lamina) tend not to be unstable. Those involving facets, pedicles, and/or vertebral
bodies have the ability to be unstable, meaning they allow abnormal movement of the spine
with the potential of entrapping the cord or nerve roots. Axial loading with about 30o of cervical
flexion can lead to fracture dislocation [10]. Compression with flexion tends to yield fracture of
the vertebral body. This can lead to “teardrop” fractures where pieces of bone may be
retropulsed into the spinal canal. These and those with vertical compression leading to a
“burst” fracture of the vertebral body can lead to angulation (> 11o) and compression of the
spinal canal. Subluxation (e.g., > 2-3 mm or antero- or retrolisthesis) and/or dislocation can
occur with such anterior spinal column or pedicle fractures or when the facets perch or “jump”
over each other and “lock” in place. Traumatic disc herniation and/or ligamentous injuries (such
as in the initial case presented in this article) can also compromise the canal and render the
spine unstable. This is not meant to be an exhaustive listing of injuries to the spinal column; the
reader is encouraged to review vertebral anatomy, if not also biomechanics, elsewhere.
Vascular injuries (e.g., dissection, pseudoaneurysm formation) may occur as a result of blunt
force to the cervical carotid artery, jugular vein, or vertebral artery; injuries to the latter may
involve fractures of or entrapment at the edges of the transverse processes of cervical
vertebrae 2-6, where the vertebral arteries travel within the foramina transversaria. Associated
stretch injuries to nerve roots and/or the brachial plexus may make difficult discerning acute
SCI versus abnormalities from those pathologies. These tend to be unilateral and affect a single
limb.
© 2013 Neurocritical Care Society Practice Update
DIAGNOSIS
Imaging Neck Injuries and “Clearing” the Cervical Spine
This article will discuss three of the many cervical spine radiographic imaging guidelines. The
National Emergency X-Radiography Utilization Study (NEXUS) criteria were designed to attempt
to identify those at low risk for cervical fracture/subluxation/dislocation [11]. The patient
should be without posterior midline cervical tenderness. Problematically, the absence of
midline cervical tenderness does not rule out cervical pathology. The patient should not be
intoxicated, should be of normal mental status, and not have any painful injuries that might
distract attention from the examiner; these criteria are to allow valid neurological examination.
Finally, the NEXUS low-risk patient should not have any focal neurological deficits. The patient
meeting these five NEXUS criteria is said to be at low risk of cervical injury and may not need
roentgenographic or other imaging of the neck or the spinal cord. These may be coupled with
the Canadian Cervical-Spine Guidelines, which are intended to identify patients who should
receive imaging [12,13]. According to these often-used guidelines, a patient should receive
imaging if he/she meets ANY of the following criteria: midline cervical tenderness, age > 65
years, “dangerous mechanism” of injury, neurological symptoms, he/she must remain supine,
had the immediate onset of neck pain, or is unable to fully rotate the neck. More recently, the
2013 Guidelines suggest an approach based on level of consciousness, ability to undergo valid
examination (as for the NEXUS criteria), the presence or absence of neurological symptoms or
other injuries [14]. Radiographic evaluation of the cervical spine is not recommended for the
awake asymptomatic patient. That is someone without neck pain or tenderness, who has a
normal neurological examination, is without other injury that may detract from accurate
evaluation, and who is able to complete full active functional range of motion. For such
patients, any cervical immobilization may be removed, and no spine imaging is recommended.
For the awake patient with any of the symptoms just mentioned, computed tomography (CT) of
the cervical spine is the recommended imaging modality. Radiographs are no longer
recommended if CT scanning is available. The traditional three views (anteroposterior, lateral,
and odontoid +/- “swimmer’s” view) are recommended only when CT is not available and are to
be supplemented with CT, when available, for any suspicious or poorly seen areas. Plain
tomograms were often used to obtain odontoid views; however, the equipment to even
perform this study has become obsolete and is increasingly difficult to find. If the imaging is
normal, the neck should be immobilized (i.e., properly-fitting hard cervical collar in neutral
position) until the patient is without symptoms. The collar may be removed after adequate and
normal dynamic flexion and extension radiographs or a normal MRI obtained within 48 hours of
injury. If the patient is obtunded or unevaluable (e.g., painful other injury distracting from
adequate neurological examination or intoxicated) then the same initial CT imaging paradigm is
recommended. Further evaluation should be by return of consciousness with absence of
symptoms or by the same MRI paradigm. In unevaluable patients, flexion/extension films
appear to be of marginal benefit and are not recommended to clear the cervical spine.
© 2013 Neurocritical Care Society Practice Update
ASIA Impairment Scale
The American Spinal Injury Association (ASIA) has published a standardized ordinal impairment
scale for communicating the functional severity of SCI. The scale and useful bedside diagrams
and charts for dermatomes and functional muscle groups by spinal level are available online at
www.asia-spinalinjury.org.
 ASIA A: Complete injury: no motor or sensory function preserved in sacral segments S4-S5
 ASIA B: Incomplete injury: sensory but NOT motor function preserved below neurological
level and includes sacral segments (“motor complete”)
 ASIA C: Incomplete: motor function preserved below neurological level and > ½ of key
muscles below neurological level have muscle grade <3 (“motor useless”)
 ASIA D: Incomplete: motor function preserved w/ muscle grade > 3 (“motor useful”)
 ASIA E: Normal function
The scale has predictive ability as to the chances of regaining functional status [15]. About 25%
of injuries present appearing complete (ASIA A); of these, up to 90% will not regain function,
but as many as 15% will improve, with 3% regaining useful motor function. About 15% of
patients present motor complete with some preserved sensory function (ASIA B); of these, 54%
will regain motor function. About 40% of patients present with incomplete motor loss (ASIA CD); of these, 86% will regain the ability to ambulate. These odds may now be improved (see
section on Early Surgery below).
SCI Syndromes
The reader is reminded to elsewhere review “classic” syndromes of the spinal cord. These may
occur in the setting of trauma or traumatic SCI may mimic any of these and/or other named
syndromes of the spinal cord:
– Transverse myelopathy
– Central cord syndrome –so-called “man in a barrel” presentation of arms affected > legs.
This syndrome most frequently occurs among older persons with cervical spondylosis;
however, it also may occur in younger individuals. It is the most common form of
incomplete SCI, representing about 9% of SCI. Prognosis is generally good to obtain at least
some functional recovery; however, persons > 70-years old, those with complicating preexisting comorbidities, and/or severe other injuries may not recover well.
– Anterior spinal artery syndrome – motor affected with preservation of proprioception;
associated with hyperflexion injuries and/or cord contusion from extruded disc material or
retropulsed bone
– Brown-Sequard syndrome – lateral hemi-cord, ipsilateral motor, contralateral sensory’ most
commonly seen with penetrating SCI
– Posterior cord syndrome – proprioception affected >> motor
– Transient quadriparesis – may be mistaken for or represent a form of spinal shock
© 2013 Neurocritical Care Society Practice Update
TREATMENT
Management of patients with acute traumatic SCI, particularly those with cervical injuries, is
recommended to take place in a setting with cardiopulmonary monitoring. The three major
areas of therapy include surgery, pharmacological therapy (e.g., corticosteroids), and critical
care issues, the latter of which include, but are not limited to, airway management and
ventilation, hemodynamics, venous thromboembolism prophylaxis, prevention and treatment
of complications, and fever control, specifically as they apply to the management of this specific
patient population. The reader is encouraged to review the consensus guidelines for managing
acute cervical spine and spinal cord injuries, updated in 2013 [16].
Airway Management
Much of this topic, as particularly it relates to SCI, has been discussed in previously. The key
points are: Remember to avoid hyperextension, rotation, or other movement of the neck
during intubation. Awake, fiberoptic intubation is preferred; in-line stabilization without
traction is an alternative when a fiberoptic laryngoscope or bronchoscope is unavailable. A
spinal level above C5 will almost necessarily mean diaphragmatic compromise. Those with a C5C8 level often, but not always, will need some degree of acute mechanical ventilatory support.
Hemodynamics
Neurogenic shock is an anatomical possibility for any lesion above the final takeoff for the
cardiac sympathetics (T1-T4). Some degree of the anatomical functional sympathectomy is
nearly ubiquitous in traumatic cervical SCI. This may render the heart unable to increase cardiac
output by increasing its rate and/or stroke volume and leaves peripheral arteries unable to
tense except by hormonal means; these effects may lead to hypotension. The resulting effect
may be hypoperfusion of smaller downstream arterioles and capillaries in the watershed
regions of the spinal cord, thus exacerbating secondary vascular injury to the cord. The
minimum systolic BP to tolerate is said to be 90 mm Hg; this is derived from the general shock
literature. The recommendation is to maintain mean arterial pressure (MAP) 85-90 mm Hg for
the first seven days after SCI [17]. The duration is loosely based on the time until scar begins to
form at the site of injury, and, presumably, damage from the initial injury has completed its
course and secondary vascular injury should become moot. There are at least six case series
with historical controls, yielding class III evidence of the potential clinical effectiveness of this
practice [18]. Given the level of evidence, this author finds it hard to fret over the seven days’
duration of such therapy, and this author with titrate patients from phenylephrine infusions if
there is nothing else about the patient’s care that is keeping the patient in the ICU
environment. While, to some, this MAP goal may seem high (vs. the goal minimum MAP of 6570 mm Hg for non-neurogenic shock), the person with a BP of 120/80 mm Hg has a MAP of 93
mm Hg. Care must be taken regarding venous pooling of administered IV fluids, as sympathetic
and muscular tone is decreased. As such, after the first couple of liters of saline resuscitation
(as per the initial resuscitation of the injured patient in Advanced Trauma Life Support), one
should then consider exogenous administration of α agonists, such as phenylephrine, to
© 2013 Neurocritical Care Society Practice Update
chemically substitute for the missing sympathetic input on the vessels. Such volume and
algorithmic paradigm is intended as an example here; obtaining euvolemia (as directed by
standard endpoints (e.g., urine output, lactate clearance) should be the usual goals of initial
resuscitation. If some β agonism is also needed or cardiac output falls in the face of pure α
agonism from the increased afterload on the heart, one can use norepinephrine. Dopamine, in
this situation, tends to produce more tachycardia than the increase in BP seen with its use.
Vasopressin infusion is another secondary consideration, as are cardiac inotropes (e.g.,
dobutamine, milrinone, inamrinone); however, these latter drugs may also decrease afterload
while increasing cardiac output, and the net result may be a fall in BP. Careful, if not continuous
BP monitoring (e.g., arterial catheter) is required when using these drugs. It is also important to
remember that the now unopposed parasympathetic tone may lead to reflex bradycardia,
particularly with vagally stimulating maneuvers (e.g., oral or endotracheal suctioning); IV
atropine pretreatment or rescue treatment may be useful in symptomatic situations related to
this.
Venous Thromboembolism Prophylaxis
Patients with para- or tetraparesis after SCI represent a group with among the highest acute
risk of VTE among hospitalized patients, with unprotected patients running upwards from a
40% risk of developing VTE. Current recommendations are for the use of prophylaxis acutely for
anyone with motor deficits, especially severe ones preventing ambulation. Low molecular
weight heparins (LMWH), rotating beds, or a combination are recommended [19]. Alternatively,
low dose subcutaneous heparin (e.g., 500 units q8 hr) in combination with pneumatic
compression stocking devices is also recommended. This should begin within 72 hours of injury,
according to available guidelines. The timing to commence VTE chemoprophylaxis is dependent
upon several factors. First, there is a dearth of data regarding beginning therapy in the first day
or so after injury. Arguably, this is because of discomfort in conducting randomized trials of
heparin or LMWH in the first day or two after injury. There are observational data that
beginning chemoprophylaxis after the first day appears safe vis-à-vis hemorrhage risk. One
possible exception is the administration of LMWH within 24 hours of spinal surgery (e.g.,
decompression, fixation) or other procedures (e.g., lumbar puncture or drains) that may violate
the dura. There is a warning that LMWH may increase the chances of local bleeding in such
procedures within this time frame; no such warning exists for the use of low-dose
subcutaneous heparin plus SCDs in this clinical scenario, where the use of such appears safe
and effective. Some have in the past used oral anticoagulation alone (e.g., warfarin,
anisindione) in fixed low doses; this practice is not recommended. Also not recommended as
routine prophylaxis are inferior vena caval filters (e.g., Greenfield). Filters do nothing to prevent
lower body deep venous thrombosis, and smaller emboli can still travel through or from the
filter to the lungs via the right heart. The filters themselves may dislodge and embolize to the
right heart. Patients may develop inferior vena caval obstruction from clot suspended in the
filter preventing blood flow through the filter and are associated with an increase risk of DVT
formation. Such filters are recommended for select patients who either fail anticoagulants (e.g.,
allergic reaction) or are not candidates for LMWH (e.g., ongoing bleeding). The recommended
duration of primary prophylaxis is three months.
© 2013 Neurocritical Care Society Practice Update
Pharmacotherapy for SCI
Several drugs have been shown NOT to improve patients’ neurological function after SCI. These
include naloxone, GM-1 ganglioside, and 21-aminosteroids. Perhaps the most studied, storied,
and controversial issue in SCI care is that of corticosteroids. There have been several
randomized trials of their use for SCI; the most “famous” and controversial of these were the
National Acute Spinal Cord Injury Study II and III [20,21]. These studies used
methylprednisolone, desiring action as a membrane stabilizer; the tirilazad studies suggest that
there is not a substantial anti-edema effect. Time to administration appears to be key for any
effect seen in these studies, with a maximum studied time window of 8 hours. Dosing regimens
were derived from weight-based animal studies: 30 mg/kg IV over the first hour and 5.4 mg/kg
IV over the following 23-47 hours. While the 2002 Guidelines left methylprednisolone infusion
as an option for administration [18], the most recent 2013 Guidelines do not recommend its
use [16]. There is criticism of the studies regarding the time criteria, the question of injury
severity and its relation to treatment efficacy, whether unilateral motor measurements are
clinically meaningful (no functional outcome measures), and questions as to the standardization
of concurrent treatments. Many of these perceived limitations are differences on clinical trials
methodology of the time. Cited are concerns over complications without clear evidence, to
those authors, of benefit. Modern neurocritical care may well obviate some, if not many, of the
previous concerns over the real, but now better understood possible clinical complication of
methylprednisolone use. The reader is encouraged to seek the source documents and reach
her/his own conclusions for everyday clinical practice.
Early Surgery
One must achieve emergent reduction of unstable fractures, dislocations, or subluxations,
particularly in the patient with any neurological symptoms. For closed reduction, one must take
care to not overly distract the injured area with traction lest ligamentous injury or laxity allow
further distracting injury. The reader is encouraged to read elsewhere regarding closed
reduction under roentgenographic guidance (i.e., “traction”), indications for non-operative
bracing (i.e., “halo” or hard cervical collar), and indications for surgery. Unstable
fractures/subluxations/dislocations most commonly go to open reduction and internal fixation.
The Surgical Timing in Acute Spinal Cord Injury Study (STASCIS) was completed and published in
the past year [22]. In short, the study suggested benefit to early (< 24 hours after ictus vs. later)
decompressive surgery for symptomatic cervical SCI, when decompression of the canal was
indicated (e.g., traumatic disc rupture, fracture/subluxation, etc). With this approach, the odds
of improving at least two grades on the ASIA scale (e.g., ASIA B  D or E) were more than
doubled (OR 2.83, 95% CI 1.10-7.28, P = 0.03). Complications were similar between the two
study groups.
© 2013 Neurocritical Care Society Practice Update
Therapeutic Hypothermia
In laboratory investigations, no treatment appears quite as promising as therapeutic
hypothermia. The current issue remains translating this putative success into an approved
human clinical therapy. The issue began to receive copious public interest after the case of
football player whose recovery was widely credited to therapeutic hypothermia. He was said to
be complete (ASIA A) below the clavicles. Of note, he received methylprednisolone infusion in
the ambulance as well as IV chilled saline and ice packs to the groin. IN the ED, he was
hemodynamically stable with a temperature of 36.6oC. His C3-4 facet dislocation was
operatively reduced about three hours after injury. The following day, he was cooled for several
days at 33oC, recovering strength about 15 hours post-injury [23]. Was this the effect of
hypothermia, or of the combination of steroids and early open reduction with adjunctive
hypothermia? Such is the potential confounding where steroids and other aspects of care have
varied in the setting of varied hypothermia protocols. While there is cogent biological rationale
for therapeutic hypothermia after SCI, for now, its use is considered experimental. Concerns
include that animal studies have not revealed consistent benefit to either systemic or local (e.g.,
bathing the spinal canal contents in chilled saline such as at the time of operation) hypothermia
and that there are insufficient existing human data in the clinical scenario [24]. A proposed
study is under revised submission to the NIH to test the hypothesis that three days at 33oC is
beneficial after SCI.
Other Recovery Strategies Under Investigation




Stem cells
Axonal bridging across scar
Rehabilitation strategies – e.g., microarray electrical stimulation
Biomedical assistive and restorative devices
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© 2013 Neurocritical Care Society Practice Update
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traumatic spinal cord injury. J Neurosurg Anesthesiol. 2003;15:215-29.
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Spine and Spinal Cord Injuries. Neurosurgery. 2013;72:1-259.
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Spinal Cord Injury. J Neurotrauma. 2011;28:1479-14-95.
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Spine and Spinal Cord Injuries. Clin Neurosurg. 2002;49:407-98.
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Patients With Cervical Spinal Cord Injuries. Neurosurgery. 2013;72:244-54.
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© 2013 Neurocritical Care Society Practice Update
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© 2013 Neurocritical Care Society Practice Update
TRAUMATIC SPINAL CORD INJURY QUESTIONS
1. Some have suggested worse outcomes for patients with SCI who receive endotracheal
intubation. What is a speculated cause?
a) Traction during in-line stabilization distracting unstable fractures or subluxations
b) Episodic hyperventilation/hypoventilation
c) Intubating delays surgical decompression
d) latrogenic pneumothorax
2. Spinal cord injury above T5 may result in what type of hemodynamic shock?
a) Cardiogenic
b) Spinal
c) Obstructive
d) Neurogenic
3. Resuscitation after SCI includes all of the following concepts EXCEPT:
a) Patients should receive fluids liberally until blood pressure normalizes
b) Infusion of an alpha agonist may be necessary soon after initial volume
resuscitation
c) Follow usual ATLS resuscitation parameters re: plasma and red blood cell
infusion
d) Saline is initially limited up to a couple of liters
e) Resuscitation may continue to an MAP of 85-90 mmHg
4. Which one of the following is NOT an acceptable associated condition when clearing the
cervical spine?
a) Alert and oriented
b) Normal neurological examination
c) Absence of neck pain
d) Extremity fracture
e) No alcohol on board
5. Central cervical SCI has the following characteristics:
a) Motor deficits usually affect the legs more than the arms
b) Absence of increased T2 MRI signal is a poor predictor of recovery
c) Most patients recover some neurological function below the level of the injury
d) It occurs commonly in persons less than 50 years of age
6. The most common organ injured in transabdominal gunshot wounds to the spine is:
a) Small bowel
b) Colon
c) Liver
d) Abdominal vascular structures
© 2013 Neurocritical Care Society Practice Update
7. A 41-year-old man is brought in after a car accident. He was wearing a seat belt. He is said
to be weak in all extremities, and his blood pressure is unstable with an unwavering heart
rate. He has jumped cervical facets. He is taken to the OR for an emergency open reduction
and internal fixation. Which of the following statements is true?
a) Reduction of his subluxation should be performed as soon as possible
b) Surgical stabilization of the cervical spine should be deferred until after 24 hours
c) There is little need to evaluate for cervical vascular injuries
d) Detailed neurological examination can be deferred until after reducing his facets
e) A hard cervical collar alone is sufficient until the time of surgical reduction
8. In the 2013 Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries
[16], all are correct EXCEPT:
a) Augmenting BP to an MAP of 85-90 mm Hg is considered an option
b) Prophylactic hypothermia is considered experimental
c) The majority of patients are managed non-operatively
d) Steroids are considered a necessary part of medical management
9. Notorious for being missed:
a) Fracture-subluxation on CT scan of the cervical spine
b) Spinal cord injury
c) Associated carotid-vertebral injuries
d) Ligamentous injuries
e) All of the above
10. Spinal shock is characterized by the following parameter:
a) Permanent neurological deficit below the level of radiographic SCI
b) Unstable blood pressure
c) Recovery of initially non-functioning spinal levels below the level of apparent
functional loss
d) Bradycardia with vagal stimulation
© 2013 Neurocritical Care Society Practice Update
TRAUMATIC SPINAL CORD INJURY ANSWERS
1. The correct answer is A. Endotracheal intubation has been associated with worse outcomes
in patients with SCI. Inadvertent traction on or hyperextension of an unstable spine during
attempted in-line stabilization have been incriminated as causes for the observed worse
outcomes. Only highly skilled personnel should perform intubation by direct laryngoscopy in
patients with possible cervical spine injury, using in-line traction without distracting
traction.
2. The correct answer is D. Cervical and upper thoracic spinal cord injury may result in
neurogenic shock, a distributive type of hemodynamic shock. There is loss of sympathetic
tone resulting in vasomotor paralysis and unopposed vagal tone.
3. The correct answer is A. During initial resuscitation after SCI, saline infusion is limited, as
excessive fluids, in the face of loss of vasomotor tone, may lead to venous pooling.
Completion of resuscitation, especially in the face of neurogenic shock may well require
infusion of alpha agonists after a couple of liters of saline. A MAP of 85-90 mmHg is the
target option, in theory, to facilitate perfusion of the centripetal smaller arterial branches of
the spinal cord.
4. The correct answer is D. Extremity fracture can be a source of severe pain and distress for
the patient, potentially distracting him from examination. The patient must meet all the
other listed criteria and not have any suspected brain injury.
5. The correct answer is C. Prognosis for traumatic central cord injury varies, but most people
have some recovery of neurological function. Evaluation of abnormal signals on MRI images
can help predict the likelihood that neurological recovery may occur. The syndrome is seen
most commonly in persons over age 50. The syndrome produces the classical “man in a
barrel”, with the arms being affected usually more so than are the legs.
6. The correct answer is A. The small bowel occupies the most space and thus is most liable to
injury after transabdominal gunshot wounds to the spine. Colon, liver and vascular
structures are descendingly less common.
© 2013 Neurocritical Care Society Practice Update
7. The correct answer is A. The patient has neurogenic shock, indicating at least some degree
of either cervical SCI or extramedullary sympathetic dysfunction. This is an unstable spine
dislocation that may be associated with ligamentous injury and/or facet fracture. It should
be reduced as soon as possible with roentgenographic guidance to avoid over-distraction,
should the longitudinal or other ligaments be incompetent. The STASCIS study suggests that
stabilization of the spine within the first 24 hours after injury may well improve outcome
versus waiting beyond that time period. Cervical carotid-vertebral injuries may occur in
association with such severe forceful “whiplash” mechanism of injury. A cervical collar
alone, without reduction of the facets, is unacceptable. Complete neurological examination
should be undertaken bother before and after reduction to ensure the procedure has not
caused further injury.
8. The correct answer is D. Majority of cervical spine injuries are managed non-operatively.
The Guidelines now recommend against giving methylprednisolone infusions.
9. The correct answer is E. About 5% of cervical fractures are missed, and about 2/3 of these
patients have further spinal-cord damage as a result. About 30% of cases of delayed
diagnosis of cervical spine injury develop permanent neurological deficits. Ligamentous
injuries may be missed where the facets may have perched or jumped, and then have fallen
back into place after the distracting injury. In the absence of suspicion and adequate
neurological examination, that the patient has suffered associated carotid-vertebral injury
or SCI may be overlooked [25].
10. The correct answer is C. Spinal shock is characterized by return of function to spinal levels
below the permanent injury. Answers B and D are features of neurogenic shock.