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Acute Traumatic Spinal Cord Injury 2021
Acute Traumatic Spinal Cord Injury 2021
Injury
a,b c b,
Ilyas Eli, MD , David P. Lerner, MD , Zoher Ghogawala, MD *
KEYWORDS
Spinal cord injury Apoptosis Corticosteroids Mean arterial pressure
Quantitative magnetic resonance imaging
KEY POINTS
Traumatic spinal cord injury is a common occurrence throughout the world with significant
morbidity, including permanent disability from motor, sensory, and autonomic
dysfunction.
Hyperacute management of suspected or confirmed spinal cord injury includes maintain-
ing airway, breathing, and circulation with special consideration for early airway stabiliza-
tion via intubation while maintaining spinal precautions. Further management involves
avoidance of hypotension and external spinal stabilization with cervical collar and back-
board as appropriate.
Computed tomography scan and MRI are necessary to assess the extent of bony, liga-
mentous, and spinal cord injury to assist with surgical planning.
Intensive care unit management with close monitoring of airway and blood pressure with
vigilant monitoring for complications, including bowel and bladder dysfunction, pressure
ulceration, and infection, is required.
INTRODUCTION
Acute traumatic spinal cord injury (SCI) is typically associated with devastating out-
comes. The injury to the spinal cord results in damage to motor, sensory, and auto-
nomic functions of the spinal cord but also takes a toll on a patient’s well-being,
including their physical and psychological state.
The literature provides many descriptions of the pathophysiology and management
of acute SCI, yet there continue to be controversies regarding the overall manage-
ment. Numerous guidelines have been published, by the American Association of
Neurological Surgeons/Congress of Neurological Surgeons (AANS/CNS) in 2002
and 2013, The Paralyzed Veterans of America in 2008, and AO Spine in 2017, which
provide sufficient framework to reference in the management of SCI.1–5 This review
a
Department of Neurosurgery, Clinical Neurosciences Center, University of Utah, Salt Lake City,
UT, USA; b Department of Neurosurgery, Lahey Hospital and Medical Center, Burlington, MA,
USA; c Department of Neurology, Lahey Hospital and Medical Center, Burlington, MA, USA
* Corresponding author. Department of Neurosurgery, Lahey Hospital and Medical Center, 41
Mall Road, Burlington, MA 01805.
E-mail address: zoher.ghogawala@lahey.org
EPIDEMIOLOGY
The incidence of SCI in the United States is 54 cases per 1 million people, resulting in
approximately 17,810 new cases per year.6–8 Worldwide incidence ranges from 10.4
to 83 cases per million persons per year.9,10 SCI results in major morbidity and mor-
tality and is associated with lifetime health care costs ranging from $1.1 to $5.4 million
and innumerable costs to the community and society.11 SCI typically affects men
more often than women, with 78% of new cases being in male individuals.12 The
average age of patients at the time of injury is approximately 43 years, but there is a
bimodal distribution with a peak in adolescents/young adults and a second peak in
the elderly population (older than 65 years of age).13 Motor vehicle accidents account
for 38.6% of SCIs, whereas falls account for 32.2% of cases, violent activity (eg, gun-
shots) accounts for 14.0%, sports-related activity accounts for 7.8%, surgery ac-
counts for 4.2%, and 3.2% accounts for all other causes (Fig. 1).11
and reflexes in the hyperacute setting of SCI. The immediate phase is also associated
with cellular necrosis owing to the mechanical injury to cell membranes and microhe-
morrhages owing to the vascular injury.19,20
The acute phase occurs from 2 hours to 2 weeks after injury. The early acute phase
(2–48 hours) comprises increasing inflammation, edema, and hemorrhage. Acute
phase injuries are caused by free-radical generation, ionic dysregulation, excitotoxic-
ity (owing to glutamate-mediated pathways), immune-related neurotoxicity, and
further vascular disruption that all result in progression of axonal injury and cellular ne-
crosis.21–26 The subacute phase, which occurs from approximately day 2 to 2 weeks
after injury, refers to the phagocytic response to clear cellular debris and initiate early
axonal growth. During this phase, damaged astrocytes undergo cellular edema and
necrosis, whereas astrocytes on the periphery of the injured tissue proliferate and
function to reestablish ionic hemostasis and the blood-brain barrier and to restrict im-
mune cell inflow. A deleterious consequence of astrocytic proliferation is scar forma-
tion, which prevents axonal regeneration because the scar functions as a physical and
chemical barrier.16,27,28
The intermediate phase occurs after week 2, lasts up to 6 months, and includes
continual maturation of the astrocytic scar and the beginning of axonal sprouting.29
The chronic phase starts at 6 months after injury and continues through the lifetime
of the patient. During the chronic phase, there are further scar maturation and the for-
mation of syrinxes. The process of Wallerian degeneration persists and requires
several years for the injured axons to be fully eliminated.30 Furthermore, maturation
of the lesion is evidenced by the presence of myelomalacia and cystic cavitations.21,31
Potential therapeutic interventions target these primary and secondary phases to opti-
mize recovery and spinal cord regeneration.
MANAGEMENT
Hyperacute Management
Initial management of patients with SCI is started at the scene of the injury. Nearly 25%
of SCI cooccurs with brain, chest/abdomen, or major extremity injury.32 As with all
medical emergencies, the first evaluation focuses on ABCs (airway, breathing, and cir-
culation) and then comprehensive emergency management of the injured patient as
indicated by Advanced Traumatic Life Support guidelines. Patients with the following
should be considered for spinal immobilization33:
Blunt trauma
Spinal tenderness or pain
Patients with an altered level of consciousness
Neurologic deficits
Obvious anatomic deformity of the spine
High-energy trauma
Presence of a distracting injury or intoxication from drugs or alcohol
Patients with suspected fractures of the thoracic and lumbar regions should un-
dergo thoracolumbar precautions and immobilization using a backboard and logroll
techniques for turning and transfers.34
Patients with SCI benefit from being transferred directly to a level 1 trauma center
equipped with specialized physicians (emergency medicine, trauma surgeons, neuro-
radiologists, neurosurgeons, spine surgeons, and intensivists), nurses with experience
and skill in managing acute SCI patients, and imaging (computed tomography [CT]
and MRI) capabilities that allow for immediate evaluation. Early transfer of SCI patients
474 Eli et al
to specialized SCI centers has been proven to yield improved patient outcomes.35 The
mode of transport to higher-level care centers, either by ground or by air, has not been
shown to produce a difference in outcomes.36
On arrival to an emergency department, the primary survey requires focused atten-
tion and stabilization of ABCs. Next, a rapid neurologic examination should be per-
formed, consisting of a Glasgow Coma Scale assessment with attention to
movement of all 4 extremities, as well as pupil size and reactivity. In the secondary sur-
vey for suspected SCI, the entire spinal column and paravertebral musculature should
be examined for deformity and focal tenderness, and a neurologic examination as
detailed in later discussion should occur. During this assessment, cervical and thora-
columbar spine precautions should be maintained.
Airway/Breathing
Patients with suspected or confirmed cervical SCI require close respiratory moni-
toring. Patients with injury rostral to C5 are more likely to require intubation and venti-
lator support.1 Patients in respiratory distress should undergo immediate controlled
intubation while cervical spine precautions are taken. Exaggerated bradycardia can
occur during intubation because of an abnormal, unopposed parasympathetic
response to tracheal stimulation during suctioning and endotracheal tube insertion.37
Subjective complaint of dyspnea should be taken seriously because early neuromus-
cular respiratory failure results in hypoventilation with normal oxygen saturation. For
patients able to participate in examination, bedside assessment with a single breath
count test can provide an indirect evaluation of forced vital capacity, and a value
less than 12 is concerning for imminent respiratory failure.38 As noted above, the tem-
poral progression of SCI can result in worsening spinal cord edema and perfusion,
which may worsen respiratory status in a delayed fashion.39 Focus should then be
directed toward hemodynamic monitoring. Resuscitation is initiated with the goal of
preventing hypotension, which can occur with blood loss and neurogenic shock.
Circulation
As noted above, polytrauma is common with SCI. Shock may be present and is of
particular concern in patients with SCI because periods of hypotension can worsen
neurologic outcome.40,41 Hemorrhagic, cardiogenic, and restrictive shock should all
be considered in trauma patients, but neurogenic shock can also develop in those
with SCI above the T4 level.42 Neurogenic shock results from effective sympathec-
tomy and unopposed parasympathetic activity, which manifests as hypotension and
bradycardia.43 Bradycardia is a characteristic finding in neurogenic shock and should
raise suspicion, although its presence is not invariable. Initial management includes
fluid resuscitation followed rapidly by vasopressor or inotrope addition.44 Vasopressor
and inotropes are discussed in more detail later.
Disability
A full clinical examination should be performed to determine the level of SCI using the
American Spinal Injury Association (ASIA) International Standards for Neurological
Classification of SCI.45 The ASIA injury score involves a detailed examination of motor
and sensory functions, including rectal sensation, which provides the best description
of a person’s neurologic status after injury (Fig. 2).46 The strength score is based on
the MRC (Medical Research Council) scale of 0 to 5 for motor strength in all 20 muscle
groups in the entire body. Sensation assessment is based on whether it is absent (0
points), altered (1 point), normal (2 points), or untestable. The ASIA scale also records
the degree of injury (complete or incomplete) on a 5-element scale (Table 1). Practi-
tioners should be aware that the ASIA scale can be inaccurate in the hyperacute
Traumatic Spinal Cord Injury 475
Fig. 2. ASIA classification of SCI. (ª 2020 American Spinal Injury Association. Reprinted with
permission.)
setting because of “spinal shock.” The overall identification of baseline functional abil-
ities and impairments is essential in determining recovery, prognostication, and eligi-
bility for clinical trials.34
Imaging plays an essential role in the diagnosis and guidance of management in SCI.
Early imaging allows for the identification of the structural injury to the spinal column,
which will determine surgical and nonsurgical treatment. The injury can then be clas-
sified using the AO Spine thoracolumbar or subaxial cervical spine injury classification
systems or the thoracolumbar injury classification system (TLICS).47–49 The TLICS
classification system is based on 3 categories: morphology of injury, integrity of the
Table 1
American spinal injury association scale
posterior ligamentous complex, and neurologic status (Table 2).50 The total sum of
points based on severity in each category determines whether the patient is likely or
not to benefit from surgical intervention. CT scans provide a clear radiographic image
of the bony destruction to the spinal column (Fig. 3). CT serves as an initial imaging
modality, as it is fast and reliable. Subsequently, MRI provides further understanding
of the injury, which may or may not involve the disc space and ligaments and can show
whether an epidural or subdural hematoma exists (Fig. 4).
SURGICAL MANAGEMENT
Table 2
Thoracolumbar injury classification and severity score system
Point
Injury Category Value
Injury morphology
Compression 1
Burst 2
Translation or rotation 3
Distraction 4
Posterior ligamentous complex status
Intact 0
Injury suspected or indeterminate 2
Injured 3
Neurologic status
Intact 0
Nerve root involvement 2
Spinal cord or conus medullaris injury
Incomplete 3
Complete 2
Cauda equina syndrome 3
Fig. 3. CT scan demonstrating the bony destruction in a T6-T7 fracture dislocation injury.
478 Eli et al
least 2 AIS grades in 5.5% of patients in the early group and 10% in the late group
(P 5 .017). A meta-analysis of 18 studies from 1996 to 2012 demonstrated that early
surgery was associated with a higher total motor score improvement in 7 studies,
neurologic improvement in 6 studies, and shorter hospital length of stay in 6 studies.
The studies pooled in the meta-analysis were heterogeneous in nature, and the
studies were concerning for publication biases.53 A Canadian multicenter cohort
study54 looked at 84 patients with cervical, thoracic, or lumbar SCI who underwent
either early, defined as less than 24 hours from injury (35 patients), or late (49 patients)
Traumatic Spinal Cord Injury 479
surgery. The results showed that a greater portion of patients who underwent early
surgery had at least a 2-grade AIS improvement (P 5 .01).
Many of the studies evaluating the timing of surgical decompression demonstrate
benefit from early decompressive surgery, despite the criticisms of the biases and
study designs. Further studies, such as the multicenter prospective, observational Eu-
ropean study (SCI-POEM), are currently in process. On the basis of existing data, the
AO Spine guidelines currently suggest early decompressive surgery when possible.55
MEDICAL MANAGEMENT
Role of Corticosteroids
The use of steroids remains controversial in the treatment of acute SCI. Initial interest
in the use of steroids was based on a rationale of augmenting anti-inflammatory mech-
anisms and thus promoting cell survival by limiting inflammation-mediated secondary
injury. Although early data suggested a benefit for steroid administration, multiple sub-
sequent studies investigating the role of steroids have found no benefit for their
use.56–58 The National Acute Spinal Cord Injury Study investigated the role of very-
high-dose methylprednisolone (bolus of methylprednisolone 30 mg/kg followed by
an infusion of 5.4 mg/kg/h for 48 hours) in acute SCI. It showed no improvement of out-
comes as assessed by its primary endpoints among patients treated with steroids.
Secondary subgroup analysis showed significant motor recovery in patients who
received methylprednisolone within 8 hours of injury, but the study also demonstrated
the major adverse effects of high-dose steroids.42 In the study, 48-hour administration
of high-dose steroids resulted in increased risk of pneumonia and sepsis, whereas
lower complication rates were observed with a shorter (24-hour) course of high-
dose steroids.56–58 A Cochrane Review analyzing 6 studies of methylprednisolone in
acute SCI found an overall 4-point increase in ASIA motor score when steroids
were administered within 8 hours of injury.59 The AANS/CNS guidelines from 2013
do not recommend the use of methylprednisolone for the treatment of SCI.60 The ratio-
nale for this exclusion was the lack of level I and II evidence in support of the treatment
and the presence of level III evidence that demonstrated possible deleterious effects.
However, the AO Spine guidelines from 2017 state that high-dose methylprednisolone
given intravenously for 24 hours should be offered within 8 hours of SCI in patients
without medical contraindications.2 Thus, the role of steroids in acute SCI remains
controversial, with no level I or II evidence to suggest its benefit.
evidence. The duration of MAP augmentation is variable in practice and ranges from
5 days to 7 days after injury.64 The current AANS/CNS guidelines recommend main-
taining MAP goals for 7 days.5 The recommendation is based on study protocols
from studies in the 1990s based on animal study results measuring spinal cord
swelling at 5 days after injury.62,65 Other studies have MAP goal duration up to
7 days, but no randomized studies exist to compare different MAP goal duration
with outcomes. Studies whereby MAP goals were augmented for 5 days only after
SCI did not show any decline in neurologic findings.66–69
Close blood pressure monitoring and augmentation require the placement of an
arterial line, and previously used pulmonary artery catheterization for cardiac output
optimization in the intensive care unit setting.61,62 Pulmonary artery catheterization
is less common than previously practiced, and only those with training and practice
should use the invasive monitoring. Because the MAP goal of greater than 85 mm
Hg may be greater than an individual’s baseline blood pressure, augmentation with va-
sopressors may be required. The AANS/CNS guidelines do not have recommenda-
tions on preferred vasopressor or inotrope, but the Consortium for Spinal Cord
Medicine recommends the use of norepinephrine and dopamine for SCI in the cervical
and upper thoracic regions.1,55 These medications have both alpha-adrenergic and
beta-adrenergic effects, which counter the potential neurogenic shock associated
with these levels of SCI. For lower thoracic SCI whereby the mechanism of hypoten-
sion is due to vasodilation, phenylephrine, a purely alpha-agonist, is recommended.
Although use of vasopressors can help achieve MAP goals and improve spinal cord
perfusion, there are risks (Table 3). Dopamine has been associated with a 10% major
complication rate compared with a 3% major complication rate with the use of phen-
ylephrine. The major complications include ST segment elevation, elevated troponins,
atrial fibrillation, and ventricular tachycardia.68 Dobutamine is not used because of
vasodilatation and reflex bradycardia. Epinephrine is also not used, as it can result
in arrhythmias.68 Norepinephrine has been commonly used for blood pressure
Table 3
Commonly used vasopressors/inotropes physiologic response and complications
Mean Systemic
Arterial Heart Cardiac Vascular
Medication Pressure Rate Output Resistance Activity Complications
Norepinephrine Increase Increase Increase Increase A>b Arrhythmia; peripheral
ischemia
Phenylephrine Increase Decrease Decrease Increase a Reflex bradycardia;
peripheral ischemia
Epinephrine Increase Increase Increase Increase a>b Tachyarrhythmia; stress
cardiomyopathy/
cardiac ischemia
Dopamine Increase Increase Increase Increase a5b Low dose can cause
hypotension;
tachyarrhythmias;
tissue ischemia
Dobutamine Similar Increase Increase Decrease b>a Tachyarrhythmias;
cardiac ischemia
Milrinone Similar Increase Increase Decrease cAMP > Vasodilation; can
inotropic decrease blood
pressure
augmentation because of its mixed alpha and beta effects, which decreases vasocon-
striction and bradycardias. One study showed that administration of norepinephrine in
SCI increased spinal cord blood flow and PaO2 compared with phenylephrine.70 Over-
all, optimal medication for blood pressure augmentation depends on the level of injury
and patient risk factors (namely underlying cardiac function), but close monitoring of
hemodynamics and potential complications is necessary regardless of choice.
LATEST THERAPIES
Quantitative MRI
MRI is a critical diagnostic tool used to understand the extent of injury in the setting of
SCI. Emerging advances in MRI modalities serve to improve the understanding of SCI.
Quantitative MRI techniques, such as magnetization transfer, magnetic resonance
relaxation mapping, and diffusion imaging, all have the utility of evaluating the micro-
structural neural features, which allows for a better understanding of the myelination
status and axonal degeneration/regeneration.78–80
Diffusion tensor imaging (DTI) measures the direction and amplitude of diffusion of
water molecules inside tissue. In axons, the diffusion of water is restricted by cell
membrane and myelin sheath, which results in a high diffusion gradient in the direction
that is parallel to the white matter tracts and lower diffusion perpendicular to the white
482 Eli et al
matter tracts. In SCI, whereby there is disruption of the normal architecture, this re-
sults in increased radial diffusivity because a new perpendicular pathway for water
diffusion exists. Two metrics used in DTI allow for user-friendly display for interpreta-
tion: fractional anisotropy evaluates the extent to which diffusion is limited in a direc-
tion and mean diffusivity assesses overall diffusion.81 Changes seen after SCI using
DTI metrics can be used to correlate with clinical function and can be monitored
throughout the diagnosis and recovery phases of patients with SCI.
The measurement of relaxation and magnetization transfer parameters is a way to
connect imaging modality with histologic myelin content, iron deposition, and
neuronal mapping. Pending further development, this modality feature can provide
insight and serve as an imaging biomarker for tracking glial cells and neural structures
in SCI.82
Using DTI data, a diffusion tensor tractography (DTT) can be derived using a compu-
tational method that reconstructs major nerve bundles in 3-dimensional spaces based
on the anisotropy properties. DTT can distinguish the distorted and injured nerve fibers
from intact areas. DTT can thus be used in the preoperative planning of surgical inter-
vention by providing insight into the degree of damage and a view of the shape of the
contused spinal cord.83
CLINICAL TRIALS
There are numerous clinical trials currently ongoing for the treatment of acute SCI that
targets the primary and secondary phases of injury focusing on neuroprotection and
neuro-regeneration.
Multiple pharmacologic agents are being investigated in clinical trials (Table 4).
Table 4
Ongoing clinical trials
SUMMARY
Acute SCI results in devastating outcomes with significant disability to the patient and
is associated with significant ongoing health and societal costs. Acute management is
geared toward preventing hypotension, early identification of injury level, and early
decompression with stabilization of the spinal column. The role of steroids continues
to remain controversial with no evidence to suggest a benefit. Blood pressure
augmentation is currently the standard practice for up to 7 days after injury. Emerging
technologies include quantitative imaging modalities and invasive spinal cord moni-
toring, which promise to improve the understanding of SCI. Finally, numerous ongoing
clinical trials are focused on neuroprotection and neuro-regeneration. Although acute
hospital management allows for the greatest possible recovery, rehabilitation serves
an important role in improving functional outcome.
Early management of traumatic spinal cord injury follows common airway, breathing, and
circulation assessment. Disability evaluation during the secondary survey should include
assessment of spinal level involved using a standardized approach. The authors advocate for
using the American Spinal Injury Association grading system.
The American Academy of Neurological Surgery does not recommend the use of high-dose
methylprednisolone in the setting of acute spinal cord injury. Other medical management
includes blood pressure augmentation to maintain a mean arterial pressure of greater than
85 mm Hg for 7 days after the acute injury.
AO Spine recommends early spinal stabilization when possible. Although there is potential
bias in prior trials, early (<24 hours from injury) decompression may result in improved motor
and functional status of patients.
DISCLOSURE
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