Keywords
airway management - bradycardia - blood pressure targets - intraoperative neuromonitoring
- neurogenic shock - respiratory arrest - resuscitation - spinal cord injury - spinal
shock - surgical decompression
Introduction
Acute spinal cord injury (SCI) is potentially irreversible and can be devastating,
affecting between 250,000 and 500,000 people every year worldwide.[1] Severe (i.e., complete) SCI presents as a total loss of motor and sensory function
and temporary depression of reflexes, reflecting an absence of communication between
the nerves below the lesion and the brain. In an incomplete injury, some signals persist,
which manifests in varying degrees of movement and sensation below the level of injury
and rarely in extinction of reflexes.[2] The pathophysiology of injury occurs in a two-step process consisting of the primary
mechanical insult and secondary pathobiological consequences.[3]
A greater understanding of these mechanisms and awareness of their potentially devastating
consequences have led to primary prevention efforts and a surge of research in mitigating
secondary injury. Protective measures such as improved safety equipment are reducing
the effects of car accidents, sports-related injury, and falls.[4]
[5]
[6]
[7] Early delivery of specialized medical and surgical care is now routine in high-resource
settings.[1] This care comprises immediate spinal immobilization with simultaneous consideration
of airway, breathing and circulatory demands, hemodynamic augmentation, and expedient
neurologic and radiographic evaluation for early surgical intervention.[8]
[9] These advances have likely played a role in both improved early survival and a decrease
in incidence of severe (complete) SCI relative to incomplete SCI.[10]
[11] Developed countries such as the United States, Finland, and Australia are seeing
greater percentages of incomplete quadriplegia from high cervical SCIs than in the
past.[12]
[13]
[14] This trend is thought to be attributed to advances in early resuscitation and rapid
airway management for an increasingly older population experiencing falls.[11]
[15]
A lack of longitudinal data collected in low- and middle-income countries makes international
trends in incidence and prevalence of SCI difficult to estimate and predict.[15]
[16] However, if early survival rates climb globally, we can expect to see a growing
population of high spinal cord injuries with concomitant ventilator dependency in
extended care settings.[11] Despite this increase in prehospital and hospital survival, there have been no meaningful
reductions in long-term mortality rates since the 1980s, and the gap in life expectancy
between the general population and individuals with SCI is increasing.[14] Fortunately, the current focus of research efforts and care delivery now centers
on preventing neural damage and promoting axonal regrowth through molecular agents
and early, aggressive physical rehabilitation.
In this two-part review, we first provide a brief background on SCI and its sequelae,
including the pathophysiology and timeline of injury, and then discuss the latest
developments in initial management and anesthetic considerations during surgery. In
the second part, we discuss the medical management of SCI in the intensive care unit,
focusing on evidence-based current practices. We conclude by reviewing the current
data on neurologic and functional recovery and promising neuroprotective approaches
and neuroregenerative therapies.
Pathophysiology
The mechanisms causing neurologic dysfunction in acute SCI involve a temporal sequence
of pathobiological events ([Fig. 1]).[3]
[17] Primary injury to the cord by acute compression, contusion (most common), distraction,
laceration, rotation, or severing results in immediate neurovasculature damage, for
example, through shearing of axons or ischemia from blood vessel compression.[18] The extent of primary injury depends on the degree of the initial insult and the
underlying condition of the cord and nerve roots (i.e., preexisting degenerative disease).
In most cases, functional deficits are disproportionate to the initial anatomical
damage, owing to the deleterious phases of injury and progressive neuronal deterioration.[3] Surgical and medical interventions during the acute and intermediate phases of SCI
have the greatest promise for halting and potentially partially reversing the damage
caused by secondary injury.[19]
Fig. 1 Timelines of primary and secondary mechanisms of acute spinal cord injury. The primary
injury incites a cascade of biomolecular changes related to the body's inflammatory
response to the initial trauma, termed “secondary injury,” which begins within seconds
and lasts for years. Disruption of the endothelium of blood vessels supplying the
cord causes hemorrhage, swelling, and subsequent thrombosis and vasospasm, which decreases
perfusion to the cord. This also allows for increased permeability for inflammatory
cells to invade the neuronal milieu and release cytokines such as interleukin (IL)-1,
IL-6, and tumor necrosis factor-α, which promote apoptosis. Additionally, cellular
membrane disruption leads to ionic dysregulation, free radial production, necrosis,
and release of glutamate, which has an excitotoxic effect on neurons and glial cells.
The influx of astrocytes and microglia cells to help mitigate the inflammatory response
causes the formation of a glial scar at the site of injury. These processes occur
during the acute (up to 72 hours after injury) and intermediate phases (days to weeks
after injury). In the months to years following SCI (chronic phase), the glial scar
may form a syrinx, or a fluid-filled cavity, at the site of injury. Scar formation
can also lead to tethering of the cord.
Initial Assessment
According to the Advanced Trauma Life Support guidelines, initial management of a
patient with potential SCI includes early transfer to a specialized center and rapid
assessment of injuries using the Airway, Breathing, Circulation, Disability, Exposure
(ABCDE) approach.[20] Patients must be assessed in the field and transported using full spinal immobilization
of the cervical, thoracic, and lumbar regions until each region is cleared or definitively
stabilized. “Spinal precautions” must be taken and are intended to limit further mechanical
injury to the highly vulnerable cord.[21] These include placement of an adequately fitting rigid cervical collar, use of a
backboard, and log rolling patients every 4 hours. If there is concern for intracranial
injury with elevated intracranial pressure (ICP), the bed or stretcher should be tilted
in the reverse Trendelenburg position to elevate the head.
Airway, Breathing:
The highest priority is to ensure an unobstructed airway and adequate oxygenation
and ventilation. Unlike current guidelines for advanced cardiac life support, airway
management in the trauma patient remains the first essential step.[20] Respiratory compromise in traumatic SCI can occur due to associated facial, neck,
or chest injuries. Complete SCI above the C3 level prompts apneic respiratory arrest.
Cervical or thoracic cord injury with phrenic or intercostal nerve paralysis leads
to hypoventilation and hypercapnic–hypoxemic respiratory insufficiency. A definitive
airway with positive-pressure ventilation should be provided as needed. The standard
of care is rapid-sequence intubation (RSI) with in-line spinal immobilization.[20] In some patients, direct laryngoscopy can be used successfully without manipulating
the neck. However, video laryngoscopy obtains better views of the glottis in less
time than standard laryngoscopy when intubation is performed in a neutral neck position
unless active bleeding or copious secretions compromise image clarity.[22] A hyperangulated video laryngoscope or optical stylet may provide better glottic
visualization in cervical SCI patients with additional risk factors for difficult
intubation, such as obesity and restricted mouth opening.[23]
Circulation:
Simultaneously, the hemodynamic status of the patient should be assessed. Occult
hemodynamic instability may be unmasked by induction agents and positive-pressure
ventilation if not yet apparent. Cervical and thoracic SCI can interrupt intermediolateral
cell column output prompting neurogenic shock from the disruption of sympathetic outflow
with undeterred parasympathetic activity.[24] Peripheral vascular tone, cardiac contractility, and heart rate may abruptly diminish,
resulting in circulatory collapse that can develop immediately and may last for weeks.
In polytrauma patients, circulatory shock from hypovolemia and cardiogenic causes
must be considered first before the symptoms of profound hypotension and bradycardia
are attributed to neurogenic shock. Immediate management of neurogenic shock involves
fluid resuscitation to restore intravascular volume followed by vasopressors, if necessary,
to avoid hypotension.[20] If an endotracheal tube is not immediately warranted, resuscitation prior to intubation
may help blunt the effects of RSI. Class III evidence supports maintaining a mean
arterial pressure (MAP) of 85 to 90 mm Hg for a minimum of 5 to 7 days, as discussed
later in Part II.[25]
[26]
[27]
[28]
[29]
[30]
Disability (neurologic status):
The next step after airway, breathing, and circulation concerns are addressed is
a neurologic assessment to help determine the extent of injury. In general, impairment
of motor and sensory function occurs in a distribution below the level of injury.
For example, injury to the cervical cord can lead to tetraplegia, whereas injury to
the thoracic or lumbar spine would result in lower extremity paraplegia. Additionally,
cervical injuries may affect the diaphragm and respiratory function. However, injury
to either the upper or lower cord can result in bowel and bladder dysfunction. The
neurologic manifestations of SCI can be assessed using the American Spinal Injury
Association (ASIA) Impairment Scale (AIS) consisting of a dermatomal-based sensory
examination, myotomal-based motor examination, and a rectal examination[31] ([Fig. 2]). Severity and level of injury are assigned based on the findings of these examinations.
The level of neurologic injury is defined as the lowest functioning nerve root with
intact sensation and grade 3 or greater motor function. (See [Fig. 2] for a description of motor grades.) Severity is classified as complete or incomplete:
from ASIA A, representing complete SCI with no motor and sensory function below the
level of injury, to ASIA E, corresponding to normal sensory and motor function (but
other neurologic phenomena, such as abnormal reflexes, may be present).
Fig. 2 International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI)
Worksheet from the American Spinal Injury Association (ASIA) and the International
Spinal Cord Society (ISCOS). (©2019 American Spinal Injury Association. Reprinted
with permission.)
While immediate neurologic assessment using the AIS provides standardized, detailed
information that guides radiographic assessment and treatment, determining whether
injuries are complete or incomplete often requires resolution of spinal shock.[32] “Spinal shock” is the term describing the immediate depression of all fundamental
functions of the spinal cord caudal to the injury, including motor, sensory, autonomic,
and reflex activity, when the cord is suddenly traumatized.[33] Areflexia or hyporeflexia seen in spinal shock is a result of spinal motoneuron
hyperpolarization from the loss of descending supraspinal background excitation and
increased presynaptic inhibition. Spinal shock evolves in phases and terminates in
a period of hours to sometimes weeks after the initial injury, with certain reflexes
recovering earlier than others.[33] Patients typically develop hyperreflexia as neurons recover due to synaptic reorganization,
such as augmentation of latent synapses on spinal motoneurons, upregulation of receptors
on the surface of partially denervated spinal cord cells, and nonsynaptic diffusion
neurotransmission through extracellular fluid.[33] Commonly mistaken for each other, neurogenic shock is not synonymous for spinal
shock, but it can be considered a manifestation of the spinal shock syndrome.
Exposure (radiographic assessment):
The choice of imaging depends on the clinical suspicion of injury, the modalities
available, and the hemodynamic and respiratory status of the patient. Computed tomography
(CT) of the spine is superior to plain radiographs and can be performed as the initial
imaging modality due to ease and speed of access.[34] All patients who have sustained blunt trauma or a fall and have an altered mental
status should receive CT scans of the brain, cervical spine, and chest/abdomen/pelvis
with dedicated spine image reformats.[35] In alert, unintoxicated patients with no midline tenderness, no distracting injuries,
and no neurologic deficits, spinal imaging is not needed according to the NEXUS (National
Emergency X-ray Utilization Study) criteria.[36]
[37] The use and timing of magnetic resonance imaging (MRI) in acute SCI is controversial
and depends on clinical circumstances and institutional resources. In high-resource
SCI centers, MRI is typically obtained within 48 to 72 hours of injury after cardiopulmonary
stabilization to fully assess the neural elements, soft tissues, and ligamentous structures.[38] While CT is better than MRI in assessing bony structures, MRI can provide valuable
information regarding extent and mechanism of SCI and is more sensitive for detecting
epidural hematomas. MRI is needed if a spinal hematoma, ligamentous injury, or traumatic
disc herniation is suspected or seen on CT scan. Additionally, patients can have nonpenetrating
unpronounced vascular injuries associated with cervical SCI, particularly to the extracranial
carotid and vertebral arteries.[39] Among traumatic SCI patients, this blunt cerebrovascular injury (BCVI) is an independent
risk factor for increased morbidity and mortality.[39]
[40]
[41] Patients benefit from screening with CT angiography (CTA) if they have signs or
symptoms of BCVI, such as expanding hematoma, bruits, or neurologic symptoms of posterior
circulation insufficiency.[42]
[43] Some argue for screening of all trauma patients with cervical SCI regardless of
the presence of symptoms since there is often a latent, asymptomatic period before
the natural pathology of carotid or vertebral artery injury leads to neurologic ischemic
events.[42]
[44]
[45]
[46] A meta-analysis of 10 studies evaluating which of 9 screening criteria are associated
with BCVI demonstrated a five times greater likelihood of BCVI in trauma patients
with cervical spine fractures compared with those without.[47] Early identification of BCVI may allow for the initiation of treatment before devastating
cerebral ischemia occurs.[41]
[46] While digital subtraction angiography remains the gold standard imaging modality
for detecting BCVI, it is time-consuming, not universally available, and invasive
with a risk of serious complications. Although false-positives and false-negatives
have been reported with CTA, it is fast, readily available and noninvasive and has
an acceptable sensitivity and specificity for detecting BCVI.[48] Further studies are needed to evaluate expansion of BCVI screening criteria to include
all cervical SCI and the diagnostic yield of CTA since overscreening is costly and
associated with unnecessary radiation and contrast exposure.[48]
[49]
Operative Management of Neurologic Injury
Operative Management of Neurologic Injury
Early surgery:
Goals of surgery are to decompress the cord and to realign and stabilize the spine.
Early relief from compressive forces reduces ischemia and alleviates trauma from bone
fractures and disc fragments. This limits the effects of secondary injury and optimizes
the environment for neurologic recovery. The surgical team may place an alert and
oriented patient with a cervical fracture dislocation injury in traction either instead
of or prior to surgical intervention.[50] This includes application of a halo ring or Gardner-Wells tongs with serial increases
in traction weight.[17] In complete SCI, however, surgical stabilization is warranted as soon as safely
possible. Early intervention is also important in incomplete SCI to help preserve
existing neurologic function with the hope of recovering some function. The landmark
Surgical Timing in Acute Spinal Cord Injury Study (STASCIS), a prospective analysis
of 313 patients with cervical CSI, showed that after adjusting for injury severity
and glucocorticoid therapy, patients who underwent spinal cord decompression within
24 hours of SCI (mean 14.2 ± 5.4 hours) were more than twice as likely to have an
improvement of at least two AIS grades at 6 months postinjury than those who underwent
surgery after 24 hours (mean 48.3 ± 29.3 hours).[51] Currently, there is insufficient evidence that early surgery improves long-term
outcomes.[52] Future study is needed to determine the effect of very early interventions (<8 hours
or <12 hours after SCI) on recovery.
Anesthetic considerations:
The anesthesiologist's main goals when caring for acute SCI patients undergoing surgical
decompression are to minimize secondary injury and to improve the outcome of the procedure.
This begins with a thorough evaluation of the extent of the patient's injuries, medical
history, and prehospital and hospital course since injury, if time allows it. A directed
physical examination, airway assessment, and review of imaging should also be performed,
keeping in mind that SCI patients often sustain facial, intracranial, and thoracoabdominal
trauma ([Table 1]).
Table 1
Suggested anesthetic guidelines for the management of surgery for acute spinal cord
injury
|
Abbreviations: EMG, electromyography; ETT, endotracheal tube; IONM, intraoperative
neuromonitoring; MAP, mean arterial pressure; MILS, manual in-line stabilization;
SCI, spinal cord injury; SSEP, somatosensory evoked potentials; TcMEP, transcranial
motor evoked potentials.
|
|
Preoperative preparation
|
Expeditious chart review, including medical history, circumstance of injury, hospital
course, and images
Directed physical examination and detailed airway assessment
Difficult airway equipment readily available
|
|
Premedication
|
Early preoxygenation
Limit anxiolytic premedication
Provide preinduction anticholinergic medication in high SCI
Preinduction arterial catheterization
|
|
Induction
|
Careful titration of induction agents with prophylactic fluid/vasopressors
Succinylcholine is contraindicated >48 h postinjury
|
|
Airway
|
Video/direct laryngoscopy and endotracheal intubation with MILS in emergent scenarios
or an uncooperative patient
Awake fiberoptic bronchoscope intubation with topicalization of the airway can be
considered in cooperative patients
|
|
Maintenance
|
MAP of 85–90 mm Hg with fluids and vasopressors
IONM with TcMEP, SSEP, and EMG using a tailored anesthetic technique
|
|
Emergence
|
Wean sedation for neurologic assessment
Leave ETT in situ for complete high cervical SCI
Extubate with consideration of patient and surgical factors (length, positioning,
volume administered, future interventions necessary) in all other patients
|
Standard monitors, including continuous pulse oximetry, electrocardiogram, blood pressure,
capnography, oxygen analyzer, and temperature, are necessary for rapid intervention
on precipitous deterioration that may exacerbate spinal cord tissue hypoxia and ischemia.[53] Premedication with anxiolytics should be avoided in patients with upper cord injury.
Central respiratory depression from benzodiazepines can intensify respiratory muscle
weakness, leading to alveolar hypoventilation. Furthermore, benzodiazepines are associated
with delirium and cognitive impairment in older individuals due to increased sensitivity
and decreased metabolism and are best avoided in elderly SCI patients.[54] Preoxygenation is paramount and can be continued through apneic oxygenation after
induction in patients at risk for aspiration.[55]
Hypotension must also be averted and insertion of an arterial catheter prior to induction
is recommended. While the reverse Trendelenburg position is best for lung expansion,
to reduce aspiration risk, and for traumatic brain injury patients with elevated ICP,
this position may worsen hypotension in patients with high SCI. Guidelines suggest
that MAP be maintained within 85 to 90 mm Hg throughout the case.[25] However, this is not supported by class I or II evidence.[26]
[27]
[28]
[29]
[30] MAP exceeding 90 mm Hg increases the risk of bleeding and obscures visualization
of the operative field due to vascular congestion, whereas MAP less than 85 mm Hg
is believed to worsen secondary spinal cord injury.
Normocapnia, normothermia, and euglycemia should be maintained throughout the procedure.
Frequent blood gas surveillance may be necessary since patients with SCI may have
concurrent pulmonary injury causing a ventilation–perfusion mismatch and end-tidal
carbon dioxide readings that inaccurately reflect arterial carbon dioxide pressure.
Arterial catheterization is indispensable in SCI surgery and allows for not only tight
blood pressure control but also frequent blood gas monitoring, sampling of important
laboratory values, such as hemoglobin (Hb), lactate, coagulation parameters, and electrolytes,
and volume status assessment with arterial tracing pulse pressure variation.[56] The likelihood of massive blood loss increases with each additional instrumented
level, and preemptive placement of adequate venous access with at least two large-bore
intravenous catheters is prudent. Central venous catheterization may be indicated
if injuries to extremities preclude access or for the administration of vasoactive
agents.
For patients with cervical and high thoracic SCI, an airway management plan must involve
maintenance of spinal immobility. Techniques for mask ventilation and instrumentation
of the airway may need to accommodate cervical spine immobilization devices such as
a halo or rigid collar. Manual in-line stabilization (MILS) of the cervical spine
provided by an assistant standing at the head of the bed or reaching across the chest
can be performed with the anterior portion of a rigid collar removed and is associated
with less movement of the spine during intubation than collar immobilization alone.[57] A properly performed jaw thrust maneuver, achieved by translating the condyles of
the mandible out of the temporomandibular joint and then pulling the mandible forward,
is the safest method to open the airway of a patient with cervical SCI and can be
performed in patients with a rigid collar without moving the head or neck. Awake fiberoptic
bronchoscopy is commonly used to intubate stable, cooperative patients prior to cervical
spine surgery.[58] Alternative devices such as intubating laryngeal mask airway, rigid optical stylet,
and hyperangulated video laryngoscopy with MILS are associated with decreased first
attempt failure rate and less cervical spine motion than direct Macintosh laryngoscopy
with MILS and are preferred in emergency situations or for patients who would not
tolerate an awake procedure due to their mental state.[23]
[59]
[60] Cricoid pressure during RSI is best avoided in patients with lower cervical SCI.
Instead, a gentle backward-upward-rightward pressure maneuver can be used to facilitate
laryngoscopic view if necessary.[20] Airway manipulation and tracheal suctioning in patients with complete high thoracic
and cervical SCI can trigger severe bradycardia and sinus arrest due to unopposed
efferent parasympathetic activity.[61] Pretreatment with anticholinergic medications prior to induction is advised in these
high-risk patients. Resting bradycardia associated with acute upper SCI can be treated
with small doses of glycopyrrolate, or with ephedrine for simultaneous MAP augmentation.
Atropine should be readily available throughout the surgical procedure for severe
bradycardia. Cutaneous pacing with a placement of anterolateral pacer pads prior to
surgical preparation and draping may be necessary in patients with high SCI.
Routinely used induction agents include propofol, ketamine, etomidate, and sodium
pentothal. Agents that decrease systemic vascular resistance, such as propofol, should
be used with caution in SCI due to the risk of profound hypotension from sympathetic
denervation and decreased venous return to the heart.[62]
[63] Concurrent intravenous fluid bolus administration for preload augmentation and vasopressor
infusion during induction may be required as prophylaxis for hypotension. In patients
with lower SCI, pure vasoconstrictors such as phenylephrine can be safely used alongside
fluid to mitigate vasodilation from the peripheral sympathectomy caused by the injury
further compounded by anesthetic agents. However, with injuries disrupting the sympathetic
cardio-accelerator fibers (T1 to T4), vasopressors with inotropic properties are needed,
such as norepinephrine, dopamine, or epinephrine.[64]
[65] Depolarizing neuromuscular blocking agents, such as succinylcholine, should be avoided
in patients with SCI after 24 hours postinjury due to an exaggerated and potentially
life-threatening intracellular potassium efflux.[66] This is because acetylcholine receptors (AChRs) are upregulated and occupy all of
the muscle membrane after denervation injury, not only the neuromuscular junction.
Furthermore, immature AChRs have a longer open channel time when depolarized and a
greater potential for sustaining a more prolonged potassium leak. Choice of maintenance
anesthesia agents depends on multiple factors such as the duration of the planned
procedure, level of hemodynamic stability, patient comorbidities, and intraoperative
neuromonitoring (IONM) techniques (see the IONM section below).
While excessive intraoperative fluid resuscitation to meet MAP goals should be avoided
to prevent pulmonary and spinal cord edema, precise clinical endpoints to guide therapy
have not been established. Euvolemia is a good initial goal, and fluid losses, both
urine and blood, should be calculated frequently. Lactate levels, acid-base status,
and trends in pulse pressure variation can further guide fluid management. Choice
of intravenous fluid is often dictated by regional and institutional availability.
While there is insufficient evidence that colloid solutions are superior to balanced
electrolyte solutions, colloids may be useful to minimize total volume of administered
fluid while improving intravascular retention and microcirculatory hemodynamics with
minimal capillary leakage.[67]
Fluids are typically the primary volume replaced until transfusion thresholds are
crossed. This could be ongoing large-volume surgical bleeding or a specific Hb or
hematocrit value. There is a lack of data on values below which blood should be transfused
in acute SCI.[68] However, spinal cord tissue offers little anaerobic reserve, and the injured cord
has a very low neurologic threshold to hypoxia/ischemia in the face of anemia. It,
therefore, can be argued that the risk of anemia in acute SCI weighs more heavily
than the risks associated with blood transfusion, and a liberal (Hb of 10 g/dL) transfusion
approach may be preferred to a restrictive one.[68]
Intraoperative neuromonitoring:
Patients with SCI benefit from IONM, particularly those with incomplete cord injury,
which helps ensure that surgery does not exacerbate motor or sensory deficits. Ideally,
IONM should be initiated immediately after the airway is secured and prior to surgical
positioning on the operating room table. Level I evidence supports the use of intraoperative
somatosensory evoked potential (SSEP) and transcranial motor evoked potential (TcMEP)
monitoring.[69] Additionally, electromyography can be used to detect and prevent nerve root injury
from decompression or pedicle screw fixation.[70]
One way in which anesthetic agents induce unconsciousness is by depressing synaptic
activity. While anesthetic effects vary by synapse location, the greatest effects
occur on TcMEP muscle responses and cortical potentials. Inhalational agents including
isoflurane, sevoflurane, and desflurane have greater effects than intravenous anesthetics.
Inhalational anesthetics cause a dose-related decrease in amplitude and an increase
in the latency of cortical SSEPs.[71]
[72] In healthy patients, adequate SSEPs can usually be recorded at 0.5 to 1 MAC of volatile
agents. However, for patients with SCI and neurologic impairment, even low levels
of inhalation agents may abolish potentials and make monitoring impossible. TcMEP
responses are even more sensitive to the effects of volatile anesthetic than SSEPs.
Total intravenous anesthesia is encouraged when TcMEP responses are monitored during
surgical treatment for SCI. Whichever the choice of anesthesia, its level must remain
constant during critical monitoring periods to avoid iatrogenic changes from baseline
and misleading interpretation of responses.
Regardless of IONM signal changes, a neurologic assessment may be requested by the
surgical team after emergence from anesthesia but before exiting the operating room.
Bispectral index (BIS) and other processed electroencephalographic monitoring are
helpful in determining the depth of anesthesia to facilitate safe emergence and a
timely spinal assessment prior to extubation.[73] Patients with a complete, high cervical SCI will require assisted ventilation and
therefore should be left intubated if a tracheostomy is not already in place. Multiple
factors influence the decision to extubate patients with incomplete and lower SCI,
including the length of surgery, positioning during surgery, volume of blood and fluid
administered, and associated injuries that may require additional interventions in
the near future.
Conclusion
Patients with suspected SCI should be brought to facilities that specialize in their
care to help decrease mortality and improve prognosis. Initial management involves
early identification of injuries, aggressive resuscitation with attention to associated
conditions, and definitive surgical treatment. The anesthesiologist plays a vital
role in preventing further injury to the vulnerable spinal cord during surgical decompression.
