Keywords
spinal cord injury - spinal cord - emergency management
Introduction
Spinal cord trauma refers to injuries compromising vertebral column and spinal cord.
Worldwide, it constitutes one of the main causes of mortality and morbidity, especially
in young adults. It’s estimated that every year there are 2 to 3 new cases for every
100,000 habitants, although incidence may vary depending on the regional variations.
The clinical presentation is bimodal according to age, the first group is between
15 and 30 years of age, and it’s generally caused by transit accidents, falls from
high heights, sports injuries, and violent actions. The other peak of incidence is
seen in population older than 65-years-old; it is seen in developed countries as life
expectancy becomes higher. In this population, falls from great heights are more frequently
cause of vertebral and cord injuries.[1] Mortality of spinal cord trauma is highly variable, depending on several factors
such as the relationship with the severity (American Spinal Injury Association [ASIA]
A–C vs. D), the extension (local vs. in multiple levels) and the spinal segment injured,
as well as the coexistence of additional distal injuries in the vertebral column and
spinal cord. However, because of its hemodynamic and ventilatory repercussions, cervical
and upper thoracic injuries more frequently require treatment in the intensive care
unit ([Table 1]).
Table 1
Physiopathology of spinal cord injury[2]
|
≤ 2 h
|
≤ 48 h
|
≤ 14 d
|
≤ 6 mo
|
≥ 6 mo
|
|
Phase
|
Primary immediate
|
Acute early
|
Secondary subacute
|
Intermediate
|
Chronic/late
|
|
Abbreviations: IL-6, interleukin-6; IL-1β, interleukin-1 beta; ROS, reactive oxygen
species; TNF-α, tumor necrosis factor-alpha.
|
|
Physiopathological process
|
Primary mechanic injury
Gray matter hemorrhage
Axonal disconnection
Hemorrhagic necrosis
Microglial activation with liberation of cytokines (IL-1β, TNFα, IL-6, among others)
|
Cytotoxic and vasogenic edema
Production of ROS: lipid peroxidation
Excitotoxicity mediated by glutamate
Continuous hemorrhages and necrosis
Neutrophil infiltration
Loss of permeability of blood–brain barrier
Early demyelination (oligodendrocyte apoptosis)
Neuronal death
Ischemic events (systemic shock, spinal shock, hypotension, hypoxia)
|
Macrophages infiltration
Astroglial cicatrization (reactive astrocytosis)
Blood–brain barrier repair and resolution of edema
|
Astroglial scar consolidation
Cyst formation
Stabilization of injury
|
Prolonged Wallerian degeneration
Persistence of noninjured and nondemyelinated axons
Beginning of structural plasticity and functional processes in noninjured medular
tissue
|
Initial Approach Including Immobilization
Initial Approach Including Immobilization
In the primary evaluation of the patient in the intensive care unit, it’s recommended
to apply the consigned recommendations from the life support protocol for spinal cord
traumatic injuries.[3] These include “ABDC” evaluation, prioritizing airway permeability, ventilation,
and circulation, while spinal immobilization measures are established.[4]
[5]
[6] To immobilize the vertebral column, a cervical rigid neck brace, cephalic immobilization,
and spinal board must be used for all unconscious patients, as well as for conscious
patients referring spinal pain. Immobilizations must be maintained until any spinal
or medullary injury is discarded or when definitive treatment is given.[6]
[7]
[8] Patients at risk of vertebral column injury are those who present any of the following
conditions:
-
Altered mental status
-
Intoxication
-
Spinal pain or deformity
-
Suspected limb fracture or suspected distraction injuries (long bones fractures, visceral
injuries that require surgical evaluation, extensive burns, superior thorax injuries,
lacerations, abrasions or extensive crushing; any injury that causes acute functional
alteration that prevents physical, mental, or neurologic examination)
-
Patients with focal neurological deficits
However, those patients who are conscious, alert, symptomatic, without cervical pain,
without sensorial or motor anomalies or any other injuries that alter the physical
examination, may be transported without cervical immobilization; this facilitates
airway manipulation and ventilation, and decreases the risk of aspiration. Immobilization
is not recommended in penetrating injuries, because the probability of cervical instability
is quite low and may delay resuscitation.[9]
The second phase of evaluation is focused on distinguishing the spinal or medullary
injuries. The whole vertebral column and prespinal muscles must be visualized and
palpated in search of deformities or local pain. The presence of tympany may be suggestive
of medullary injury.[9] The findings in the neurological examination must be compared with the medullary
disability and standardized classification scale proposed by The ASIA that includes
standardized neurological classification of spinal injuries into category A (complete);
categories B, C, and D (incomplete); and category E (normal).[10] According to the findings of the neurologic examination, the spinal injuries may
be classified in some of the following clinical syndromes, that is, complete transection
syndrome, hemisection syndrome or Brown-Séquard syndrome, central cord syndrome or
Schneider’s syndrome, anterior medullary syndrome, central cord syndrome, and cauda
equina syndrome.
Additionally, the probable injury level must be identified clinically, because of
the strong implications in the radiologic evaluation, management, and prognosis. Neurologic
evaluation has to be repeated daily during the first 72 hours after the injury, because
this is the time when major changes are seen. In the patients with complete medullary
section syndrome, during the first 3 to 5 days after the injury, myotatic reflexes
may be lost. This period of time is known as medullary shock (this is not the same
as a neurogenic shock of medullary origin), whose outcome is clinically determined
by the return of the bulbocavernosus reflex (Osinski reflex). If complete medullary section syndrome findings are persistent even when
the bulbocavernosus reflex has returned, the probability of neurologic recovery is
very low.
Imaging Evaluation
There is no “gold standard” for the diagnosis of spinal cord traumatic injuries; however,
the rational use of conventional radiologic tests, computed tomography (CT) scan,
and magnetic resonance imaging (MRI) allows identifying almost all clinically relevant
injuries. Currently, the most recommended method to identify vertebral injuries is
CT scan, because of its availability, sensibility, and specificity; on the other hand,
conventional radiology techniques must be considered as a diagnostic approach only
when CT scan is not available.[11] Imaging studies indication must be based on the clinical finding of the patient.
In those patients who are conscious and show sensitive response, the approach will
be made considering that the sensitive level secondary to cervical injuries is above
the injured segment; in upper thoracic segments, one level below; in lower thoracic
segments, two segment below; and those in the medullary cone and cauda equina produce
well defined syndromes. However, all vertebral segments caudal to the neurologic injury
must be examined systematically. In those patients with an altered state of consciousness
(i.e., moderate and severe cranioencephalic trauma, intoxication, shock and so on),
examination of the vertebral column by CT is indicated. For the assessment of cervical
column, a three-projection radiography (anterior–posterior, lateral, and odontoid)
technique is recommended only when CT is not available; if any anomaly is found or
if bone structures are hardly distinguished, the assessment must be complemented with
CT scan.[11] MRI is a key element in patients whose neurologic examinations is altered, since
it allows diagnosing medullary injuries, which are seen as increase in signal in the
sequence T2, and distinguishing epidural collections, and discoligamentous complex
injuries that may cause medullary compression or mechanical instability; this findings
may result useful to determine the treatment of the injury. In those patients who
do not present neurologic deterioration, MRI is recommended according to surgeon’s
criteria, who after evaluating the specific characteristics of the injury will determine
its usefulness.
Treatment
In the emergency management, therapeutic actions should look for the following principles:
-
Maintain ventilator function, and treat its respective alterations.
-
Identify and treat hemodynamic alterations.
-
Stop deterioration of neurologic damage.
-
Prevent systemic complications.
-
Promote early rehabilitation.
Respiratory Care
Respiratory alterations are the principal cause of death in patients with spinal cord
injury (SCI), that’s why the standardized approach is vital, as this is associated
with a lower incidence of complications, fewer days with mechanical ventilation, intensive
care unit stay, and lower attention costs.[12] The majority of patients with high quadriplegia will present respiratory alterations
due to compromise of diaphragmatic innervation (C-C-5) since the beginning, or will
develop it in the first 5 days after the traumatic event secondary to ascending medullary
edema.[13] Therefore, respiratory management of these patients generally includes intubation,
mechanical ventilation, and tracheostomy, especially when the injury is found above
C5 level.[12] It’s very important to note that during rapid sequence intubation, succinylcholine
must be avoided during the first 48 hours due to the high risk of lethal hyperkalemia.[13] In those patients who do not present respiratory failure at admission, an integral
assessment of ventilatory mechanic must be performed; this includes physical examination
and measurement of forced expiratory volume in 1 second, forced vital capacity and
peak expiratory flow, which will be used to monitor the respiratory mechanic daily
and allow anticipation of respiratory failure. For atelectasis prevention, in intubated
patients relatively high volumes of air (10–15 mL/kg) should be considered to solve
or to prevent atelectasis; in nonintubated patients the use of respiratory incentives
is recommended every hour. Tracheostomy with chronic airway management may be used
in patients with persistent respiratory compromise and unmanageable airway secretions.[14] For patient whose injury is above C5 level, a diaphragmatic pacemaker implant should
be considered because diaphragmatic weakness secondary to denervation and muscular
atrophy is the main cause of respiratory failure in these types of patients.
Cardiovascular and Hemodynamic Care
Cardiovascular and Hemodynamic Care
Therapeutic strategies need to be directed to maintain mean arterial pressure between
85 and 90 mm Hg during the first 7 days after the traumatic event to guarantee medullary
perfusion.[15] In patients who present with hypotension, fluid resuscitation must be optimized,
rule out other injuries as potential cause of hypotension and if the goal arterial
pressure is not achieved, norepinephrine infusion must be started with a dose of 0.05
µg/kg/min, which will be entitled to guarantee medullary perfusion. However, fluid
resuscitation must be performed carefully to avoid fluid overload in these patients
with high risk of pulmonary edema.[16] Some patients with upper thoracic or cervical injuries may present sympathetic insufficiency,
which may present as extreme symptomatic bradycardia that can progress to cardiac
arrest; because of this, such alterations require observation and appropriate treatment
with chronotropic drugs (atropine or adrenaline). Some refractory cases will need
to be treated with temporal transthoracic or transvenous pacemakers.
Gastrointestinal Care
The start of enteral nutrition must be early, preferably before 72 hours after the
traumatic event.[17] Prophylaxis for stress-induced gastric mucous ulcers is indicated in all patients
with thoracic or cervical injuries, as well as in those with mechanical ventilation.
Routinely it’s recommended the use of proton-pump inhibitors or H2 receptor antagonist,
which will be suspended only once mechanical ventilation is suspended as well and
enteral intake goals have been accomplished for at least 48 hours. Gastric emptying
delay manifests as nausea, vomiting, and abdominal distension. In the patients with
a tube for enteral nutrition, the gastric residue should be monitored strictly every
4 hours, and should never be more than 250 mL. In the event that gastric emptying
is delayed, it is recommended to start treatment with metoclopramide and erythromycin,
and in case of persistence, progress the nasogastric tube to post-pyloric tube. The
first measure to avoid constipation is prevention by digital stimulation and laxative
drug such as bisacodyl at a dose of 10 mg once daily. In those cases, in which defecation
is not accomplished 72 hours after the initial dosage, the dose may be increased up
to 10 mg bid and sorbitol (30 mL bid PO or nutrition tube) may be added.
Urogenital Care
In the initial medullary shock phase, the spinal reflex activity in the areas below
the injury stops completely; this is translated as lower urinary tract areflexia that
implies neurogenic bladder with passive filling and overflow incontinence.[5] The duration of this stage is variable from days to weeks before the bladder reflex
activity is restored.[5]
[18] In the acute phase, once the presence of clinical signs suggestive of urethral trauma
(urinary meatus bleeding, vaginal introitus bleeding, hematuria, free-floating prostate,
perineal hematoma) have been ruled out, an imminent vesical catheterization should
be performed, this procedure is associated with a lower incidence of urinary tract
infections, compared with permanent catheterization; thus, it constitutes the election
method in patients with SCI.[5] Other options are associated with less risk of urinary tract infection such as “urofunda”
(urologic sheath) or bladder training.[18]
Priapism is another acute and generally auto-limited event, caused by an increase
of the arterial blow flow in the cavernous sinusoids with oxygenated blood overload
without causing ischemia or acidosis therefore, sequels are rare. It solves spontaneously
in 62% of patients within a maximum period of 5 hours with no need of specific treatment.
It’s managed with conservative treatment with topical application of ice in the perineum.
Measures such as drainage of the corpus cavernosum penis, intracavernous injection
of α-adrenergic drugs (phenylephrine, adrenaline), are not recommended.[18]
Venous Thromboembolic Disease Prophylaxis
Venous Thromboembolic Disease Prophylaxis
The incidence of deep venous thrombosis in patients with SCI varies from 9 to 100%.
The strategies used for prevention in thromboprophylaxis include low-molecular-weight-heparin
(LMWHs), unfractionated heparin, antithrombotic stockings, intermittent pneumatic
compression devices, and inferior vena cava filters. The current recommendation is
the start of early antithrombotic prophylaxis (<72 hours) and combined that includes
a LMWH, which must be used in association with intermittent pneumatic compression
devices and electric stimulation, because drug prophylaxis alone is poorly effective.
Unfractionated heparin should be used for cases where LMWH is not available or contraindicated.[19] In the patients that require surgical treatment, LMWH must be suspended 12 hours
before the programmed surgery and restarted in the 24 hours posterior to the surgery.[20] The recommended duration of thromboprophylaxis is 3 months.
Conclusions
The initial approach of the patient requires optimization of vital signs (arterial
pressure, ventilation, and oxygenation), as seen in the protocols for polytraumatized.
Immobilization must be used routinely in patients with suggestive findings of spinal
injury and in those whose clinical examination is nonreliable until injuries can be
ruled out with imaging studies. In those patients that require imaging assessment
and do not present neurologic deterioration, CT scan is the election imaging study;
while those patients who present findings suggestive of neurologic injury have to
be assessed additionally with MRI. In the actuality, there is no pharmacological treatment
that is useful to improve the functional prognosis of patients with traumatic medullary
injuries. Steroids (methylprednisolone) don’t improve vital or functional prognosis
and may cause severe complications, even fatal outcome.[21] Intensive treatment must be focused on the prevention and management of ventilatory
and cardiovascular abnormalities related to muscle weakness and loss of autonomic
innervation. A huge percentage of morbidity and mortality is related to gastrointestinal
and urinary alterations and venous thromboembolic disease, so the treatment of these
alterations should be established promptly in the acute phase of the traumatic event.
