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 CRITICAL
CARESPINAL
TRAUMA |
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Injuries to the Cervical Spine Georges
Desjardins, MD FRCPC Introduction Epidemiology Pathophysiology The circulation of the spinal cord is more vulnerable to injury than that of the brain. Immediately following blunt trauma or compression, hemorrhages are seen in the central gray matter. A zone of hemorrhage, edema and necrosis spreads from the central area to involve, in severe injuries, the entire diameter of the cord within 6 to 24 hours. Damage to the gray matter involves only two or three segments at the level of injury. This will cause an interruption of nerve conduction in the fiber tracts, which isolates the region of the body below the level of injury from cerebral control. There is progressive loss of function after the initial impact for the first 24 hours related to associated secondary injury, edema, disc compression, hematoma and hypoperfusion to the spinal cord. As edema sudsides or circulation is reestablished, the function in some areas may improve slightly; in the absence of further injury, the pattern is usually stable after the first day. The rest of the patient’s progress can be divided in an acute and chronic phase. Acute phase of spinal cord injuries (4-6 weeks) The immediate response to spinal cord compression
is a massive sympathetic stimulation and reflex parasympathetic
activity that usually lasts for 3 to 4 minutes and is mediated
by alpha-adrenergic receptors. The hemodynamic effects are severe
hypertension and reflexe bradycardia or tachyarrhythmias.A
After this initial response, loss of neurologic function
below the injured will cause what is called spinal shock. There
is flaccid paralysis of voluntary muscles, areflexia, loss of
sympathetic tone ( hypotension and bradycardia in high thoracic
or cervical injuries, increased vascular capacitance ), poikilothermia
and flaccidity of the GI tract and the bladder with generalized
ileus and urinary retention.
Treatment of cervical spine trauma begins with the
realization that patients with head, neck, facial, and multiple
injuries may also have cervical spine instability. In the hospital,
life-threatening situations are identified and treated during
the initial and secondary surveys following the “A,B,C” of trauma
resuscitation. The rest of the resuscitation phase should focus
on the prevention of secondary injuries to the spinal cord with
early fracture stabilization and reduction, early ventilatory
support and adequate spinal perfusion (correction of hypotension).
Recently, a multicenter trial has shown the usefulness of high
dose steroids in the treatment of blunt spinal cord injuries.
A bolus of methylprednisolone, 30 mg/kg, followed in 1 hour by
an infusion of 5.4 mg/kg/hr for 23 hours, was associated with
improvement in both sensory and motor recovery if started within
8 hours of trauma. Body temperature should be monitored at all
times. Reflex vascular activity, sweating, and shivering are abolished
in spinal shock; thus patients with high-level lesions are generally
poikilothermic. Hyperglycemia which commonly occurs in patients
with severe systemic stress, has been associated with worse neurologic
outcome in animal studies. We recommend tight blood glucose control
in the acute phase.
Progression to the chronic
phase
Sympathetic tone returns to some extent in 4 to
7 days. Resting blood pressure returns to, or toward normal and
there may be a mild hypertensive response (autonomic hyperreflexia)
to various stimuli such as pain or bladder distention below the
level of the lesion. Reflex activity returns after 4 to 6 weeks
and the chronic phase begins. This is characterized by spastic
motor paralysis with hyperactive tendon reflexes, occasionally
severe autonomic hyperreflexia, and some return of involuntary
bladder function.
A patient who sustains paralysis with no sign of
distal sparing may have a complete and irreversible cord lesion.
When the period of spinal shock is over, which is heralded by
the return of the bulbocavernosus reflex (elicited by pulling
on the glans penis, tapping the clitoris, or tugging on an indwelling
urinary catheter and obtaining a rectal sphincter response), a
definitive diagnosis can be made. If the reflex has returned and
complete paralysis continues, there will be no neural recovery.
Two additional considerations are particularly important
to the anesthesiologist in the chronic phase: supersensitivity
of cholinergic receptors and autonomic hyperreflexia.
Supersensitivity of cholinergic
receptors
In response to denervation, cholinergic receptors
proliferate beyond the end plates of voluntary muscle fibers,
eventually to invest the entire cell membrane. The muscle becomes
"supersensitive” and contracts maximally in response to a
concentration of acetylcholine only 10-4 to 10-5 that needed to
initiate contraction in normal muscle. Potassium ion is released
suddenly along the entire length of the fiber rather than gradually
as the action potential propagates. This produces a rapid rise
in serum potassium levels. Succinylcholine induces an identical
response and may be associated with a serum potassium increase
of 4 to 10 meq/L.
The extent of this increase is roughly proportional
to the amount of paralyzed muscle mass. Within 3 minutes of succinylcholine
administration, the serum potassium reaches a peak and may cause
irreversible ventricular dysrhythmias and cardiac arrest. Because
of muscle supersensitivity, the severity of this reaction is virtually
independant of the dose of succinylcholine administered. Although
hyperkalemia can be modified somewhat by prior administration
of a nondepolarizing muscle relaxant, paralyzing doses are required
to eliminate it altogether. Supersensitivity becomes clinically
significant within about a week following denervating injury and
lasts for at least 6 months to 2 years. Thus, although succinylcholine
is safe in the first days of paraplegia, it should be avoided
completely after the third or fourth day.
Autonomic hyperreflexia
The chronic phase in which spinal reflexes reappear
is characterized by autonomic hyperreflexia in a high proportion
of patients. Cutaneous, proprioceptive, and visceral stimuli,
such as urinary bladder distention, may cause violent muscle spasm
and autonomic disturbances. The symptoms of autonomic hyperreflexia
are facial tingling, nasal obstruction, severe headache, shortness
of breath, nausea and blurred vision. The signs are hypertension,
bradycardia, dysrhythmias, sweating, cutaneous vasodilation above
and palor below the level of the spinal injury, and occasionally
loss of consciousness and seizures. The precipitous blood pressure
increase may lead to retinal, cerebral, or subarachnoid hemorrhage,
increased myocardial work and pulmonary edema. Patients with chronic
spinal cord lesions above T-6 are particularly at risk for this
response: 85 % will display autonomic hyperreflexia at some time
during the course of daily living. Of course, surgery is a potent
stimulus to autonomic response even in patients who give no history
of the problem.
The neuroanatomic pathway of this syndrome have
been known for a long time (figure 2). Afferent impulses enter
the isolated spinal cord and elicit reflex autonomic output over
the entire sympathetic outflow below the level of injury, which
is not modulated by higher centers as in the neurologically intact
subject. This causes vasoconstriction below the level of injury
and resultant hypertension, which stimulates baroreceptors and
may cause bradycardia via intact vagal pathways to the heart and
vasodilation via intact pathways above the injury.
Therapeutic methods to reduce the hypertension of
autonomic hyperreflexia must act below the level of injury. Ganglionic
blockers, alpha-adrenergic blockers, catecholamine depleters,
direct vasodilators, and general or regional anesthesia have been
recommended for prevention or treatment of autonomic hyperreflexia.
Cervical Spine Fracture
management
Evaluation of the possibility
of a cervical spine fracture There is a key association
between cervical spine injury and neck pain or tenderness in alert
trauma patients. Alert patients without neck pain or tenderness
should not have a cervical injury and should not require further
cervical spine evaluation, neck immobilization, or special precautions
during airway management. This criteria must be applied stringently,
however. If a patient has the slightest amount of neck discomfort,
is not fully alert, or has other very painful injuries, cervical
spine precautions must be maintained until the absence of lesion
is demonstrated.
The standard radiologic evaluation
consists of 3 views: the cross-table lateral, anterior- posterior,
and open-mouth view. All 7 vertebrae must be examined because
20%-30% of all C-spine injuries are at C-7. Pulling the arms and
shoulders caudad may be necessary to see C-7. If this is insufficient,
raising the arm closest to the film over the head and depressing
the opposite arm (the swimmer’s view) may expose it. In doubt,
computed tomography (CT) scan is considered the “gold standard”.
It is superior to plain films in identifying injuries at C-1 or
C-2, showing fine detail and resolving tissue densities. Fractures
in an axial plane are difficult to identify by CT scan and ligamentous
injuries may not be appreciated.
A radiologist should evaluate
emergency C-spine films, but the anesthesiologist should have
the skill in reading them also, as the condition of the spine
will usually affect the approach for airway management. Evaluation
includes the alignment of the vertebrae, the condition of the
bones and cartilage, and the width of the soft tissue spaces and
intervertebral spaces.
Alignment is best assessed
by tracing four anatomic lines on the cross-table lateral view.
Compression fractures appear as wedging and increased density
of the anterior part of the vertebral body or loss of more than
3 mm body height anteriorly. Spinous processes, vertebral bodies,
and transverse processes should be aligned from one level to the
next on the anteroposterior view. On the open-mouth view, the
gap between the lateral masses of C-1 and the dens should be equal
on the right and the left sides, and the lateral masses should
not extend beyond the body of C-2. Deviation indicates a fracture
of the vertebral arch of C-1, a Jefferson fracture. Assessment
of cartilage includes the disk spaces and facet joints. The disk
spaces should be uniform and of roughly equal height and width
at all levels. The facet joints, the articulations between the
lamina and pedicles of adjacent vertebrae, should be roughly the
same width at all levels.
Widening of the soft tissue
spaces suggests hemorrhage, edema, abscess, foreign body, or tumor,
and may be the only sign of an injury at C-1 or C-2. The space
between the anterior border of C-2 and the pharyngeal air density
should be no wider than 7 mm. The space between the air density
and the body of C-7 should be no greater than 2 cm. This is the
rule of 27: 2 cm maximum width at C-7 and maximum width at C-2
of 7 mm. Finally, atlantal fractures can be either stable or unstable.
In all cases, the atlantal ring is broken in at least 2 places.
Fractures of the ring in which the transverse ligament is intact
are stable, whereas fractures associated with ligament rupture
are unstable. Posterior movement of the dens greater than 3 mm
behind the anterior ring of the atlas implies significant injury
to the transverse ligament.
The cross-table lateral view
if used alone will be missing 15%-25% of cervical spine injuries.
The combination of the cross-table lateral, anterior-posterior,
and open-mouth views will be missing 8% of fractures. The missed
injuries were often unstable in the above studies. As the sensitivity
of plain films is only 75%-90%, negative plain radiographs cannot
be used as sufficient criteria for ruling out a cervical spine
fracture, especially if a patient is at high risk. High risk patients
include front-end motor vehicle accidents (>35 mph) without seatbelts,
head-first falls and equivocal C-spine roentgenograms. They are
believed to have at least a 10% chance of having a C-spine injury.
Given a 10% false-negative rate, a set of plain films negative
for spine injuries reduces the probability of an injury to 1%
(not 0%).
Cervical spine immobilization
The trauma patient's neck
must be immobilized as soon as help arrives at the scene of the
accident until complete evaluation shows that there is no injury.
Soft collars are unsatisfactory for immobilization because they
permit 75% of normal neck movement. Rigid collars, such as the
Philadelphia and the extrication collars, reduce flexion and extension
to about 30% normal and rotation and lateral movement to about
50%. The best immobilization method is to secure the patient to
a hard board from the head to feet, place sandbags at either side
of the head and put a rigid collar around the neck. This decreases
movement to about 5% of normal.
Airway management
Many airway management plans
would be reasonable for patients with potential cervical spine
injuries because there is no evidence for the superiority of any
individual tracheal intubation technique. The urgency of airway
intervention is the most important factor in planning airway management
for patients with potential C-spine injuries. Other considerations
include the assessment of the risk of cord injury with head and
neck movement, the airway anatomy, the patient’s degree of cooperation,
and the anesthesiologist’s expertise.
The safety of orotracheal
intubation for patients with potential C-spine injury has been
documented in recent years. For patients requiring immediate and/or
urgent airway control, we recommend rapid sequence induction followed
by orotracheal intubation with cricoid pressure and manual in-line
immobilization of the head and neck.Precise cervical spine in-line
immobilization should be maintained throughout the intubation
maneuvers. This technique, also called manual in-line axial traction
is an active process done by a second individual who is responsible
for applying a varying amount of force to counteract the movements
of the laryngoscopist, in an attempt to stabilize the cervical
spine. The patient lies supine with the head in neutral position;
an assistant applies manual in-line immobilization by grasping
the mastoid processes, whereupon the front of a rigid collar can
be removed safely; the collar can impede mouth opening, does not
contribute significantly to neck stabilization during laryngoscopy,
and will be an obstruction if surgical airway is required. This
technique of emergency airway management involves a minimum of
three, but ideally four individuals: the first to pre- oxygenate
and intubate, the second to apply cricoid pressure, the third
to maintain manual in-line immobilization of the head and neck
and the fourth to give intravenous drugs and assist.
For non-urgent and elective
airway control, we believe that awake, fiberoptic intubation technique
should be used. Although there is no proof that this method minimizes
C-spine movement, it does not depend on atlanto-occipital extension
and the head and the neck stabilizing devices can be left in place.
Conclusion References
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