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Georges Desjardins, MD FRCPC
Assistant Professor of Anesthesiology
University of Miami, Miami, FL
Anesthesiologists are often involved in the initial resuscitation and management of trauma victims with possible cervical spine injuries. They should recognize the situations in which such injuries are likely, be familiar with evaluation of the cervical spine, understand the pathophysiology of the spinal cord injuries and evaluate the risks and benefits of alternative approaches to anesthesia and airway management. We will review the management of injuries to the cervical spine and spinal cord, from the initial fracture to the chronic phase of the disease.
Few diseases or injuries have greater potential for causing death or devastating effects to the quality of life than cervical spine trauma. It involves people of all age; the age frequency peaks are 15-35 years and greater than 65 years of age. Cervical spine injuries occur in 1.5%-3% of all major trauma cases. The type of accidents include motor vehicle accidents (50%-70%), falls (6%-10%), diving accidents, blunt head and neck traumas, penetrating neck injuries and contact sports injuries. The incidence of cervical spine injuries in head trauma victims is 1%-3% in adults and 0.5% in children, no higher than the figures for trauma victims in general. At least 20% of the patients will have more than one cervical spine fractures. Twenty to 75% of the cervical spine fractures are considered unstable and 30%-70% of these have associated neurologic injuries to the spinal cord. In traumatized patients, 3%-25% of spinal cord injuries occur during field stabilization, transit to the hospital, or early in the course of therapy. This implies that, in order to prevent additional neurologic disability, care of any severely injured patient must include neck stabilization until cervical fracture is ruled out. Since the prognosis for recovery from complete cervical cord lesions is poor, emphasis must be placed first on preventing injury and second on preventing extension of neurologic injury once trauma has occurred.
The goals of resuscitation should be stabilization of the cervical spine, prevention of secondary injury, reduction of the fracture as soon as possible and protection of the spinal cord.
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.
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.
Many airway management of the trauma victim 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.
Anesthesiologists should be able to recognize situations in which cervical spine injuries are likely, be familiar with the evaluation of the cervical spine, understand the pathophysiology of spinal cord injuries and evaluate the risks and benefits of alternative approaches to anesthesia and airway management.
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