CH 25

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Alan M. Levine, M.D.
Copyright 2003 Elsevier Science (USA). All rights reserved.
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25
Initial Evaluation and Emergency Treatment of the Spine-Injured Patient
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Munish C. Gupta, M.D. Daniel R. Benson, M.D. Timothy L. Keenan, M.D.
BASIC CONSIDERATIONS
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Incidence, Etiology, and Demographics

Injury to the spinal column can be devastating. Some degree of neurologic decit occurs in 10% to 25% of patients at all levels of injury,10, 89 in 40% at cervical spine levels,10, 12, 89 and in 15% to 20% at thoracolumbar levels.10, 27 Even with the development of specialized spinal injury centers, the cost to society per patient remains staggering.28 The ultimate solution rests in prevention of the original injury, but in the meantime, those managing a patient with a spine injury can minimize the risk of further damage by using accepted techniques of initial transportation and treatment. A thorough understanding of the demographics, anatomy, and pathophysiology of spinal cord injury, use of logical algorithms for initial evaluation and treatment, and knowledge of the potential complications seen with specic patient populations are critical for optimal patient management. The magnitude of the problem and the difculties with past studies on the incidence rates of spinal injuries prompted the U.S. Centers for Disease Control and Prevention to establish spinal cord injury surveillance systems.23 The most recent estimates of incidence are generally unchanged from the previous estimates36, 112 of approximately 4.0 to 5.3 per 100,000 population.114 This incidence corresponds to 12,000 new spinal cord injuries every year for which treatment is sought and an additional 4800 patients who sustain spinal cord injuries but die before arrival at the hospital.112 The causes of spinal column and spinal cord injury are illustrated in Figure 251.10, 12, 13, 27, 89, 112 The most signicant cause of spinal column injury is motor vehicle accidents (45%), followed by falls (20%), sports-related accidents (15%), acts of violence (15%), and miscellaneous causes (5%). At the extremes of age, the role of falls increases from 9% in the 0- to 15-year-old group to 60% in those older than 75 years.112 The male-to-female ratio is
4:1. When a neurologic decit is associated with spinal column injury, the overall survival rate for all levels of injury is 86% at 10 years.111 The survival rate drops off for patients injured after age 29 to about 50% at 10 years. In patients older than 55 years, in nonwhites, and in quadriplegics, the leading cause of death is pneumonia. Accidents and suicides are most common in those younger than 55 years of age, in nonwhites, and in paraplegics.111 Although improvements in prevention and treatment have been slow in developing, they are clearly represented in the national statistics. The National Spinal Cord Injury Data Base reported fewer complete injuries and a higher percentage of incomplete spinal cord injuries in 1985 than in 1973,112 an improvement that can be attributed to better initial management. These changes evolved from severe deciencies in the emergency medical services, which were described in a classic report released by the National Academy of Sciences National Research Council Committee on Shock and the Committee on Trauma in 1966.22, 49 Progress in prevention was seen in a 14-year report from the National Football Head and Neck Injury Registry,115 which noted a decrease in the number of football-related cases of permanent quadriplegia and cervical fractures between 1976 (34 and 110 cases, respectively) and 1984 (5 and 42 cases, respectively). This decrease was attributed to tackling rules instituted in 1975 in which deliberate spearing and the use of the top of the helmet as the initial point of contact were banned. The establishment of spinal cord injury centers and the improvement in prehospital management of patients with spinal cord injuries have been of signicant benet in the overall outcome of such patients. The concept of a spinal cord injury center as a separate unit began at the Ministry of Pensions Hospital, Stoke Mandeville, England, under the supervision of Sir Ludwig Guttman in 1943. Founding of this unit was followed by the establishment in 1945 of a unit in Toronto, Canada, and later by the creation of eight units in Veterans Affairs hospitals in the United States. When compared with the outcomes in other centers, such
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Falls 20%
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MVA 45% Sports 15%
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Other 5%
Acts of violence 15%
FIGURE 251. Causes of spinal column and spinal cord injury. Abbreviation: MVA, motor vehicle accidents.
specialized facilities in the United States are credited with a shorter length of hospitalization, a lower rate of complications (e.g., urinary tract infection, pulmonary complications, decubitus ulcers), and therefore an overall lower cost of patient care. In addition, these centers have greatly lowered the percentage of complete versus incomplete injuries, with a decrease of 65% to 46% in one study113 and 20% to 9% in another.79
Anatomy and Pathophysiology

Understanding the conclusions drawn from the initial physical examination of a spine-injured patient requires a basic knowledge of the osseous and neurologic structures of the spinal column. Details of osseous structures and fracture patterns are presented in Chapters 28 through 31. Knowledge of fracture patterns allows the examining physician to assess the relative stability of the injury, the risk of an associated neurologic decit, and the indications for treatment. SPINAL CORD ANATOMY The spinal cord lls about 35% of the canal at the level of the atlas and then about 50% in the cervical and thoracolumbar segments. The remainder of the canal is lled with cerebrospinal uid, epidural fat, and dura mater. The cord has a variable diameter, with swellings in the cervical and lumbar regions for the exiting nerve roots of the plexuses. The myelomere, or segment of cord from which a nerve root arises, lies one level above the same-numbered vertebral body in the cervical and high thoracic levels. For example, the T7 myelomere lies at the level of the T6 vertebral body. The lumbar and sacral myelomeres are concentrated between the T11 and L1 vertebral bodies. The end of the spinal cord (i.e., the conus medullaris) is most commonly located at the level of the L1L2 intervertebral disc. The conus medullaris consists of the myelomeres of the ve sacral nerve roots.
The spatial relationships of the gray and white matter structures remain consistent throughout the length of the cord, but their proportions change according to the level. Because the white matter carries the long tract bers from the sacral, lumbar, thoracic, and cervical levels, it constitutes more of the cervical than the sacral crosssectional area. The gray matter, with its concentration of lower motor neurons, is predominant in the cervical and lumbar swellings, where the axons exit to the upper and lower extremities. Accurate examination of a patient with a spinal cord injury depends on understanding the reex arc and the organization of motor and sensory elements. Figure 252 presents a cross-sectional view of the spinal cord in the cervical region. The upper motor neuron, which originates in the cerebral cortex, crosses to the opposite side in the midbrain and then descends in the lateral corticospinal tract to synapse with its respective lower motor neuron in the anterior horn of the gray matter. The sacral bers of the corticospinal tract are the most peripheral and the cervical bers the most central (see Fig. 252). The lower motor neurons in the gray matter are organized with the extensor neurons anterior to the exor neurons. Upper motor neurons not crossing in the midbrain descend in the smaller ventral corticospinal tract. The ascending sensory input originates in an axon from a cell body located in the dorsal root ganglion within the vertebral foramen. Sensory input enters the posterior horn of the gray matter and travels beyond, depending on the type of sensation. Pain and temperature sensations cross immediately to the opposite level of the cord and ascend in the lateral spinothalamic tract. Touch sensation also crosses immediately and ascends diffusely but is carried primarily in the ventral spinothalamic tract. Proprioceptive position and vibratory sensation bers ascend in the posterior column (funiculus cuneatus, funiculus gracilis) and cross higher in the brain stem. The posterior column is structured with the sacral elements more peripheral and posterior relative to the lumbar, thoracic, and cervical levels. The reex arc (Fig. 253; e.g., bulbocavernosus) is a simple sensory motor pathway that can function without using ascending or descending white matter long tract axons. If the level of the reex arc is both physiologically and anatomically intact, the reex can function despite disruption of the spinal cord at a higher level. Below the level of the conus medullaris (L1L2 interspace), the spinal canal is lled with the cauda equina, with the motor and sensory roots yet to exit their respective intervertebral foramina distally. These roots are less likely to be injured because they have more room within the canal and are not tethered to the same degree as is the spinal cord. Furthermore, the motor nerve root is the lower motor neuron axon (peripheral nerve), which is known to be more resilient to trauma than central nervous tissue.
PATHOPHYSIOLOGY OF SPINAL CORD INJURY The pathophysiology of spinal cord injury can be divided into two partsprimary and secondary. Primary injury
CHAPTER 25 Initial Evaluation and Emergency Treatment of the Spine-Injured Patient
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Fasciculus gracilis Fasciculus cuneatus POSTERIOR S S L T
Lateral corticospinal tract L S Print Graphic
FIGURE 252. Transverse view of the spinal cord in the cervical region. Note that the sacral structures (S) are most peripheral in the posterior columns and the lateral corticospinal tracts. The extensors are also more lateral than the exors in the gray matter. Abbreviations: C, cervical structures; L, lumbar structures; T, thoracic structures.
CT Flexors Extensors
Presentation Lateral spinothalamic tract ANTERIOR Anterior corticospinal tract Anterior spinothalamic tract
occurs at the moment of impact to the spine. When the energy transmitted to the spinal column musculature, ligaments, and osseous structures exceeds the exibility of the spinal column, the spinal column and cord become
injured. Primary injury to the spinal cord can develop in two waysdirect injury by means of excessive exion, extension, or rotation of the spinal cord and indirect injury by impaction of displaced bone or disc material. Injury
FIGURE 253. The bulbocavernosus, a reex arc that is a simple sensorimotor pathway, can function without using ascending or descending white matter long tract axons.
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secondary to contusion and compression is most common and causes physiologic interruption rather than physical transection of the spinal cord. Secondary injury to the spinal cord occurs after the initial direct injury to neural tissue. The complicated events that take place on a chemical, cellular, and tissue level are not completely understood, however (Fig. 254). The cascade is interrelated and eventually leads to cavitation, largely because of cell death (Fig. 255). Cell death can occur as a result of necrosis or apoptosis. Necrosis is brought on by cellular swelling and mitochondrial and membrane damage. Apoptosis is programmed cell death that occurs normally but is evident to a greater extent in spinal cord injury. Chromatin aggregation and intact cellular organelles can be seen by electron microscopy, which can differentiate between apoptosis and necrosis.72 The three best known factors leading to cell death are exocytosis, inammatory mediators, and free radicals, but other factors can also be involved. Release of excitotoxins from damaged or hyperactive cells can liberate increased amounts of neurotransmitters, such as glutamate and aspartate. These excessive neurotransmitters can bring about an increase in Ca2+ entry into cells and cause an imbalance in the homeostasis of mitochondrial function
Normal spinal cord
Compression injury
Hemorrhage Print Graphic Acute stage Primary changes (minutes after injury) -Central hemorrhage Cavity formation
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Early secondary changes - Multiloculated cavitation of cord with apoptosis at the edges of the cavities
Wallerian degeneration and cell death of ascending tracts above lesion Late secondary changes - Central cavitation - Cell death of Wallerian degeneration and cell death oligodendrocytes of descending tracts below lesion in white matter
FIGURE 254. An illustrated sequence of the progression from acute primary to late secondary injury. (From Lu, J.; Ashwell, K.W.; Waite, P. Advances in secondary spinal cord injury: Role of apoptosis. Spine 25(14):18591866, 2000.)
Apoptotic cells
and swelling, which eventually leads to cell death. Free radicals such as O2, OH, and nitric oxide have been found to take part in cell injury through lipid, protein, and nucleic acid damage. Inammatory mediators such as prostaglandins and cytotoxins are produced by inammatory cells that enter the area of spinal cord damage through a break in the blood-brain barrier. Cytokines such as tumor necrosis factor- can lead to damage to oligodendrocytes. Arachidonic acids break down to prostaglandins, and eicosanoids can lead to an increase in free radicals, vascular permeability, change in blood ow, and cell swelling. The anatomic and morphologic changes in the spinal cord after injury have been well dened.3, 30, 31 Within 30 minutes of injury, multiple petechial hemorrhages are seen within the central cord gray matter. Direct disruption of the myelin sheath and axoplasm is also seen. Over the course of 1 hour, these changes extend progressively to the posterior of the cord. Several hours after injury, the hemorrhages tend to coalesce and progressive longitudinal necrosis is seen. Histologic and ultrastructural changes characteristic of edema are seen within 6 hours and are most severe 2 to 3 days after trauma. At 1 week after injury, cystic degeneration of the previously necrotic areas of the cord develops. Clinically, progressive neurologic deterioration after the initial spinal cord injury is uncommon.106 It is difcult to dene a point in the anatomic injury cascade at which secondary injury factors become important, but the recent success of some pharmacologic agents directed at the agents of secondary injury implies that intervention is possible to some degree. The initial mechanical injury disrupts neuronal activity in several ways. Microvascular endothelial damage and thrombus formation decrease local blood ow dramatically in the central gray matter without reperfusion. This effect is in contrast to the reperfusion that is frequently seen in the peripheral white matter at about 15 minutes after injury and that is probably induced by vasospasm. Primary injury also leads to altered systemic vascular tone and hypotension, thus worsening this probably reversible white matter hypoperfusion. Relative cord ischemia can play a major role in the secondary metabolic derangements of nervous tissue. A decrease in membrane-bound sodium potassium adenosine triphosphatase (N+,K+-ATPase) causes severe alterations in the product of high-energy phosphorylation and the subsequent lactic acidosis. Abnormalities in electrolyte concentration are believed to be associated with abnormal axonal conduction. Membrane damage and direct damage to intracellular organelles cause severe derangements in calcium homeostasis. Large intracellular shifts of calcium (Ca2+) induce further mitochondrial dysfunction with decreased energy production and eventual cell death. Uncontrolled inux of Ca2+ leads to the activation of phospholipases A2 and C, thereby resulting in accelerated breakdown of cellular membranes and the production of arachidonic acid and free radicals.59 Many recent advances in the treatment of acute spinal cord injuries have attacked this secondary injury cascade at various levels, with varying degrees of success.
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Spinal cord injury
Edema, tissue ischemia and anoxia cell energy supply

FIGURE 255. Pathways involved in cell death after spinal cord injury. (From Lu, J.; Ashwell, K.W.; Waite, P. Advances in secondary spinal cord injury: Role of apoptosis. Spine 25[14]:18591866, 2000.)
BBB breakdown and cell membrane injury
Release of excitotoxins from damaged and hyperactive cells
Microglial activations activity of antioxidants
extracellular glutamate Print Graphic Ca in cells ( Na in cells) Presentation
ion pumping Free radical release from cell metabolism and tissue breakdown
Proinflammatory cytokines NOS activation
Na in cells ( Ca in cells)
Phospholipase, Damage endonuclease, to cellular protein kinase Mitochondrial Repair macromolecules activation damage mechanisms Caspase Cytochrome C and calpain Survival release activation Activation of promoters apoptosis (Bcl-2, promoters Bcl-xL) Cell death (Bax, Bad)
SPINAL CORD REGENERATION The promotion of regeneration of spinal cord axons after injury so that the cord again becomes functional is a monumental challenge that has been approached in many ways. The use of neurotrophic factors such as nerve growth factor, brain-derived neurotrophic factor, neurotrophic factor 3, and ciliary neurotrophic factor has been shown to be helpful in vitro in regenerating axons. Delivery of these factors by cells programmed to secrete them has helped in long-term release directly inside the central nervous system (CNS) so that they do not also have to cross the blood-brain barrier. Growth-inhibiting factors have been identied that may inhibit axonal regeneration in the CNS. Antibodies to these factors increase the regeneration of axons.97 Electrical stimulation has also been shown to effect axonal growth, but the exact mechanism is not clear. Peripheral nerve and Schwann cell transplants have shown the ability to lead to regeneration of motor pathways.24, 51 Fetal spinal cord tissue has been successfully transplanted in neonates. Considerable functional recovery along with growth and regeneration of the cells has been observed.21, 116 Similar success has not occurred with transplantation in adults. Transplantation of olfactory glial cells, which appear to continue to divide in adulthood, has been reported to regenerate corticospinal tracts in an adult rat.70
Classication of Neurologic Injury

An initial responsibility of the examining physician in evaluating a patient with a spinal cord injury is to determine the extent of neurologic decit. A patient with an incomplete neurologic decit has a good prognosis for
at least some functional motor recovery, whereas functional motor recovery is seen in only 3% of those with complete injuries in the rst 24 hours after injury and never after 24 to 48 hours.12, 108 According to the Standards for Neurological Classication published by the American Spinal Injury Association (ASIA), a complete injury is one in which no motor and/or sensory function exists more than three segments below the neurological level of injury.5 Likewise, an incomplete injury is one in which some neurologic function exists more than three segments below the level of injury. Critical to this determination is the denition of level of injury. The ASIA denes it as the most caudal segment that tests intact for motor and sensory functions on both sides of the body. A muscle is considered intact if it has at least antigravity power (grade 3 out of 5) and if the next most cephalic level is graded 4 or 5.5 These denitions can make determination of completeness of an injury somewhat difcult. At least one study has found the simple presence or absence of sacral nerve root function to be a more stable and reliable indicator of the completeness of an injury.118 The concept of sacral sparing in an incomplete spinal cord injury is important because it represents at least partial structural continuity of the white matter long tracts (i.e., corticospinal and spinothalamic tracts). Sacral sparing is demonstrated by perianal sensation, rectal motor function, and great toe exor activity (Fig. 256). Electrical detection of sacral sparing by dermatomal somatosensory potentials has been reported but is not in common use.99 Comparison of the normal anatomy in Figure 252 with that of the injury depicted in Figure 257A reveals how preservation of only the sacral white matter is possible. Sacral sparing is dened as continued function of the sacral lower motor neurons in the conus
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medullaris and their connections through the spinal cord to the cerebral cortex. The presence of sacral sparing therefore indicates an incomplete cord injury and the potential for more function after the resolution of spinal shock. At the time of physical examination in the emergency room, sacral sparing may be the only sign that a lesion is incomplete; documentation of its presence or absence is essential. Waters and coauthors118 found that the presence of external anal sphincter or toe exor muscle power or the presence of perineal sensation accurately predicted the completeness of injury in 97% of 445 consecutive patients. In addition, for prognostic purposes, no patients with initial sacral sparing were found to have had complete injuries. After a severe spinal cord injury, a state of complete spinal areexia can develop and last for a varying length of time. This state, conventionally termed spinal shock, is classically evaluated by testing the bulbocavernosus reex, a spinal reex mediated by the S3S4 region of the conus medullaris (see Fig. 253). This reex is frequently absent for the rst 4 to 6 hours after injury but usually returns within 24 hours. If no evidence of spinal cord function is noted below the level of the injury, including sacral sparing, and the bulbocavernosus reex has not returned, no determination can be made regarding the completeness of the lesion. After 24 hours, 99% of patients emerge from spinal shock, as heralded by the return of sacral reexes.107 If no sacral function exists at this point, the injury is termed complete, and 99% of patients with complete injuries will have no functional recovery.107 One
exception to this dictum is an injury to the distal end of the spinal cord itself. A direct injury to the conus medullaris can disrupt the bulbocavernosus reex arc and thus make its absence an unreliable indicator of spinal shock. CLASSIFICATION SYSTEMS After a determination of its completeness, an injury can be further classied according to the severity of the remaining paralysis. Classication systems are useful because they allow patient outcomes to be compared within and between clinical studies. The most commonly used classication system is that of Frankel and colleagues,39 which divides spinal cord injuries into ve groups (Table 251). The ASIA has put forth the Motor Index Score, which uses a standard six-grade scale to measure the manual muscle strength of 10 key muscles or functions in the upper and lower extremities (Fig. 258). All the individual muscle groups, both right and left, are measured, with a possible maximal score of 100. The disadvantage of the Frankel score is that an innite continuum of injury severity is divided into ve discrete groups. However, because recovery and repair of injured neural tissue must occur through the injury site for an injury to move to a higher grade, improvement by one Frankel grade, especially improvement by two grades, is functionally quite signicant. On the other hand, the ASIA Motor Index Score represents injuries along a continuum, but an improvement does not necessarily
S3 S4 S5
S3 S5 S4
FIGURE 256. Sacral sparing may include perianal sensation, rectal tone, and great toe exion.
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Dorsal columns
Dorsal columns
T C
Lateral corticospinal tract
S L
T C
CT S L
CT S L
Lateral spinothalamic tract
Central cord syndrome
Posterior cord syndrome
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Dorsal columns Dorsal columns
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S L
T C
S L
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CT S L
CT
S L
Anterior cord syndrome
Brown-Sequard syndrome
FIGURE 257. A, This illustration of a central cord syndrome can be compared with Figure 252 to appreciate the spinal cord abnormality. An incomplete spinal injury can affect the more central but not the peripheral bers, thereby preserving the sacral white bers. Abbreviations: C, cervical structures; L, lumbar structures; S, sacral structures; T, thoracic structures. B, Anterior cord syndrome. The dorsal columns are spared, so that the patient retains some deep pressure sensation and proprioception over the sacral area and lower extremities. C, Posterior cord syndrome, a very rare traumatic lesion with clinical features similar to those of tabes dorsalis. D, Brown-Sequard syndrome, also known as hemisection syndrome. Patients have motor paralysis on the ipsilateral side distal to the lesion and sensory hypesthesia on the contralateral side distal to the level of the lesion.
represent recovery in the injured spinal segment. Instead, the improved score may represent recovery in the most caudal level of function in a complete injury or a generalized recovery of motor strength in previously weak but functioning muscles.
TABLE 251
INCOMPLETE SPINAL CORD INJURY SYNDROMES If an incomplete spinal cord injury is diagnosed by the protocols discussed, it can usually be described by one of several syndromes (Table 252). As a general rule, the greater the function distal to the injury, the faster the recovery and the better the prognosis.73 Central Cord Syndrome. Central cord syndrome, the most common pattern of injury, represents central gray matter destruction with preservation of only the peripheral spinal cord structures, the sacral spinothalamic and corticospinal tracts (see Fig. 257A). The patient usually presents as a quadriplegic with perianal sensation and has an early return of bowel and bladder control. Any return of motor function usually begins with the sacral elements (toe exors, then the extensors), followed by the lumbar elements of the ankle, knee, and hip. Upper extremity functional return is generally minimal and is limited by the
Frankel Classication of Neurologic Decit

Type A B C D E Characteristics
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Absent motor and sensory function Sensation present, motor function absent Sensation present, motor function active but not useful (grades 2/5 to 3/5) Sensation present, motor function active and useful (grade 4/5) Normal motor and sensory function
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Presentation
FIGURE 258. The worksheet for the American Spinal Injury Association (ASIA) motor index score. The motor strengths for the 10 muscles on the left side of the worksheet are graded on a scale of 0 to 5. All scores are added, for a total maximal score of 100. (Copyright, American Spinal Injury Association, from International Standards for Neurological and Functional Classication, Revised 1996.)
degree of central gray matter destruction. The chance of some functional motor recovery has been reported to be about 75%.109 Anterior Cord Syndrome. A patient with anterior cord syndrome has complete motor and sensory loss, with the exception of retained trunk and lower extremity deep pressure sensation and proprioception.98 This syndrome carries the worst prognosis for return of function, and only a 10% chance of functional motor recovery has been reported (see Fig. 257B).108 Posterior Cord Syndrome. Posterior cord syndrome is a rare syndrome consisting of loss of the sensations of
deep pressure and deep pain and proprioception, with otherwise normal cord function. The patient ambulates with a foot-slapping gait similar to that of someone aficted with tabes dorsalis (see Fig. 257C). Brown-Sequard Syndrome. Brown-Sequard syn drome is anatomically a unilateral cord injury, such as a missile injury (see Fig. 257D). It is clinically characterized by a motor decit ipsilateral to the spinal cord injury in combination with contralateral pain and temperature hypesthesia. Almost all these patients show partial recovery, and most regain bowel and bladder function and the ability to ambulate.109
TABLE 252
Incomplete Cord Syndromes

Syndrome Central Anterior Posterior Brown-Sequard Root
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Frequency Most common Common Rare Uncommon Common Description Usually quadriplegic, with sacral sparing; upper extremities affected more than lower Complete motor decit; trunk and lower extremity deep pressure and proprioception preserved Loss of deep pressure, deep pain, and proprioception Ipsilateral motor decit; contralateral pain and temperature decit Motor and sensory decit in dermatomal distribution Functional Recovery (%) 75 10 >90 30100
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Root Injury. The spinal nerve root can be injured along with the spinal cord at that level, or an isolated neurologic decit of the nerve root can occur. The prognosis for motor recovery is favorable, with approximately 75% of patients with complete spinal cord injuries showing no root decit at the level of injury or experiencing return of function.108 Those with higher cervical injuries have a 30% chance of recovery of one nerve root level, those with midcervical injuries have a 60% chance, and almost all patients with low cervical fractures have recovery of at least one nerve root level.109
pressure above 85 mm Hg results in a better neurologic outcome.
Resuscitation
Patients with spinal injuries are frequently the victims of major trauma and as such are at high risk for multiple injuries. Experience with such patients has documented a clear relationship between head and facial trauma and cervical spine injuries and between specic intrathoracic and abdominal injuries and thoracolumbar fractures. The evaluation and management of hypotension in these multiply injured patients have been the subject of much discussion. Although hemorrhage and hypovolemia are signicant causes of hypotension, one must be aware of the syndrome of neurogenic shock in patients with cervical and high thoracic spinal cord injuries. Neurogenic shock is dened as vascular hypotension plus bradycardia occurring as a result of spinal injury. In the rst few minutes after spinal cord injury, a systemic pressor response occurs through activation of the adrenal medulla. This state of hypertension, widened pulse pressure, and tachycardia subsequently gives way to a drop in pressure and pulse. Neurogenic shock is attributed to the traumatic disruption of sympathetic outow (T1L2) and to unopposed vagal tone, with resultant hypotension and bradycardia.50, 85 Hypotension with associated tachycardia is not caused by neurogenic shock, so another cause must be sought. A review of 228 patients with cervical spine injury revealed that 40 (69%) of 58 patients with systolic blood pressure lower than 100 mm Hg had neurogenic shock.103 The remaining 18 patients had hypotension caused by other associated major injuries. Another study demonstrated that victims of blunt trauma with associated cervical spinal cord injury rarely sustain signicant intra-abdominal injuries (2.6%).2 Nonetheless, hemodynamic instability strongly suggested occult intra-abdominal injuries. The degree of hypotension and bradycardia and the incidence of cardiac arrest are directly related to the Frankel grade. For example, in a study of 45 patients with acute cervical spinal cord injury, 87% of Frankel A patients had a daily average pulse rate lower than 55 beats per minute, 21% had a cardiac arrest, and 39% required the administration of atropine or a vasopressor. Among the Frankel B patients, 62% had average pulses lower than 55 beats per minute, and none had cardiac arrest or needed vasopressors.85 A more recent study demonstrated that spinal cord injury secondary to penetrating trauma is distinctly different from that caused by blunt trauma with respect to the origin of hypotension.119 Penetrating injuries rarely result in neurogenic shock. Of 75 patients with a penetrating spinal cord injury, only 5 (7%) showed classic signs of neurogenic shock, and of the patients in whom hypotension developed, only 22% were found to have a neurogenic origin of their shock. As in all patients with major trauma, hypotension should be assumed to be caused by an injury involving major blood loss, especially in those with penetrating trauma.119 No matter what the cause of the hypotension, support
MANAGEMENT
Accident Scene Management

The initial evaluation of any trauma patient begins at the scene of the accident with the time-honored ABCs of resuscitation, such as the advanced trauma life support (ATLS) method described by the American College of Surgeons.1 The ABC (airway, breathing, and circulation) method can be described more accurately as A (airway), B (breathing), and C (circulation and cervical spine). All patients with potential spine injuries arriving at the emergency department should be on a backboard with the cervical spine immobilized. A spinal column injury should be suspected in all polytrauma patients, especially those who are unconscious or intoxicated and those who have head and neck injuries. Suspicion of a spine injury must begin at the accident scene so that an organized extrication and transport plan can be developed to minimize further injury to neural tissue. Regardless of the position in which found, the patient should be placed in a neutral spine position with respect to the long axis of the body. This position is achieved by carefully placing one hand behind the neck and the other under the jaw and applying only gentle stabilizing traction.49 An emergency two-piece cervical collar is then applied before extrication from the accident scene. Any patient wearing a helmet at the time of injury should arrive at the emergency room with it still in place unless a face shield that cannot be removed separately from the helmet is obstructing ventilation, a loose-tting helmet is preventing adequate cervical spine immobilization, or the paramedic has been trained in helmet removal.4 A scoop-style stretcher is now recommended for transfer; previously recommended maneuvers such as the four-man lift and the logroll have been shown to cause an excessive amount of motion at thoracolumbar fracture sites.77 The victim on a scoop stretcher is then placed immediately onto a rigid fulllength backboard and secured with sandbags on either side of the head and neck and the forehead taped to the backboard.86 The method of transportation and initial destination are determined by a multitude of factors, including but not limited to the medical stability of the patient, distance to emergency centers, weather conditions, and the availability of resources. Vale and colleagues117 have shown that keeping the mean blood
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of blood pressure is critical in the early hours after spinal cord injury. As described previously, localized spinal cord ischemia is an important cause of late neurologic disability. As the injured spinal cord loses its ability to autoregulate local blood ow, it is critically dependent on systemic arterial pressure.32 Hypotension needs to be aggressively treated by blood and volume replacement and, if indicated, by emergency surgery for life-threatening hemorrhage and appropriate management of neurogenic shock. The initial treatment of neurogenic shock is volume replacement, followed by vasopressors if hypotension without tachycardia persists despite volume expansion. The patients legs should be elevated to counteract venous pooling in the extremities. Fatal pulmonary edema can result from overinfusion of a hypotensive patient with a spinal cord injury.50 Endotracheal suctioning is a cause of severe bradycardia and can induce cardiac arrest, which is attributed to vagal stimulation. Repeated doses of atropine may be necessary to maintain the heart rate, and vasopressors may be necessary to maintain blood pressure. Use of a gentle sympathomimetic agent (e.g., phenylephrine) may also be helpful.
Assessment
After the patient arrives at the emergency department, rapid assessment of life-threatening conditions and emergency treatment are begun in a logical, sequential manner as dictated by the ATLS protocols.1 The primary survey includes assessment of airway, breathing, circulation, disability (neurologic status), and exposure (undress the patient) (ABCDE). As resuscitation (described earlier) is initiated, a secondary survey is begun that includes evaluation of spinal column and spinal cord function. The evaluation usually starts with a physical examination, with a more detailed history elicited later. The only part of the initial assessment that absolutely pertains to the spine is the emergency need for a lateral cervical spine radiograph (from the occiput to the superior end-plate of T1) to establish the safest means of maintaining an airway. A patient suspected of having a spine injury should, before intubation, have the airway maintained with a jaw thrust maneuver rather than a head tilt method. An unconscious or intoxicated patient is difcult to assess in terms of pain and motor sensory function. Careful observation of spontaneous extremity motion may be the only information that can be obtained about spinal cord function, and a detailed examination may have to be delayed until the patient can cooperate. An unconscious patients response to noxious stimuli and the patients reexes and rectal tone can provide some information on the status of the cord. Similarly, spontaneous respirations with elevation and separation of the costal margins on inspiration indicate normal thoracic innervation and intercostal function. Unconscious patients should be rolled onto their side with the cervical spine immobilized while on a full-length backboard, and the entire length of the spine should be inspected for deformity, abrasions, and ecchymosis. The spine should be palpated for a step-off or interspinous widening. The locations of lacerations and abrasions on the skull
are critical for determination of cervical injuries. Occipital lacerations suggest exion injuries, whereas frontal or superior injuries suggest extension or axial compression, respectively. The presence of a single spinal injury does not preclude inspection of the rest of the spine. Any associated head and neck trauma should increase the suspicion of cervical spine injury, and any thoracic or abdominal trauma (e.g., shoulder or lap seat belt markings) should raise suspicion of a thoracolumbar spine injury. Clear patterns of associated injuries should be recognized. For example, in addition to the relationship between head trauma and cervical spine injury, the presence of multiple fractured ribs and chest trauma can suggest thoracic spine injury. Massive pelvic injuries are frequently associated with exion-distraction injuries of the lumbar spine. Finally, falls from heights resulting in calcaneal or tibial plafond fractures are frequently associated with injuries to the lumbar spine. A responsive patient who is hemodynamically stable can be examined in greater detail. Inspection and palpation of the entire spine should be performed as described for an unconscious patient. The patient should be asked to report the location of any pain and to move the upper and lower extremities to help localize any gross neurologic decit. If possible, the patient should be questioned about the mechanism of injury, any transient neurologic symptoms or signs, and any preexisting neurologic signs or symptoms. The upper (Fig. 259) and lower (Fig. 2510) extremities are examined for motor function by nerve root level. The motor examination includes a digital rectal examination for voluntary or reex (bulbocavernosus) anal sphincter contraction. The sensory examination includes testing of the dermatomal pattern of the proprioceptive and pain temperature pathways, as described previously (Fig. 2511). The sharp dull sensation of a pin tip is considered to reect a pain pathway (lateral spinothalamic tract), and this sensation should also be tested in the perianal region. The presence of pinprick sensation around the anus or perineal region may be the only evidence of an incomplete lesion. Proprioception (posterior columns) can be tested easily by having the patient report the position of the toes as up, down, or neutral as the examiner moves them. Temperature sensation (lateral spinothalamic tract) is difcult to establish in the often loud and busy emergency room setting, and testing for this function is usually deferred until a later time. The areas of sensory decit should be accurately recorded, dated, and timed on the medical record progress note or a spinal injury ow sheet. It is also recommended that the sensory level be marked, dated, and timed in ink on the patients skin at the affected level. The practice of marking the sensory level on the skin can avoid much uncertainty when a number of examiners are involved. Figure 2512 reviews the locations of the upper and lower extremity stretch reexes and their nerve roots of origin. If spinal shock is present, all reexes may be absent for up to 24 hours, only to be replaced by hyperreexia, muscle spasticity, and clonus. If a spine injury patient with a neurologic decit has a concomitant head injury, it is important to distinguish between the cranial upper motor neuron lesion and a spinal cord lower motor neuron injury.
C5 C6
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FIGURE 259. An examination of the upper extremities must include, at a minimum, the muscle groups that are designated by their respective nerve root innervation. These are C5, elbow exion; C6, wrist extension; C7, nger extension; C8, nger exion; and T1, nger abduction. The strength (0 to 5) should be listed on the time-oriented ow sheet.
C7
Presentation
C7 C8 T1
L5 L1-L2
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L3-L4
L5-S1 Presentation S1
FIGURE 2510. An examination of the lower extremities needs to include at least these muscle groups, designated by their respective nerve root innervation: L1L2, hip abductors; L3L4, knee extension; L5S1, knee exion; L5, great toe extension; and S1, great toe exion.
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The presence of extremity stretch reexes in a patient without spontaneous motion of the extremities or a response to noxious stimuli implies an upper motor neuron lesion. The absence of these reexes in the same setting implies lower motor neuron injury of the spinal cord. The plantar reex in the lower extremity is elicited by
stroking the plantar aspect of the foot rmly with a pointed object and watching the direction of motion of the toes. A normal plantar reex is plantar exion of the toes. An abnormal plantar reex (Babinskis sign), in which the great toe extends and the toes splay out, represents an upper motor neuron lesion. Similar information can be obtained by running a nger rmly down the tibial crest;
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Presentation
FIGURE 2511. Sensory dermatome chart. Note that C4 includes the upper chest just superior to T2.
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L4
C5
FIGURE 2512. Stretch reexes and nerve roots of origin.
C6
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C7 Presentation S1
abnormal great toe extension with splaying of the toes (Oppenheims sign) constitutes evidence of an upper motor neuron lesion. Other signicant reexes include the cremasteric, the anal wink, and the bulbocavernosus reexes. The cremasteric reex (T12L1) is elicited by stroking the proximal aspect of the inner part of the thigh with a pointed instrument and observing the scrotal sac. A normal reex involves contraction of the cremasteric muscle and an upward motion of the scrotal sac, whereas an abnormal reex involves no motion of the sac. The anal wink (S2, S3, S4) is elicited by stroking the skin around the anal sphincter and watching it contract normally; an abnormal reex involves no contraction. The bulbocavernosus (S3, S4) reex (see Fig. 253) is obtained by squeezing the glans penis (in a male) or applying pressure to the clitoris (in a female) and feeling the anal sphincter contract around a gloved nger. This response can usually be elicited more easily by gently pulling the Foley catheter balloon against the bladder wall and feeling the anal sphincter contract. The bulbocavernosus reex examination in a catheterized female can be misleading; the Foley balloon can be pulled up against the bladder wall and thus be felt by a ngertip that is past the anal sphincter, with this response being misinterpreted as contraction of the anal sphincter. Not uncommonly, a more detailed history is delayed until the patient is hemodynamically stable and the overall neurologic status can be determined. In addition to a routine review of systems, the patient should be specically questioned regarding previous spine injury, previous neurologic decit, and details of the mechanism of injury. If the patient cannot respond, an attempt should be made to interview family members in person or by telephone. At some time during the physical examination, the initial lateral cervical spine radiograph should be available for review. It should rst be examined to ensure that the interval from the occiput to the superior end-plate of T1 can be seen clearly. If the radiographic appearance is normal, the remainder of the cervical spine series is obtained. Interpretation of the lm is discussed in Chapter 26. Under no circumstances should spine precautions be removed until the cervical spine and any suspicious areas
of the thoracolumbar spine have been cleared radiographically. In the assessment of a polytraumatized patient, the association between thoracolumbar fractures and other high-energy internal injuries (i.e., aortic and hollow viscus injuries) must be kept in mind. Because these patients thoracolumbar spines cannot be cleared of injury on clinical grounds, anteroposterior and lateral thoracic and lumbar spine lms should be obtained on a routine basis. In addition, the 10% incidence of noncontiguous fractures must be kept in mind in a patient with multiple injuries.61 For example, the presence of a thoracolumbar burst fracture requires review of a complete plain radiographic series of the cervical, thoracic, and lumbar spine in any patient who is unable to fully cooperate or accurately report pain during the physical examination.
Special Studies
After the initial cross-table lateral cervical spine radiograph, a complete cervical spine series should be obtained. Several studies have reported that a technically adequate radiographic series consisting of a cross-table lateral view, an anteroposterior view, and an open-mouth odontoid view is almost 100% sensitive for detecting cervical injuries.29 In the trauma situation, it can be difcult to see the atlantoaxial articulation and the cervicothoracic junction, so additional studies may be needed. A limited computed tomographic scan through the C7 to T1 levels can rule out signicant cervicothoracic junction injuries; however, most studies have shown such imaging to have very low yield. In addition, computed tomography may be required to clear the C1C2 levels if plain radiographs are equivocal.94 In an awake, conversant patient, the physical examination can be used to guide further imaging studies. Numerous studies have demonstrated the occurrence of concomitant spinal fractures.61 Therefore, if a cervical fracture is identied, especially in a patient with a spinal cord lesion, radiographs of the entire thoracic and lumbar spine are indicated. Magnetic resonance imaging (MRI) has found an increasing role in the evaluation of patients with spine
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injuries. In a patient who has a clinical spinal cord injury and minimal or no bony or ligamentous injury on other imaging studies, MRI is useful for the identication of soft tissue (ligamentous or disc) injuries, as well as abnormalities of the spinal cord itself. Findings on MRI have been shown to have some prognostic signicance with respect to the severity of spinal cord injury and neurologic recovery.55, 83 In children, the syndrome of spinal cord injury without radiographic abnormality (SCIWORA) has been described,8, 56 and more recently, the use of MRI to better dene these injuries has proved useful.48 MRI has found an important role in the evaluation of intervertebral discs in cervical dislocations35, 91 (see later discussion and ligamentous description66). Transportation of a cervical spine injury patient in skull traction can be done safely with the patient in a hospital bed, on a gurney, or in a Stryker frame, as long as a traction pulley unit is used. The use of a Stryker frame has been associated with loss of reduction after turning and with worsening of neurologic decits, especially in those with lumbar spine injuries.102 Traction can be compromised while the patient lies on the radiographic table and the rope hangs over the table edge without the use of a pulley. Disturbance of the magnetic eld of MRI by the ferrous elements of traction equipment presents a problem, but solutions are being sought. A traction system has been described in which nonferrous zinc pulleys are bolted to an aluminum ladder with water traction bags attached to the halo ring by nylon traction rope.76 A patient with a high cervical spine injury and dependence on a ventilator who needs MRI studies must be ventilated by hand or with a nonferrous ventilator.80 A patient with a thoracolumbar spine injury is easier to manage because plastic construction backboards can now be used during conventional radiographic and MRI studies. Experimental in-board traction sets can allow transport of cervical cord injury patients without the danger of free weights.
Intervention
Once a spine-injured patient is resuscitated adequately, the mainstay of treatment is prevention of further injury to an already compromised cord and protection of uninjured cord tissue. Realignment and immobilization of the spinal column remain critical to this end. Other life-threatening issues in a multiply injured trauma patient may take precedence over time-consuming interventions related to the spine. Perhaps the most rapidly evolving interventions toward limiting the degree of neurologic injury have been pharmacologic. PHARMACOLOGIC INTERVENTION The most studied and clinically accepted pharmacologic intervention for a patient with a spinal cord injury has been high-dose intravenous methylprednisolone (MPS). The efcacy of glucocorticoids has been studied since the mid-1960s. In animal studies, high doses of MPS given intravenously after spinal cord injury lessened the degree of post-traumatic lipid peroxidation and ischemia, prevented neuronal degradation, and allowed improved
neurologic recovery.52 The initial National Acute Spinal Cord Injury Study (NASCIS I) attempted to work out an appropriate dosage for MPS but failed to show a difference in outcome between patients who received a 100-mg bolus per day for 10 days and those who received 1000 mg/day for 10 days. In fact, the high-dose regimen was associated with an increased risk of complications.16 A second multicenter randomized trial compared MPS, naloxone, and placebo. The results of the NASCIS II study, completed in 1990, showed that patients who were treated with MPS within 8 hours had improved neurologic recovery at 1 year, regardless of whether their injury was complete or incomplete.18, 19 Naloxone treatment was no better than the control. When MPS was given at a point longer than 8 hours after injury, patients recovered less function than did placebo controls. A predictable trend toward increased complications was seen in the steroid group, including a twofold higher incidence of wound infection (7.1%); these differences, however, were not statistically signicant. Critics of this study question the signicance of the improvement in treated patients because the neurologic grading system used did not report a true level of patient function.34 Nonetheless, this study has made acute treatment with MPS a standard of care for patients with a spinal cord injury. The NASCIS II trial established a dosing schedule of an initial intravenous bolus of 30 mg/kg, followed by a continuous infusion of 5.4 mg/kg/hr for 23 hours. Many centers are now administering a 2-g bolus of MPS in the ambulance or at the accident scene in keeping with the intuition that the earlier the steroid is administered after injury, the better the outcome. The third multicenter randomized trial, NASCIS III, is completed.20 One treatment arm in this study is the standard MPS bolus and 23-hour infusion; a second arm extends the infusion another 24 hours. The third treatment arm consists of the initial MPS bolus followed by a 10-mg/kg/day dose of tirilazad mesylate for 48 hours. Tirilazad mesylate is a 21-aminosteroid compound, a group of MPS analogues that lack the hydroxyl function necessary for glucocorticoid receptor binding. Theoretically, these drugs possess no glucocorticoid activity but are potent inhibitors of lipid peroxidation. The negative systemic side effects seen with prolonged use of high-dose MPS should be signicantly reduced.15 The study showed that the high-dose steroid regimen was effective only when given within 8 hours after injury. If the steroid bolus recommendation is administration of the bolus within 1 to 3 hours, the drip should be continued for 24 hours. If the bolus is given between 3 and 8 hours after injury, the drip should continue for 48 hours rather than 24 hours. This difference may increase the risk of complications but at the same time should make the neurologic outcome better. Reanalysis of the data from NASCIS II and III has not demonstrated a statistically solid benecial effect. Additionally, no other pharmacologic agent has been shown to be effective in modulating secondary damage. The results of these studies have inspired some heated debate in the literature.82, 101 Gangliosides are complex acidic glycolipids present in high concentration in the membranes of CNS cells. Experimental evidence has shown that these compounds
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augment regeneration and sprouting of neurons in vitro and restore neural function after injury in vivo.45 A prospective, randomized, placebo-controlled trial of GM1 ganglioside in patients with spinal cord injury showed that GM1 enhanced motor recovery when compared with placebo controls.45 However, only 16 patients received GM1 once a day for 18 to 32 days, with the rst dose given within 72 hours. All patients received initial treatment with steroids at a dose much less than the current standard dose. Analysis of the results showed that improved motor scores in both the Frankel and ASIA grading systems were attributable to restoration of power in initially paralyzed muscles rather than improvement in strength in previously weak muscles. The authors postulated that GM1 allows for enhanced recovery of effectiveness in initiating the motor response of the circumferential white matter. Current trials exploring combination therapy with GM1 and MPS are under way. The combination of the early antioxidant effects of high-dose bolus MPS and the late neuronal recovery effects of GM1 may produce greater than additive benets.44 Opiate receptor blockade has been an attractive target for pharmacologic manipulation of the injury process. Theoretically, release of endogenous opiates can cause systemic hypotension and a decrease in spinal cord blood ow. Naloxone and thyrotropin-releasing hormone (TRH) have been studied extensively in animal models and have shown variable success in improving neurologic recovery.22, 54, 78, 106 The results of the NASCIS do not support the use of naloxone in humans because it performed no better than controls. Clinical trials of a more stable analogue of TRH (longer half-life) are under way. Various other agents have shown variable promise in the laboratory but remain unproved in clinical trials. The antioxidant effects of vitamin E have been shown to be useful, but the need to give the drug before injury limits its application.6 Calcium channel blockers have been used in an attempt to minimize the calcium-modulated elements of the secondary injury cascade, but published reports have been variable and clinical use is controversial.100 An endothelial receptor antagonist has been shown to prevent and delay the degeneration of axons after spinal cord injury in rats. Osmotic diuretics used to reduce edema in head trauma (mannitol, low-molecular-weight dextran) failed to provide evidence of clinical effectiveness with regard to spinal cord injury.59, 87 Table 253 summarizes the most frequently studied drugs used for the treatment of spinal cord injury in humans. PHYSICAL INTERVENTION After administration of the standard high-dose steroid NASCIS protocol, an assessment of the overall alignment of the spinal column (and therefore the cord) should be made. Any malalignment or dislocation causing the neural elements to be under a severe degree of tension should be noted. Although treatment of the spinal injury cannot alter the initial trauma, experimental evidence has shown that immediate immobilization protects the spinal cord.33 In addition, it has been demonstrated experimentally that continued compression causes additive detrimental effects that result in ischemia and electrophysiologic changes in
TABLE 253
Pharmacologic Agents for Spinal Cord Injury

Agent Methylprednisolone (MPS) Tirilazad mesylate GM1 ganglioside Naloxone
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
Mechanism of Action Membrane stabilization by decrease in lipid peroxidation, prevention of inammatory cascade Same as MPS, lacks glucocorticoid activity Augmentation of neuron regeneration Blocks effects of endogenous opiates that cause local and systemic hypotension and spinal cord ischemia Same as naloxone
Thyrotropin-releasing hormone
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz
the injured spinal cord.47 A highly unstable situation may allow an already severely injured cord to undergo repeated injury with the slightest movement. Examination of the dorsal skin may reveal an impending breakdown over a kyphotic deformity, in which case urgent reduction is imperative. If the neurologic injury can be determined to be a complete injury (i.e., the bulbocavernosus reex is intact), realignment may proceed at a less urgent pace. An exception may be in the cervical spine, where urgent reduction may improve the rate of root-sparing recovery. In an incomplete lesion, reduction and stabilization should be performed as quickly as possible to minimize continued neurologic injury. In the cervical spine, such management frequently involves the application of skull traction. In the thoracolumbar spine, traction is less successful, so if positioning does not restore anatomic alignment, emergency surgical reduction is required. The role of pretraction MRI became a focus of debate after Eismont and colleagues,35 among others,74, 93 reported neurologic deterioration in patients with cervical dislocations after they underwent traction and reduction. The high incidence of disc herniations with facet dislocations91 prompted these authors to advocate that an MRI study be obtained before closed reduction of the cervical spine is attempted. Several large studies have refuted this contention by showing no worsening of neurologic levels with closed traction and reduction in awake, cooperative patients.25, 65, 105 Nonetheless, expediency is of the utmost importance in the reduction of patients with incomplete injuries. If it can be obtained quickly without putting an unstable patient at risk during transportation, pretraction MRI is reasonable. In many centers, such studies are difcult to obtain within several hours. MRI is required if the patient is otherwise uncooperative, fails closed reduction, or requires reduction under anesthesia for any reason. If MRI demonstrates disc herniation, anterior discectomy plus fusion is performed before other surgery is attempted. If operative reduction of a thoracolumbar dislocation is planned, MRI should be obtained and operative plans modied based on the results. After adequate alignment and stabilization, further diagnostic studies, such as computed tomography (or MRI, if not obtained previously), can be performed on a less urgent basis. Frequent neurologic examinations, preferably
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by the same physician, should be documented and recorded, especially when the patient is returned after diagnostic tests. If worsening of a neurologic decit is documented, emergency surgical decompression is indicated. In a patient with a stable or improving spinal cord injury, the timing of surgical stabilization, if needed, is controversial. In the case of a polytrauma victim, early stabilization, whether in a halo vest or by surgery, has been shown to improve overall outcome and shorten the hospital stay.37 An overview of a suggested algorithmic approach to a spine-injured patient is shown in Figure 2513. Although such an algorithm tends to oversimplify a complicated
decision-making process, adherence to a dedicated protocol provides a basic framework from which to manage these often multiply injured, complicated patients. In patients with isolated injuries, as well as those with complicated multiple injuries, a simple, reliable method of cervical and thoracolumbar immobilization is necessary to safely perform a complete evaluation. The most effective method of initial cervical immobilization is the use of bilateral sandbags and taping of the patient across the forehead to a spine board, along with the use of a Philadelphia collar (which serves to limit extension).86 In the cervical spine, a soft collar, extrication collar, hard collar, or Philadelphia collar alone is probably not
Spine-Injury Patient
Extrication Spinal stabilization Transportation
ATLS protocols Resuscitation
Plain radiographs entire spine
MPS protocol 30 mg/kg IV 5.4 mg/kg/hr x 23 hrs
NO
Neurology intact ?
YES
Plain radiographs
MRI R/O disc herniation
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Severe malalignment dislocation ? NO
YES Emergent
Closed realignment traction
YES
Severe malalignment dislocation ? NO
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Further diagnostic studies as needed CT scan, MRI
FIGURE 2513. An algorithmic approach to the spine injury patient. Abbreviations: ATLS, advanced trauma life support; CT, computed tomography; MPS, methylprednisolone; MRI, magnetic resonance imaging; R/O, rule out.
YES
Alignment adequate ? NO
YES
Further diagnostic studies as needed CT scan, MRI
Worsening neurologic deficit NO
YES Emergent
MRI R/O disc herniation
Neurology incomplete ? NO Complete injury
YES Urgent
Surgical reduction/decompression stabilization
"Elective" OR Definitive closed treatment
YES "Elective"
OR
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in an uncooperative patient. Gardner-Wells tongs can be applied with minimal skin preparation and without assistance. The halo ring allows axial traction for reduction and provides rather stable immobilization with the application of a vest, but in a busy polytrauma setting, its application requires an assistant, and it takes longer to apply than Gardner-Wells tongs. Gardner-Wells Tongs The halo should be applied for initial stabilization of cervical spine injuries only if prolonged halo vest or cast immobilization is planned. If short-term traction followed by surgical stabilization and nonhalo external immobilization is planned, the use of Gardner-Wells tongs is preferred. Gardner-Wells tongs are easily applied by one person and without anterior pin sites. Gardner-Wells tongs (Fig. 2514) are fast and easy to apply, with no assistance required. Directions for use are generally located on the tongs (Fig. 2515). The pins should be positioned below the temporal ridges at a point 2 cm above the external auditory canal and above the temporalis muscle (Fig. 2516). After shaving, the skin is inltrated with local anesthetic after the application of an antiseptic. The screws must be tightened symmetrically. The tongs are secure when the metal pressure pin protrudes 1 mm (Fig. 2517). Protrusion of the pressure indicator pin by 1 mm has been demonstrated in cadavers to provide a pull-off strength of 137 34 lb.64 Pressure indicator pin protrusion of as little as 0.25 mm can support up to 60 lb.64 It is recommended that the pin be tightened to 1 mm on the next day, but not again thereafter. Traction should be initiated at 10 lb and increased by 5to 10-lb increments. Reduction should be performed in awake patients with administration of intravenous mida-
Presentation
FIGURE 2514. MRI-compatible graphite Gardner-Wells tongs.
sufcient for immobilization.60, 86 A poster brace (e.g., four-poster brace) or cervicothoracic brace (SOMI brace) is not practical in the emergency setting. A standard long spine board is adequate for immobilization and turning of the thoracolumbar spine.77 Immobilization gear is removed only after radiographs have been interpreted as normal. An unstable or malaligned cervical spine requires either more stable immobilization or axial traction to achieve reduction. Specic indications for skull traction are discussed in Chapters 27 to 29. The concept of skull traction was introduced by Crutcheld in 1933,26 but the Crutcheld skull tongs for traction have been replaced by the Gardner-Wells40 and halo immobilization devices. Gardner-Wells tongs are a simple, effective means of applying axial traction for reduction, but they do not signicantly limit voluntary rotation, exion, or extension
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FIGURE 2515. Directions for use of the Gardner-Wells tongs are usually attached to the traction hook.
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FIGURE 2516. Correct position for the Gardner-Wells tongs is 1 to 2 cm above the external auditory canal and below the temporal ridge.
zolam if needed. Fluoroscopy or serial radiographs and serial neurologic examinations should be performed to avoid injury. In patients with neurologic symptoms or signs or 1-cm distraction of a disc space, closed reduction should be stopped and further images taken. Gardner-Wells tongs have been reported to undergo pin and spring wear with repeated use. The pins and the tongs should be inspected and replaced if necessary or the indicator given a lower pin pressure to prevent pull-out.67 Blumberg and associates11 have reported that the MRIcompatible titanium alloy Gardner-Well tongs are more predisposed to plastic deformation and slippage than stainless steel Gardner-Wells tongs. They warned against using MRI-compatible tongs for reduction, especially with weights greater than 50 lb. Tongs may be switched after reduction to a lower weight if MRI is needed. A halo ring compatible with MRI would be another option if MRI is needed. Halo Ring Application A halo ring can be applied in the emergency department when denitive treatment is anticipated to be in a halo or in cases in which distraction should not be applied through Gardner-Wells tongs. Placing a halo vest underneath the patient during transfer to the bed can help attach the ring to the vest while the patient is in traction after reduction. Open halo rings offer the advantage over previous whole rings of being able to put the ring on without putting the patients head on a head holder off the stretcher. The correct ring size is selected according to head circumference. The ring is placed around the head, the pin holes in the ring are used to identify the posterolateral pin sites, and the hair is shaved in these areas. The ring can be held in place temporarily with three plastic pod attachments. The skin is prepared, and local anesthetic is inltrated through the ring holes. Placement of the halo pins too high on the convexity of the skull can result in slippage of the ring, especially with traction. Placement of the anterior pin, as determined by skull osteology41 and by supraorbital nerve anatomy, is best at a point in the middle to lateral third of the forehead,
just above the eyebrow (Fig. 2518). Although not supported by osteologic studies, placement of the anterior pin more laterally and just into the hairline for cosmetic reasons has been reported to give good clinical results.46 This more lateral pin placement has been used by one of the authors (Benson), with similarly good clinical results. If the more lateral position is to be used, care must be taken to palpate and avoid penetration of the temporal muscle and temporal artery on each side. The posterior pin is placed in the posterolateral position on the halo ring, with care taken to avoid skin contact with the ring because pressure ulceration can result. All pins are rst secured to nger tightness. As the pins are tightened, the patient should be encouraged to keep both eyes tightly closed to avoid stretching the skin, which limits the patients ability to close the eyes. Once the pins are nger tight, the ring is inspected carefully to ensure a symmetric t. The pins are then tightened sequentially in a diagonally opposite manner (i.e., right front with left rear and left front with right rear) to 2 inch-lb, then 4 inch-lb, and nally 8 inch-lb in an adult or 4 to 6 inch-lb in a child younger than 5 years. The pins should be retightened within 24 hours (and thereafter) only if they are loose and resistant to tightening. A loose pin without resistance to tightening should be moved to another position on the skull. Traction can then be applied with the traction bar attachment. If a vest is to be applied, the size should be equal to the chest diameter measured in inches at the level of the xiphoid process. MRI-compatible halo vests with graphite rings are used routinely, as shown in Figure 2519. Fleming and co-workers38 devised instrumented halo vest orthoses with gauges that can measure pin force and showed an 83% decrease in compressive force during approximately a 3-month typical halo vest wear period. All patients had some symptoms caused by the degradation in pin force, which signied some loosening. The high stress on the bone may cause resorption and is thus one of the postulated causes of loosening. This potential complication highlights the importance of clinical vigilance during treatment of patients with halo vests. Attention to detail such as pin site care is essential, as well as alertness to
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FIGURE 2517. Pressure indication pins of the Gardner-Wells tongs should protrude 1.0 mm.
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FIGURE 2518. The anterior pin should be placed above the eyebrow in the medial to lateral third, avoiding the supraorbital nerve.
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Presentation
symptoms of loosening or other complications during treatment. Reports of complications with use of the halo ring and vest42, 46 have indicated signicant rates of pin loosening (36%), pin site infection (20%), pressure sores under the vest or cast (11%), nerve injury (2%), dural penetration (1%), cosmetically disguring scars (9%), and severe pin discomfort (18%). Skull osteomyelitis and subdural abscess have also been described. A lower rate of pin loosening and infection has been reported with an initial torque of 8 inch-lb rather than 6 inch-lb in adults.14 A prospective randomized study has, however, shown that 6or 8-lb torque does not lead to any signicant difference in pin loosening.92
The use of a halo ring in children requires special consideration43, 63, 81 because of a higher complication rate in this population.9 The calvaria develops in three signicant phases by age: (1) 1 to 2 years, when interdigitation of the cranial sutures ends; (2) 2 to 5 years, a period of rapid growth in diameter; and (3) 5 to 12 years, when skull growth ceases.43 Overall, the calvaria is thinner in a child 12 years or younger than in an adult, and the middle layer of cancellous bone may well be absent. Computed tomographic studies have demonstrated that the standard adult anterolateral and posterolateral pin positions correspond to the thickest bone in a child, and they are recommended as the site of halo pin placement.41, 43 In children younger than 3 years, a multiple-
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FIGURE 2519. MRI-compatible halo vests.
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pin, low-torque technique is recommended.81 In this age group, custom fabrication of the halo ring and vest may be required. Ten to 12 standard halo pins can be used. The pins are inserted to a torque tightness of 2 inch-lb circumferentially around the temporal and frontal sinus regions. Halo placement in children younger than 2 years is complicated because of incomplete cranial suture interdigitation and open fontanels.81
SPECIAL CONSIDERATIONS Pediatric Patients
The spine is thought to behave biomechanically as an adult spine by about the age of 8 to 10 years.8, 56, 57 Until then, spinal column injury is uncommon, usually involves soft tissues, and therefore is not seen on plain radiographs in the emergency room. In patients younger than 10 years, the most common injury occurs in the occiput to C3 region.57, 110 The entire spectrum of neurologic involvement is associated with these injuries, including cranial nerve lesions and vertebral basilar signs such as vomiting and vertigo. SCIWORA is most common in children younger than 10 years. Flexion, extension, and distraction cervical spine views and MRI scans can be helpful in identifying the level, but they should be used with extreme care to avoid further injury. After the age of 10 years, the pattern of injury is similar to that of adults, except for exion-distraction injuries in the lumbar spine. As a result of seat belt injuries, pediatric patients can have a lumbar fracture with a more proximal thoracic level of paraplegia. Initial immobilization of a pediatric patient requires an understanding of the supine kyphosis anterior translation (SKAT) phenomenon.56 A young child lying supine on a standard backboard can have the head forced into kyphosis because of the normally disproportionate relationship of the larger head and smaller trunk in a child. Cases of forced kyphosis causing anterior translation of an unstable pediatric spine have been reported.56 In normal development of a child, head diameter grows at a logarithmic rate, with 50% of adult size achieved by the age of 18 months, and chest diameter grows at an arithmetic rate, with 50% of adult size achieved by the age of 8 years. The problem can be avoided by elevating the thorax of a child on a spine board with a folded sheet to bring the shoulders to the level of the external auditory meatus or by the use of a pediatric backboard with a cutout to compensate for the prominent occiput of a young child.
years.71, 95, 104 Cervical spine injury predominates in the elderly population and accounts for 80% or more of traumatic spinal injuries. Injury to the C1C2 complex is signicantly more common in elderly people and accounts for a higher percentage of the total number of spinal injuries, with odontoid fractures being the single most common spinal column injury in these patients.96, 104 Elderly patients are more likely to have an incomplete injury.95, 104 The frequent incidence of spondylosis in this population predisposes this patient group to central cord syndromes. Most importantly, the overall mortality rate for the initial hospitalization period has been reported to be 60 times higher in patients older than 65 years than in those younger than 40 years.104 The causes of death are more commonly related to the stress of the treatment (immobilization, recumbency) than to the injury itself. Treatment of this patient population is problematic. The overall priority in treatment should be early mobilization of the patient to avoid respiratory and other complications. Although previous reports have suggested that halo vests are poorly tolerated by the elderly population,84 these patients are frequently poor operative candidates. A high index of suspicion must be maintained when evaluating an elderly patient with neck pain, even after relatively trivial trauma.
Multiply Injured Patients

Several important issues should be raised regarding multiply injured patients with spinal trauma. Delay in diagnosis of a spine injury is a signicant problem that can affect a trauma patients care. The rate of delay in diagnosis in spinal trauma is 23% to 33% in the cervical spine12, 88 and about 5% in the thoracolumbar spine. As many as 22% of all delays in diagnosis in one series occurred after arrival at a tertiary referral center.88 The main cause is a low level of suspicion, as represented by the following: (1) failure to obtain a radiograph, (2) missing the fracture on radiography, or less commonly, (3) failure of the patient to seek medical attention. A secondary neurologic decit developed in 10% of patients with a delayed diagnosis as compared with 1.5% of those in whom spinal injury was diagnosed on initial evaluation,88 but no progression of an already recognized decit was observed. Other factors associated with a delay in diagnosis include intoxication, polytrauma, decreased level of consciousness, and noncontiguous spine fractures. Knowledge of the relationships between specic injury patterns and spinal injuries should decrease the incidence of serious missed spinal injuries. Patients with severe head injuries, as evidenced by a decreased level of consciousness or complex scalp lacerations, have a high incidence of cervical spine injuries, which may be difcult to diagnose clinically.12, 58 The incidence of noncontiguous spine fractures is about 4% to 5% of all spine fractures10, 61, 62 but is higher in the upper cervical spine.68 Therefore, diagnosis of a spinal fracture should in itself be an indication for aggressive investigation to rule out other, noncontiguous spinal injuries. Conversely, the presence of a spinal fracture should heighten the awareness of the possibility of a serious, occult visceral injury. Thoracic fractures resulting in
Elderly Patients
Spinal trauma and spinal cord injury have traditionally been thought of as conditions of youth, but as many as 20% of all spinal cord injuries occur in patients older than 65 years.17 Some particular characteristics and injury patterns are specic to elderly patients. For example, elderly patients with spinal cord injuries are more likely to be female. Whereas spinal injury is commonly associated with high-energy trauma in young adults, simple falls are the most common mechanism in patients older than 65
705
paraplegia have a high incidence of associated multiple rib fractures and pulmonary contusions. Translational shear injuries at these levels have signicant associations with aortic injuries.69 A delay in the diagnosis of a visceral injury can occur in up to 50% of patients with spinal injuries.90 The relationship between the use of lap-style seat belts and Chance-type exion-distraction injuries of the thoracolumbar spine is now well appreciated.7 Almost two thirds of patients with exion-distraction injuries from lap belts have an associated injury to a hollow viscus. Overall, approximately 50% to 60% of spine-injured patients have an associated nonspinal injury ranging from a simple closed extremity fracture to a life-threatening thoracic or abdominal injury.10, 62
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SECTION

Alan M. Levine, M.D.

Copyright 2003 Elsevier Science (USA). All rights reserved.

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Incidence, Etiology, and Demographics

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MVA 45% Sports 15%

Acts of violence 15%

Anatomy and Pathophysiology

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CHAPTER 25 Initial Evaluation and Emergency Treatment of the Spine-Injured Patient

Fasciculus gracilis Fasciculus cuneatus POSTERIOR S S L T

Lateral corticospinal tract L S Print Graphic

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Normal spinal cord

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CHAPTER 25 Initial Evaluation and Emergency Treatment of the Spine-Injured Patient

Spinal cord injury

Edema, tissue ischemia and anoxia cell energy supply

BBB breakdown and cell membrane injury

Release of excitotoxins from damaged and hyperactive cells

Microglial activations activity of antioxidants

extracellular glutamate Print Graphic Ca in cells ( Na in cells) Presentation

Proinflammatory cytokines NOS activation

Classication of Neurologic Injury

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Copyright 2003 Elsevier Science (USA). All rights reserved.

CHAPTER 25 Initial Evaluation and Emergency Treatment of the Spine-Injured Patient

Lateral corticospinal tract

Lateral corticospinal tract

Lateral spinothalamic tract

Lateral spinothalamic tract

Central cord syndrome

Posterior cord syndrome

Lateral corticospinal tract

Lateral corticospinal tract

Lateral spinothalamic tract

Lateral spinothalamic tract

Anterior cord syndrome

Frankel Classication of Neurologic Decit

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Incomplete Cord Syndromes

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CHAPTER 25 Initial Evaluation and Emergency Treatment of the Spine-Injured Patient

pressure above 85 mm Hg results in a better neurologic outcome.

Accident Scene Management

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Copyright 2003 Elsevier Science (USA). All rights reserved.

CHAPTER 25 Initial Evaluation and Emergency Treatment of the Spine-Injured Patient

FIGURE 2512. Stretch reexes and nerve roots of origin.

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CHAPTER 25 Initial Evaluation and Emergency Treatment of the Spine-Injured Patient

Pharmacologic Agents for Spinal Cord Injury

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Extrication Spinal stabilization Transportation

ATLS protocols Resuscitation

Plain radiographs entire spine

MPS protocol 30 mg/kg IV 5.4 mg/kg/hr x 23 hrs

MRI R/O disc herniation