SPINAL TRAUMA

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CHAPTER 104 SPINAL TRAUMA

Thomas Kossmann, Ilan Freedman, Cristina Morganti-Kossmann

Spinal cord injury (SCI) is a devastating event for patients and their families, with many severe medical, social, and economic sequelae. Patients may be permanently disabled and may ultimately have a lifelong dependence on support services. The neurological dysfunction after traumatic SCI results from a “primary” mechanical insult, followed by a downstream cascade of “secondary” processes that disrupt normal cord anatomy and function. The primary insult is determined by the mechanism of injury, energy applied to the cord, level of SCI, and patient factors such as medical comorbid conditions and the preinjury space available to the cord. Secondary injury mechanisms include, but are not limited to, disruption of the microcirculation, loss of autoregulation, edema, ischemia, calcium toxicity, glutamate excitotoxicity, lipid peroxidation, and free radical activation.¹

Greater understanding of the pathophysiology of the secondary cascade and effective early resuscitation measures have improved the outcomes for these patients. Treatment of SCI is aimed at preserving residual neurological function, avoiding secondary injury to the cord, and restoring spinal alignment and stability. Currently, there is also burgeoning activity in basic research aimed at repair and regeneration of the injured spinal cord. This may facilitate higher levels of independence and productivity and may markedly improve the quality of life for patients with SCI.^2,³

EPIDEMIOLOGY

The incidence of SCI in developed nations is approximately 30 to 50 per million persons per year. Accordingly, 10,000 new cases of SCI are diagnosed in the United States each year. The most common mechanisms of SCI include motor vehicle accidents, falls from a height, violence, and sports-related injuries. Approximately 55% of these injuries occur in the cervical region, 15% in the thoracic region, 15% at the thoracolumbar junction, and 15% in the lumbosacral area. The incidence of SCI among boys and men is three to four times that among girls and women. The incidence peaks in adolescence and young adulthood; two thirds of all cases arise in patients younger than 30. With improvements in medical and surgical care, those who survive their initial injuries can now expect to live long lives, but the cost of caring for such patients over the course of a lifetime is substantial. The incidence of SCI is also increased in the sixth and seventh decades of life. This is a result of aging and an associated increase in cervical spondylitic disease, which narrows the spinal canal and predisposes to spinal injury.

DEFINITIONS

SCI can be categorized as incomplete paraplegia, complete paraplegia, incomplete tetraplegia, and complete tetraplegia. According to the classification of the American Spinal Injury Association,⁴ tetraplegia is the “impairment or loss of motor and/or sensory function in the cervical segments of the spinal cord.” Paraplegia refers to “impairment or loss of motor and/or sensory function in the thoracic, lumbar, or sacral segments of the spinal cord.”

SCI is deemed an incomplete injury when motor sensory function is preserved below the level of injury. Sparing of sensation in the perianal region may be the only sign of residual function. Sacral sparing may be demonstrated by preservation of some sensory perception in the perianal region and/or by voluntary contraction of the rectal sphincter.

The injury is deemed complete when all function, including rectal, motor, and sensory function, is lost. During the first few days after injury, this diagnosis cannot be made with certainty because of the possibility of spinal shock (described later). The dermatomes and myotomes caudal to the neurological levels that remain partially innervated are named the zone of partial preservation.

The neurological injury level is determined primarily by clinical examination and is defined as the most caudal spinal cord segment with normal sensory and motor function on both sides of the body. The sensory level refers to the most caudal spinal cord segment with normal sensory function. The motor level is defined similarly with regard to motor function as the lowest key muscle that has a grade of at least 3/5 (Table 104-1).

TABLE 104-1 Muscle Strength Grading

Score	Clinical Finding
0	Total paralysis
1	Palpable or visible contraction
2	Full range of motion with gravity eliminated
3	Full range of motion against gravity
4	Full range of motion but less than normal strength
5	Normal strength
NT	Not testable

The bony level of injury is that at which the vertebrae are damaged, which causes injury to the spinal cord. As spinal nerves enter the spinal canal through the vertebral foramina and ascend or descend inside the spinal canal before entering the spinal cord, there is frequently a discrepancy between the bony and neurological levels. This discrepancy becomes more pronounced the further caudal the injury is.

ANATOMY OF SPINAL CORD INJURY

Fractures of the spine are determined by the forces applied to the spinal column. Such forces include distraction and compression, flexion and extension, and combinations thereof. Fractures are also categorized by anatomical location: cervical, thoracic, and lumbar.

Cervical Injury

The cervical spine is the region most vulnerable to injury. These injuries can be classified as upper and lower cervical. Upper cervical injuries include those to the base of the skull, C1, and C2. Lower cervical injuries affect C3 to C7. Upper cervical spine injuries can be described as atlanto-occipital dislocation, C1 fractures, disruption of the transverse ligament of C1, C2 odontoid fractures, and traumatic C2 spondylosis fractures. Lower cervical spine injuries are generally classified into facet dislocations, compression fractures, burst fractures, and teardrop fractures.

Atlanto-Occipital Dislocation

This is caused by traumatic hyperflexion and extension, in which the ligamentous connections between the skull and C1 and C2 are disrupted (Fig. 104-1). Because of the highly unstable nature of this injury, these patients often either die of brainstem destruction and apnea or are profoundly neurologically impaired (ventilator dependent and tetraplegic). On occasion, a patient may survive if prompt resuscitation is available at the injury scene. This injury may be identified in up to 20% of patients with fatal cervical spine injuries and is a common cause of death in cases of shaken baby syndrome in which the infant died immediately after being shaken.

Figure 104-1 Atlanto-occipital dislocation. A, Computed tomographic scan reconstruction. The articular surface of the condyle is dislocated anteriorly. Note the space between the occipital condyle and C1. B, Three-dimensional reconstruction from computed tomographic scans.

Atlas Fracture (C1)

This injur represents 10% of all cervical fractures and usually results from axial loading, such as when a large load falls vertically on the head or in a fall in which the patient lands on the head in a relatively neutral position. The most common C1 fracture is a burst fracture (Jefferson’s fracture), which involves disruption of both the anterior and posterior rings of C1 with lateral displacement of the lateral masses (Fig. 104-2). In patients who survive, these fractures are usually not associated with SCIs but may be accompanied with significant retropharyngeal swelling. The trauma team should be alert to this possibility and should consider prophylactic intubation. Approximately 40% of atlas fractures occur in combination with fractures of the axis (C2).

Figure 104-2 Jefferson’s fracture: fracture of the anterior and posterior arc of C1 (two-part fracture).

Axis (C2) Fractures

Because of its unusual shape, the C2 vertebra is susceptible to various fracture patterns, depending on the force and direction of impact. Acute C2 fractures represent approximately 18% of all cervical spine injuries.

Approximately 60% of C2 fractures involve the odontoid process. These are classified according to the scale of Anderson and D’Alonzo. Type 1 odontoid fractures involve the tip of the odontoid and are relatively uncommon. Type II odontoid fractures occur at the waist of the odontoid and C2 body and are the most common type (Fig. 104-3). Type III odontoid fractures occur at the base of the dens and extend obliquely into the body of C2.

Figure 104-3 Dens fracture before (A) and after (B) reduction.

Posterior Element Fractures of C2

A hangman’s fracture involves the pars interarticularis, usually results from an extension injury, and represents approximately 20% of all C2 fractures. Variations of a hangman’s fracture include bilateral fractures through the lateral masses or pedicles. Approximately 20% of all axis fractures are nonodontoid, nonhangman’s fractures and include fractures through the body, pedicle, lateral mass, laminae, and spinous process.

Fractures and Dislocations (C3 to C7)

Bony injury to the lower cervical area occurs in the form of compression fracture, burst fracture, or teardrop fracture. Compression fractures arise from a flexion injury, with no greater than 25% compression of the middle column and no injury to the posterior longitudinal ligament. Burst fractures are the result of compression and flexion. Teardrop fractures are caused by flexion with rotation and compression and are notably unstable injuries (Fig. 104-4).

Figure 104-4 Teardrop fracture of C7. Multiple-slice reconstruction with clearly visible teardrop fracture of C7. This may indicate additional discoligamentary injury.

Fractures of C3 are relatively infrequent because this vertebra is positioned between the more vulnerable axis and the more mobile C5 and C6 vertebrae. C5 is the most commonly fractured cervical vertebra in adults, whereas subluxation more often occurs at the level of C5 on C6. Common injury patterns at these levels are vertebral body fractures with or without subluxation; subluxation of the articular processes; and fractures of the laminae, spinous processes, pedicles, or lateral masses. In rare cases, ligamentous disruption occurs without fractures or facet dislocations. The incidence of neurological injury increases dramatically with facet dislocations. After unilateral facet dislocation, 80% of patients develop a neurological injury (of which approximately 30% are root injuries only, 40% incomplete SCIs, and 30% complete SCIs). In the presence of bilateral locked facets, the morbidity is much worse, with 16% incomplete and 84% complete SCIs.

The Thoracic Spine

The mobility of the thoracic spine is much more restricted than that of the cervical spine, because it has additional support from the rib cage. This region requires greater force to disrupt its integrity and thus has a much lower incidence of fractures (Fig. 104-5). However, because the thoracic canal is relatively narrow, a fracture dislocation here frequently results in a severe neurological deficit. Because thoracic spine fractures result from violent forces, they are associated with a high incidence of concomitant injuries, such as rib fractures, pneumothorax, hemothorax, pulmonary contusion, cardiac contusion, and sometimes aortic shearing injury.

Figure 104-5 Magnetic resonance image of multiple fractures of the thoracic spine. The fractured thoracic vertebrae appear smaller with irregular shape and white appearance in the magnetic resonance image.

The Thoracolumbar Junction

The thoracic spine has a natural kyphosis (concave forward), whereas the lumbar spine has a lordosis (convex forward). Because of the change of curvature in the transition zone, the thoracolumbar junction acts like a fulcrum between the inflexible thoracic region and the stronger lumbar levels, which predisposes it to injury.⁵ Consequently, approximately 15% of spinal injuries are found in this region (Fig. 104-6).

Figure 104-6 Radiograph of the thoracolumbar junction, showing a T12 burst fracture.

The three-column structural concept described by Dennis is integral to evaluation of the thoracolumbar spine. According to this concept, the spine is divided into anterior, middle, and posterior columns. The anterior column comprises the anterior longitudinal ligament, anterior half of the vertebral body, and anterior half of the disk. The middle column consists of the posterior longitudinal ligament with the posterior half of the vertebral body and disk. The posterior column is composed of all structures posterior to the middle column, back to the level of the supraspinous ligament. Disruption of two or three columns at one level generates spinal instability.

Lumbar Spine

The Dennis classification also divides lumbar spine injuries into minor and major categories on the basis of radiographic criteria. Major injuries encompass compression fractures, burst fractures, flexion- and distraction-type injuries, and fracture dislocations. Minor injuries include transverse process fractures, articular process fractures, spinous process fractures, and pars interarticularis fractures.

Compression fractures usually result from failure of the anterior column with intact middle and posterior columns, frequently from an anterior flexion force accompanied by a posterior tensile force. These injuries are generally not associated with neurological deficit. With lumbar burst fractures, loss of height of the anterior and middle columns is characteristically shown on radiographs, with retropulsion of bone into the canal and widening of the interpedicle distance. These fractures are inherently unstable. Flexion and distraction injuries, frequently described as Chance fractures (Fig. 104-7), represent a failure of the middle and posterior columns in tension, with the anterior column acting like a hinge. Fracture dislocations are associated with failure of all three columns with a combination of forces, including flexion rotation, flexion distraction, or shearing. Because of their inherent instability these injuries are probably associated with a high incidence of severe SCI.

Figure 104-7 Magnetic resonance image of a Chance fracture at L3. Note the destruction of the posterior spine complex. A superior burst fracture of L3 is also evident.

Because the spinal cord ends at the L1 vertebral level, the cord itself may not necessarily be injured in lumbar fractures. Instead, insult to the cauda equina may occur. The neurological deficit here is less severe than in injuries to the spinal cord itself.

HISTOLOGY OF SPINAL CORD INJURY

According to Belanger and Levi (2000) and Park and associates (2004), the histological changes in SCI can be categorized as immediate, acute, intermediate, and late phases.^6,⁷

Immediate Phase (Initial 1 to 2 Hours)

This phase involves the mechanical tissue disruption at the time of injury (e.g., tears, distortions, compression) and vascular changes such as vasodilatation, congestion (hyperemia), and petechial hemorrhages. In many cases, no abnormalities are observed during this period (particularly in the absence of massive compression or laceration injury), inasmuch as much of the pathology of human SCI results from secondary phenomena mediated by cellular and molecular cascades. This suggests that there may be a window of opportunity during the immediate phase for downregulating the deleterious secondary events.

Acute Phase (Hours to 1 to 2 Days)

This phase is characterized by vascular alterations, edema, hemorrhage, inflammation, and neuronal and myelin changes. The edema may be vasogenic: that is, secondary to breakdown of the endothelium at the blood-brain barrier, which leads to leakage of plasma fluid into the extracellular space. Diminished blood flow to the injured region and pressure effects may in turn cause ischemic damage. Cytotoxic edema (intracellular swelling), occurring mostly in astrocytes, is observed from 3 hours to 3 days after injury. This is probably caused by factors such as glutamate, lactate, K⁺, nitric oxide, arachidonate, reactive oxygen species, and ammonia, levels of which are elevated in the extracellular space shortly after injury, altering the osmotic balance of the cells. Hemorrhage in the acute phase occurs in the gray matter after contusion injury. This is primarily a result of rupture of postcapillary venules or sulcal arterioles, either from mechanical disruption or from intravascular coagulation that leads to venous stasis and distension. The larger caliber vessels are usually spared.

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