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.

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.

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.

The high metabolic requirements of neurons make the gray matter exquisitely sensitive to ischemic injury. This can be compounded by the loss of autoregulatory mechanisms that normally control the microvascular hemodynamics tightly within the spinal cord.

The early inflammatory response is a complex process involving vascular changes, including the disruption of the blood-brain barrier and the upregulation of endothelial cell adhesion molecules that allow the activation and extravasation of cells from the bloodstream (neutrophils, macrophages, lymphocytes) into the injured tissue. These cells also release a large number of soluble immune mediators (cytokines, chemokines) that consequently activate resident glial cells.^1,3 A mild influx of neutrophils has been described as beginning within 1 day after SCI, with a peak at 2 days and a decrease by 3 days. This is in sharp contrast to other tissues, in which the neutrophilic influx is often marked. The neutrophilic response in the central nervous system (CNS) is likely to be neurotoxic in nature, because once these cells are activated and accumulated at the lesion site, they release potent free radicals that attack the integrity of the lipid bilayer of the cellular membrane. The extent of neutrophil infiltration has been associated with blood-brain barrier dysfunction and tissue damage. The neuronal and axonal changes in the acute phase include marked axonal swelling and ultimately fiber disconnection. Microscopically, this is marked by the formation of typical retraction balls. Myelin breakdown is another feature of the early period after SCI. This is initially characterized by swelling of the myelin sheaths, and ultimately by fragmentation of myelin and its phagocytosis by macrophages. Myelin loss generally occurs in association with axonal pathology. Oligodendrocytes are also exquisitely sensitive to SCI. Much of the injury to these cells appears to be necrotic, but oligodendrocyte apoptosis has also been documented both in experimental animals and in humans.

Intermediate Phase (Days to Weeks)

Microglia and astrocytes play important roles in this phase of SCI, leading to either beneficial or detrimental effects on the damaged tissue.

Late Phase (Weeks to Months/Years)

The later phases of SCI are characterized by wallerian degeneration, astroglial and mesenchymal scar formation, development of cysts/cavities and syrinx, and schwannosis.

Central Cord Syndrome

Because the motor fibers to the cervical segments are topographically arranged toward the center of the cord, damage to the central cord affects the arms and hands more severely than the lower extremities. The degree of sensory loss is variable. This syndrome is usually seen after a hyperextension injury in a patient with preexisting cervical canal stenosis (often resulting from degenerative osteoarthritic changes). The history is commonly that of a forward fall that resulted in a facial impact. The syndrome may occur with or without cervical spine fracture or dislocation. Central cord syndrome in young patients has a relatively good prognosis. Recovery usually follows a characteristic pattern. The lower extremities recover strength first, bladder function next, and the proximal upper extremities and hands last (Fig. 104-8).

Figure 104-8 Magnetic resonance image showing a central cord syndrome. Note the bleeding within the spinal cord at the C6-C7 level.

Anterior Cord Syndrome

Infarction in the territory supplied by the anterior spinal artery causes damage to the anterior two thirds of the cord. This syndrome is characterized by paraplegia and a dissociated sensory loss with loss of pain and temperature sensation. Posterior column function (position, vibration, and deep pressure sense) is preserved. This syndrome has the poorest prognosis of the incomplete injuries.

Brown-Séquard Syndrome

This disorder results from hemisection of the cord, and its pure form consists of ipsilateral motor paralysis (corticospinal tract) and loss of proprioception (posterior column), in association with contralateral loss of pain and temperature sensation beginning one to two levels below the level of injury (spinothalamic tract). The classic syndrome is rare, but variations are common. Some recovery is usually obtained, even if the syndrome is caused by a direct penetrating injury to the cord.

Neurogenic Shock versus Spinal Shock

Neurogenic shock may occur after a cervical or high thoracic (T1-T5) injury that interrupts thoracic sympathetic outflow. This results in loss of vasomotor tone and loss of cardiac sympathetic innervation. The consequent hypotension and bradycardia may cause secondary neurological injury and pulmonary, renal, and cerebral insults. Under these conditions, it may not be possible to restore a patient’s blood pressure by fluid infusion alone, because massive fluid resuscitation may generate pulmonary edema. The blood pressure can instead be restored by supplementing moderate volume replacement with judicious use of inotropes, such as dobutamine, and pressors, such as dopamine, that increase vascular tone. Muscarinic antagonists, such as atropine, can be used to treat hemodynamically significant bradycardia.

Spinal shock refers to the muscle flaccidity and loss of reflexes seen after SCI. The “shock” to the injured cord may make it initially appear completely functionless. However, because the cord is usually not completely destroyed in SCI, the duration of this state is variable; recovery usually occurs.

Penetrating Injuries

Penetrating SCIs are most commonly caused by gunshots or stabbings. A complete neurological deficit may result if the path of injury passes directly through the vertebral canal. Complete deficits can also be produced by energy transfer from a high-velocity missile (e.g., a rifle bullet) passing close to the spinal cord rather than through it. Spinal instability from penetrating injury is exceedingly rare. Associated injuries, however, should be highly suspected. Penetrating cervical injuries are combined with a high incidence of vascular lesions, whereas penetrating thoracic trauma is associated with pulmonary and cardiac injuries. Knife or gunshot trauma to the lumbar spine may be accompanied by damage to the abdominal viscera, genitourinary system, or major vascular structures, and severe infection may follow bullet injuries that traverse the colon. Penetrating injuries can be complicated by the formation of cerebrospinal fluid fistulae. All patients with penetrating spinal injuries should therefore receive treatment with tetanus prophylaxis and broad-spectrum antibiotics.

Spinal Cord Injury without Radiographic Abnormality (SCIWORA)

Because of the relatively large size of the head and the greater inherent mobility in the skeletally immature spine, combined with ligamentous laxity or disruption, children’s spinal cords are vulnerable to damage in high-energy trauma. The pediatric spine, however, because of its unique anatomical and biomechanical characteristics, may have a normal radiographic appearance even in the presence of a high-energy injury with neurological impairment. This reflects the inherent elasticity of the soft tissues, which allows spontaneous reduction after intersegmental replacement.

In a child with SCI without abnormal findings on plain radiographs, a hyperextension cervical SCIWORA should be considered. A high index of suspicion is required. Because the flexibility of the spine is reduced with increasing age, SCIWORA is rarer in the adult trauma population, but it should be suspected in all patients with a neurological deficit and apparently normal radiographs.^9,10

Prehospital Management

Initial management adheres to the guidelines of the American College of Surgeons Advanced Trauma Life Support protocol, which sequentially prescribes airway management, ventilation and oxygen, and circulatory support before neurological evaluation and resuscitation. The primary injury to the spinal cord is sustained at the time of impact and is irreversible. The caregivers’ role is to prevent and minimize secondary injury. This task begins in the field during initial resuscitation:

Patients should receive supplemental oxygen.

If the airway is compromised, a nasotracheal or orotracheal intubation should be considered with simultaneous in-line stabilization, whereby a second person manually maintains the patient’s head and the neck in neutral alignment with the torso. Cricothyroidotomy may be required if these techniques fail to secure the airway.

Large-bore intravenous access should be established, and mean arterial blood pressure should be maintained above 85 mm Hg to ensure adequate spinal cord perfusion.

Spine Immobilization

This has become established as standard care in the management of multiple trauma and begins at the accident field. Such immobilization entails placement of a hard cervical collar, transportation on a rigid long spine board, and use of log-rolling technique when the patient is turned. As prolonged spinal immobilization predisposes to decubitus ulceration and deep venous thrombosis and may compromise nursing care, the board should be removed promptly after arrival at the hospital. Log rolling is the standard maneuver to allow examination of the head and back and to transfer the patient onto and from a spine board. Ideally, five people participate in its use: one to hold the patient’s head and coordinate the roll; three to control the patient’s chest, pelvis, and lower limbs; and one to perform associated procedures. Inadequate mobilization may lead to fracture displacement, which can further compromise spinal cord function and convert a good prognosis into a devastating and life-threatening outcome.

Emergency Department Management

On arrival at the emergency department, securing the patient’s airway, breathing, and circulation is again the priority. Simultaneous evaluation and treatment should proceed. The physical examination includes a complete neurological examination and an assessment of the head and back. An accurate knowledge of sensory dermatomes and muscle innervation is necessary to determine the level of SCI. Manual in-line stabilization of the patient’s head is maintained while the cervical collar is temporarily removed so that the neck can be palpated for deformity or pain.

Prognostically, it is important to assess for any indication of preserved long tract function of the spinal cord. Signs of an incomplete injury may include any sensation (including position sense) or voluntary movement in the lower extremities and sacral sparing.

Imaging

There is a risk that spinal column injuries may be missed when other potentially life-threatening injuries are present. Radiological imaging consequently plays a pivotal role in diagnosing injuries in multiple-trauma patients. There is, however, no consensus in the literature as to which investigations are necessary to detect a clinically significant SCI or how many and which radiographs are necessary to rule out such injury (“clear” the spine). The traditional standard three-view plain film series comprises the lateral, anteroposterior, and open-mouth peg views. There is evidence that primary helical computed tomography of the entire cervical spine (with sagittal and coronal reconstructions) is more sensitive than plain films for investigating osseous integrity and competency of the spinal canal. In addition, magnetic resonance imaging offers better evaluation of soft tissues such as the intervertebral disks, ligaments, and neural elements. Major trauma centers continue to update their spine clearance protocols to reflect these innovations; some centers now routinely perform full-neck computed tomographic scans on all unconscious trauma patients and also in conscious patients with neck pain or high-risk mechanism of injury.

Surgical Treatment

The short-term goal is to place the spinal cord and nerves in the optimal position for recovery. Strategies range from an external orthosis to surgical intervention. Factors such as mechanism of injury, degree of neurological deficit, level of injury, and fracture anatomy contribute to the selection of the preferred treatment for each individual patient.

The timing, choice of surgical approach and extent of surgery in the acute management of spinal trauma are controversial. The time from injury to surgery and the degree of initial SCI appear to be important prognostic factors, but various authors have presented conflicting arguments. Some suggest that neurological recovery in patients with progressive deficits is greater if patients are treated within 8 hours of injury. Others argue that early surgery may predispose seriously injured patients to intraoperative and postoperative respiratory distress, additional bleeding, and infection and may increase the risk of adverse outcomes.

Kossmann and colleagues (2004) recommended two-staged “damage control” approach for spine trauma.¹⁴ Relatively safe procedures, such as posterior internal stabilization of thoracic or lumbar fractures or temporary external fixation of cervical fractures in a halo thoracic brace, are performed early. Once the patient is medically stable, a second operation for reconstruction of the anterior column may be performed. This delay allows for general recovery of the patient and facilitates safer anesthesia. Eventually, the definitive surgery can be electively scheduled at a time when an experienced spine surgeon is available. This may enable use of new minimally invasive techniques that are now available for the reconstruction of the anterior column of the thoracic and lumbar spine (Fig. 104-9).¹⁵

Figure 104-9 Pincer fracture of L3. A, Computed tomographic reconstruction with visible destruction of the L3 anterior column. The L2 and L4 vertebrae are acting like pincers. Because of the high flexibility of the ligaments in young patients, no further significant damage occurs in the posterior elements of the lumbar spine. B, Computed tomographic reconstruction of pincer fracture reduced with a cage. The defect of the vertebrae was replaced with an expandable cage filled with bone. With the minimally invasive surgical technique, minimal morbidity is caused by the surgical approach.

Pharmacological Therapy

Most traumatic injuries to the spinal cord do not involve actual transection of the cord but rather entail damage of the fibers from contusive, compressive, or stretch injury. Often, portions of the ascending and descending tracts remain intact. Although it is not currently known how much of the spinal cord needs to remain intact to mediate meaningful neurological function, the observation of anatomical continuity of the spinal cord has led to the notion that pharmacological treatments, if applied early, may be able to interrupt the secondary cascade and thereby improve the survival of damaged tissue.¹

Cell membrane (plasma and organelle) lipid peroxidation has been demonstrated to be a key mechanism in the secondary cascade. Post-traumatic glutamate release, activation of the arachidonic acid cascade, and production of prostaglandins result in vasoconstriction and microembolism. This leads to formation of oxygen free radicals, which cause lipid peroxidation, more often involving neurons and endothelium, thus directly impairing neuronal and axonal membrane function, with consequent microvascular damage and secondary ischemia.

New Pharmacological Approaches