Traumatic Spinal Cord Injury

Christopher E. Mandigo

Michael G. Kaiser

Peter D. Angevine

INTRODUCTION

Traumatic spinal cord injury (SCI) is a sudden event with possibly catastrophic effects that may create a medical, financial, and social burden for the individual and society. Adequate management of these patients requires knowledge of SCI, including epidemiology and pathophysiology, acute and chronic medical complications, and long-term rehabilitation and social needs.

ETIOLOGY AND EPIDEMIOLOGY

Epidemiologic data can guide the use of resources for treating and preventing SCI. The best source of this information for the United States is the National Spinal Cord Injury Database (NSCID), which has been collecting information from facilities that have participated in the Model Spinal Cord Injury System (MSCIS) since 1973. This database includes data from an estimated 13% of new SCI cases each year and has information on over 25,000 people with SCI. SCI occurs in the United States in approximately 40 per 1 million people per year, which results in about 12,000 new cases annually. This figure does not include injuries that result in fatality before hospital arrival, which may double the number of injuries. Currently, 225,000 to 300,000 people are living with SCI.

SCI primarily affects young adults aged between 16 and 30 years, but the average is increasing. The average age in the 1970s was 28.7 years; in the period 2005 to 2008, it was 39.5 years. The median age is 27 years, and 65% of SCI patients are younger than 35 years. The highest incidence occurs between ages 20 and 24 years. The most significant changes between the 1970s and 2005 to 2008 have occurred at the extremes of age. The proportion of patients older than 65 years has increased from 5% to 11%, and the proportion of children from birth to 15 years has decreased from 6% to 2%. The increasing age could arise from data collection bias, improved survival of older patients in the acute period of SCI, or in age-specific incidence rates. That is, the larger population of elderly patients requires special consideration for medical, surgical, and rehabilitative care.

TABLE 47.1 Life Expectancy after Spinal Cord Injury

		For Persons Who Survive the First 24 h					For Persons Surviving at Least 1 yr Postinjury
Age at Injury (yr)	No SCI	Motor Functional at Any Level	Para	Low Tetra (C5-C8)	High Tetra (C1-C4)	Ventilator Dependent at Any Level	Motor Functional at Any Level	Para	Low Tetra (C5-C8)	High Tetra (C1-C4)	Ventilator Dependent at Any Level
20	58	53	45	40	36	17	53	46	41	37	24
40	40	34	28	23	20	7	35	28	24	21	11
60	22	18	13	10	8	2	18	13	10	9	3
Life expectancy in years based on age and injury severity. SCI, spinal cord injury.

Seventy-eight percent of SCI patients are male. Among those injured after 2000, 63% were white, 23% were African-American, 12% were Hispanic, and 2% were from other racial or ethnic groups.

Motor vehicle accidents account for approximately 42% of cases, a relatively steady figure for 30 years. Falls account for 27% of all and are the most common cause in patients older than age 65 years. Work-related injury (10%), sports (7%), and violence, typically gunshot wounds (15%), account for most of the remaining causes of SCI. Most injuries occur on the weekends and during the summer months.

Since 2000, the most frequent neurologic category at discharge is incomplete tetraplegia (34%), followed by complete paraplegia (23%), complete tetraplegia (18%), and incomplete paraplegia (19%). Less than 1% of persons experienced complete neurologic recovery by hospital discharge. The average length of hospital stay for a patient with SCI was 15 days in 2005, and the length of rehabilitation stay was 36 days. As one might expect, length of stay for patients with neurologically complete injuries is significantly longer. The Life expectancy for patients with SCI is significantly less than those for uninjured people. Mortality rates are significantly higher during the first year after injury than during subsequent years. As shown in Table 47.1, adapted from the NSCID Web site, life expectancy rates for SCI are directly related to the severity of injury.

There are profound sociologic and economic effects from SCI. About 57% of people with SCI were employed at the time of their injury. Ten years after injury, only 32% of persons with paraplegia and 24% with tetraplegia are employed. About 80% to 90% of patients with SCI are eventually discharged to a private residence, and only 6% are discharged to nursing homes. The rest are discharged to hospitals, group living situations, or other destinations.
Most SCI patients (53%) are single at the time of injury, and those who are married, or become married, are slightly more likely to become divorced than uninjured individuals. The average yearly and lifetime costs of SCI patients are directly related to the severity and level of injury. For example, patient with high tetraplegia (injury at C1-C4) is estimated to have expenses totaling $775,000 in the first year and $140,000 for each subsequent year. A 25-year-old with a C1-C4 injury will have a lifetime expense of $3 million, and a 50-year-old will have an expense of $1.8 million. A patient with low tetraplegia (injury at C5-C8) will have expenses of $500,000 in the first year and about $55,000 for each subsequent year. Paraplegics and incomplete motor injuries cost from $225,000 to $300,000 for the first year and $15,000 to $30,000 for each subsequent year. These numbers do not reflect the additional indirect costs that relate to unemployment and loss in productivity, which average another $60,000 per year per patient.

Nontraumatic SCI affects a large number of people and can result from a number of etiologies (see Chapter 111). These include multiple sclerosis (MS), neoplastic diseases, vascular disease, inflammatory disease, infections, and degenerative spinal stenosis. This population of patients more commonly presents with incomplete lesions and over a subacute or chronic period. The extent of injury at presentation, the response to treatment, and the prognosis of the underlying disease process will guide medical therapy and the ultimate rehabilitation goals.

MECHANISM OF INJURY

It is generally accepted that acute SCI is a two-step process that involves primary and secondary mechanisms. The primary mechanism results from the initial mechanical injury due to local deformation and energy transformation, whereas the secondary mechanisms encompass a cascade of biochemical and cellular processes that are initiated by the primary process and cause ongoing cellular damage and death.

Primary SCI is most commonly a combination of the initial impact as well as subsequent persisting compression. The most frequent primary mechanism of SCI is impact of bone and ligament against the spinal cord from high translational forces, such as that generated by flexion, extension, axial rotation, or vertebral compression. These motions may result in a variety of vertebral column injuries, which can be identified through imaging studies such as plain radiographs, computed tomography (CT) scans, or magnetic resonance imaging (MRI) scans. The spinal cord may consequently be compressed, stretched, or crushed by fracture or dislocations, burst fractures of the vertebral body, or acutely ruptured intervertebral disks. Injury can result from only the initial impact without ongoing compression. These may occur from severe ligamentous injuries in which the spinal column dislocates and then spontaneously reduces or when there is preexisting cervical spondylosis or spinal stenosis. In this circumstance, a trivial injury may cause major neurologic damage even without obvious fracture or dislocation after the event.

Similarly, SCI from sharp bone fragments or stabbing or missile injuries can produce a mixture of spinal cord laceration, concussion, contusion, and/or compression. Direct injuries, like indirect injuries, may be partial or complete in their destruction of the cord.

An understanding of the mechanism of injury and the radiographic findings can provide insight into the biomechanical stability of the vertebral column after SCI. For example, flexion injuries, particularly in the cervical and thoracic regions, may cause anterior compression fractures of vertebral bodies and unilateral or bilateral facet joint dislocation, which can cause spinal cord compression and spinal instability. Severe axial loading can cause complete fracture of the vertebral body with displacement of bony fragments and disk material into the spinal canal and SCI. Any combination of forces may occur in a single case. Understanding the mechanism of injury permits a more complete assessment of the underlying cord injury and the instability of the spinal column.

Secondary mechanisms that result from biochemical cascades that occur after the initial event are a source of ongoing SCI and neurologic deterioration. These cause damage to neural tissue on the cellular level and include the pathologic effects of microvascular changes, excitatory amino acids, cell membrane destabilization, free radicals, inflammatory mediators, and neuroglia apoptosis.

PATHOBIOLOGY

GROSS PATHOLOGY

The pathology of SCI has been divided into four relatively simple groups based on gross findings: solid cord injury, contusion/cavity, laceration, and massive compression. Solid cord injury refers to a cord that grossly appears normal without evidence of softening, discoloration, or cavity formation. However, damage to the cord can be clearly seen on histologic examination. Contusion or cavity injuries have no breach or disruption in the surface anatomy, and there are no dural adhesions. Areas of hemorrhage and necrosis (eventually evolving into cysts) are readily identified in the cord parenchyma. In many instances, these lesions taper rostrally and caudally in a cone-like fashion along the ventral regions of the posterior columns. Lacerations result in clear-cut disruption of the surface anatomy. This type of injury is most often caused by penetrating missiles or sharp fragments of bone. The lesions are characterized by a break in the glia limitans, with damage to the underlying cord parenchyma. The epicenter of the injury generally shows minimal to no evidence of cavity formation; rather, the lesion is dominated by the deposition of a variable amount of collagenous connective tissue that, in most cases, is adherent to the overlying meninges. With massive compression injury, the cord is macerated or pulpified to a varying degree. This lesion is often accompanied by severe vertebral body fractures or dislocations. In many instances, the epicenter of this lesion is replaced by connective tissue scar and fragments of nerve roots. The tissue response is similar to that seen with laceration injuries where extensive fibrous scarring occurs over time.

There are additional anatomic characteristics of SCI worth noting. The lesion may be surprisingly small and may involve no more than a single spinal cord segment. There may be multiple lesions, especially with gunshot wounds. It is also rare to observe a complete transection of the spinal cord; on close examination, there is almost always a small amount of residual tissue traversing the cord.

HISTOPATHOLOGY

The histologic changes in SCI can be divided into immediate, acute, intermediate, and late phases.

Immediate Phase (Initial 1 to 2 Hours)

The immediate event, presumably arising from the primary injury, consists of the actual mechanical disruption of tissue that occurs at the time of injury, such as tears, compression, and distortions.
Vascular changes are commonly found and are characterized by vasodilatation, congestion (hyperemia), and petechial hemorrhages. In many cases, however, no abnormalities are observed during this early time period, particularly in the absence of a massive compression or laceration injury. This lack of pathologic changes in the early period reflects the observation that the pathology of SCI is also due to secondary phenomena, which include progressive edema, ischemia, hemorrhage, inflammation, hyperthermia, as well as calcium-, free radical-, nitric oxide-, and glutamatemediated cell injury.

Acute Phase (Hours to 1 to 2 Days)

Vascular changes, edema, hemorrhage, inflammation, and neuronal and myelin changes characterize this phase. Edema may be vasogenic or cytotoxic. Vasogenic edema is leakage of plasma fluid into the extracellular space from breakdown of the blood-brain barrier (BBB). Cytotoxic edema results from intracellular swelling after cell death. Edema from either mechanism may result in pressure-induced ischemia caused by diminished blood flow to the injured region. Edema is seen from 3 hours to 3 days after injury. In addition to creating pressure effects, cell swelling may also alter astroglial functions.

Injury to vessels may lead to hemorrhage, which occurs primarily in the gray matter following contusion injury. Hemorrhages are primarily due to rupture of postcapillary venules or sulcal arterioles, either from mechanical disruption by the trauma or from intravascular coagulation leading to venous stasis and distention.

The inflammatory response that follows early after injury is a complex process involving vascular changes, cellular responses, and chemical mediators. There is a mild influx of neutrophils within 1 day, a peak at 2 days, and most are gone by 3 days. It is likely that the neutrophilic response is neurotoxic in nature, as these cells normally act to eradicate infection through the release of free radicals.

Neurons are very vulnerable to injury following SCI. Most neurons die from necrosis, but neuronal apoptosis also has been observed. Acute injury is characterized by axonal swelling, manifested as retraction balls or spheroids. Myelin breakdown occurs early following SCI. It is characterized initially by swelling of myelin sheaths and ultimately by its fragmentation and phagocytosis by macrophages. The loss of myelin occurs with the destructive process and is almost always associated with axonal pathology. Oligodendrocytes, like neurons, are exquisitely sensitive to SCI and undergo necrosis and apoptosis. It is likely that the death of oligodendrocytes contributes significantly to the process of wallerian degeneration.

Intermediate Phase (Days to Weeks)

Over the ensuing days and weeks, there are prominent glial responses with the elimination of necrotic debris, the beginning of astroglial scarring, the resolution of edema, the revascularization of tissue, and restoration of the BBB.

Late Phase (Weeks to Months/Years)

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

Wallerian degeneration is the anterograde disintegration of axons and their myelin sheaths that have been transected following injury. It is characterized by distorted and fragmented myelin sheaths with absent or malformed axons. An astroglial “scar,” which comprises tightly interwoven astrocyte processes and extracellular matrix, eventually replaces the destroyed myelinated axon. Wallerian degeneration is a protracted process and may take more than a year to complete. The spinal cord may also be replaced by fibrous connective tissue and collagen. This occurs particularly after lacerating-type injuries and is stimulated by violation of the glia limitans. This abnormal healing coupled with astroglial scarring are thought to create physical and biochemical barriers to axonal migration and spinal cord healing.

Another late finding is the formation of cysts and syrinxes, which may be single, multiple, or multiloculated. Cysts and syrinxes are surrounded by an astrogliotic wall and represent the final “healing” phase of the necrotic process. These cavities are filled with extracellular fluid and commonly contain residual macrophages, small bands of connective tissue, and blood vessels. These cavities typically do not create a clinical problem, except that they do not provide a good substrate for regeneration.

Schwannosis is an aberrant intra- and extramedullary proliferation of Schwann cells with associated axons. It is similar, if not identical, to traumatic neuromas that occur in injured peripheral nerves. Varying amounts of spinal cord tissue may be replaced by schwannosis. The Schwann cells are introduced into the spinal cord after penetrating injuries. The incidence of schwannosis in human SCI is very high and directly correlates with time after injury, suggesting an ongoing mechanism. Its clinical significance is unclear. The prolific schwannosis may be a physical barrier to spinal cord healing. The aberrant axons that are part of this process may have untoward physiologic consequences and potentially contribute to pain, spasticity, and other abnormal responses observed in the chronically injured patient with SCI.

In general, the morphologic responses in human SCI are stereotyped and follow discernible patterns. Early glial (astrocytic and microglial) responses may greatly influence the outcome of SCI.

DIAGNOSIS, NEUROLOGIC ASSESSMENT, AND CLASSIFICATION

CLINICAL EVALUATION

The diagnosis and initial management in patients with SCI often are intertwined, as a large percentage of patients present acutely, often with multisystem trauma, and require rapid assessment and medical intervention.

Prehospital trauma protocols are critical to prevent further injury to the spinal cord, particularly by modifying factors that contribute to secondary spinal cord damage. Any patient with suspected SCI should be immobilized with a hard cervical collar and/or a rigid head-strap/backboard until definitive neurosurgical assessment can take place. Treatment of hypoxia and hypotension, proper monitoring of vital signs, and transfer to an appropriate trauma center will affect ultimate outcomes positively.

On arrival to the trauma center, a rapid assessment should be undertaken to assess the status of the airway, respiratory, and circulatory (ABC) systems. In addition, a cursory assessment of the neurologic status (“disability”) and removal of all clothing with attention to possible injuries missed on the primary survey (“exposure”) are now included in the initial steps of trauma protocols. Clinical signs of shock and hypoxia require immediate attention and appropriate therapy.

Specific diagnosis of SCI requires a more comprehensive neurologic exam as outlined later in the text with the steps necessary to determine the exact spinal cord impairment. Concomitant with the
physical exam, complete and accurate imaging studies of the spinal column are necessary if SCI is suspected. These can enhance the accuracy of diagnosis and determine the extent of spinal column injury, especially in a comatose, confused, or uncooperative patient. Imaging studies are not necessary when patients are awake, are alert and cooperative without evidence of intoxication, do not have evidence of neurologic injury, and have no pain or tenderness along the spine to palpation and no associated injuries distracting from the general evaluation.

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