EPIDEMIOLOGY

• There are approximately 12,000 new spinal cord injuries requiring treatment each year.

• Injury to the vertebral column occurs much less frequently than injury to the appendicular skeleton, and vertebral column fractures account for approximately 6% of all fractures.

• Fifteen percent to 20% of vertebral fractures can occur at multiple noncontiguous levels.

• Motor vehicle accidents account for approximately 50% of all traumatic spinal cord injuries.

• In patients with spinal cord injury, the overall mortality during the initial hospitalization is 17%.

• Approximately 2% to 6% of trauma patients sustain a cervical spine fracture.

• The ratio of male to female patients sustaining vertebral fractures is 4:1.

• The lifetime direct medical cost of spinal cord injury for persons injured at age 25 years is estimated to be between $1.5 and $4.6 million depending on injury severity.

  ANATOMY

• The spinal cord occupies approximately 35% of the canal at the level of the atlas (C1) and 50% of the canal in the lower cervical spine and thoracolumbar segments. The remainder of the canal is filled with epidural fat, cerebrospinal fluid, and dura mater.

• The conus medullaris represents the caudal termination of the spinal cord. It contains the sacral and coccygeal myelomeres and lies dorsal to the L1 body and L1–L2 intervertebral disc.

• The cauda equina (literally translated means “horse’s tail”) represents the motor and sensory roots of the lumbosacral myelomeres. These roots are less likely to be injured because they have more room in the canal and are not tethered to the same degree as the spinal cord. Furthermore, the motor nerve roots are composed of lower motor neurons, which are more resilient to injury than the upper motor neurons of the brain and spinal cord.

• A reflex arc is a simple sensorimotor pathway that can function without using either ascending or

  descending white matter long tract axons. A spinal cord level that is anatomically and physiologically intact may demonstrate a functional reflex arc at that level despite dysfunction of the spinal cord cephalad to that level.

  MECHANISM OF INJURY

  A long-standing and fundamental problem of classifying spinal injury based on presumed mechanism of injury is that the same mechanism of injury can result in morphologically different patterns of injury; similar morphologic patterns of injury can also be the result of different injury mechanisms, and the patterns of head deflection do not predict spinal injury patterns. Several characteristics of the injury force that determine the extent of neural tissue damage have been identified. These include the rate of force application, the degree of neural tissue compression, and the duration of neural tissue compression.

  Primary Injury

  Primary injury refers to physical tissue disruption caused by mechanical forces.

• Contusion: This sudden, brief compression by a displaced structure affects central tissues primarily and accounts for the majority of primary injuries; thus, it is responsible for the majority of neurologic deficits. Contusion injuries are potentially reversible, although irreversible neuronal death occurs along with vascular injury and intramedullary hemorrhage.

• Compression: Injury results from decreased size of the spinal canal; it may occur with translation or angulation of the spinal column, as in burst injuries or epidural hematomas. Injury occurs by:

  • Mechanical deformation interrupting axonal flow

  • Interruption of spinal vascularity resulting in ischemia of neurologic structures

• Stretch: Injury results in longitudinal traction, as in the case of a flexion–distraction injury. Injury occurs as a result of capillary and axonal collapse secondary to tensile distortion.

• Laceration: This is caused by penetrating foreign bodies, missile fragments, or displaced bone.

  Secondary Injury

  Secondary injury refers to additional neural tissue damage resulting from the biologic response initiated by physical tissue disruption. Local tissue elements undergo structural and chemical changes. These changes, in turn, elicit systemic responses. Changes in local blood flow, tissue edema, metabolite concentrations, and concentrations of chemical mediators lead to propagation of interdependent reactions. This pathophysiologic response, referred to as secondary injury, can propagate tissue destruction and functional loss.

  CLINICAL EVALUATION

• Assess the patient: Airway, breathing, circulation, disability, and exposure (ABCDE). Avoid the head-tilt–chin-lift maneuver, hypoxia, and hypotension.

• Initiate resuscitation: Address life-threatening injuries.

• Evaluate the patient’s level of consciousness.

• Evaluate injuries to the head, chest, abdomen, pelvis, and spine.

  The spine should be protected at all times during the management of a multiply injured patient. The ideal position is with the whole spine immobilized in a neutral position on a firm surface. This may be achieved manually or with a combination of semirigid cervical collars, side head supports, and strapping. Strapping should be applied to the shoulders and pelvis as well as the head to prevent the neck becoming the center of rotation of the body.

  Take extreme care when logrolling the patient to assess the spinal column, as there is significant risk of injuring the spinal cord if there is instability. Examine the skin for bruising and abrasions, and palpate spinous processes for tenderness and diastasis. The patient should be placed on a scoop stretcher or long spine board with the head and neck supported.

• Calenoff found a 5% incidence of multiple noncontiguous vertebral injuries. Half of the secondary lesions were initially missed, with a mean delay of 53 days in diagnosis; 40% of secondary lesions occurred above the primary lesion and 60% below. The region T2 through T7 accounted for 47% of primary lesions in this population but only 16% of reported spinal injuries in general.

• Injuries of the vertebral column tend to cluster at the junctional areas: the craniocervical junction (occiput to C2), the cervicothoracic junction (C7–T1), and the thoracolumbar junction (T11–L2). These areas represent regions of stress concentration, where a rigid segment of the spine meets a more flexible segment. Also contributing to stress concentration in these regions are changes at these levels in the movement constraints of vertebrae.

• Among these injuries, the most serious and most frequently missed is craniocervical dissociation.

• In trauma patients, thoracic and lumbar fractures are concentrated at the thoracolumbar junction, with 60% of thoracic and lumbar fractures occurring between T11 and L2 vertebral levels.

• Three common patterns of noncontiguous spinal injuries are as follows.

• Assess injuries to the extremities.

• Complete the neurologic examination to evaluate reflexes, sensation (touch, pain), and motor function (Fig. 8.1 and Table 8.1).

   

   

   

   

   

   

• Perform a rectal examination to test for perianal sensation, resting tone, and the bulbocavernosus reflex.

  Pattern A: Primary injury at C5–C7, with secondary injuries at T12 or in the lumbar spine Pattern B: Primary injury at T2–T4, with secondary injuries in the cervical spine Pattern C: Primary injury at T12–L2, with a secondary injury at L4–L5

  Spinal Shock

• Spinal shock is defined as spinal cord dysfunction based on physiologic rather than structural disruption. Resolution of spinal shock may be recognized when reflex arcs caudal to the level of injury begin to function again, usually within 24 hours of injury.

• Spinal shock should be distinguished from neurogenic shock, which refers to hypotension associated with loss of peripheral vascular resistance in spinal cord injury.

  Neurogenic Shock

• Neurogenic shock (Table 8.2) refers to flaccid paralysis, areflexia, and lack of sensation to physiologic spinal cord “shutdown” in response to injury.

   

   

   

• It is most common in cervical and upper thoracic injuries.

• It almost always resolves within 24 to 48 hours.

• The bulbocavernosus reflex (S3–S4) is the first to return (Table 8.3).

   

  

   

   

• Initial tachycardia and hypertension immediately after injury are followed by hypotension accompanied by bradycardia and venous pooling.

• Hypotension from neurogenic shock may be differentiated from cardiogenic, septic, and hypovolemic shock by the presence of associated bradycardia, as opposed to tachycardia.

• Treatment is based on administration of isotonic fluids, with careful assessment of fluid status (beware of overhydration).

• Recognizing neurogenic shock as distinct from hemorrhagic shock is critical for safe initial resuscitation of a trauma patient. Treatment of neurogenic shock is pharmacologic intervention to augment peripheral vascular tone. This vascular tone may be essential for effective resuscitation. Fluid overload from excessive fluid volume administration, typical in treatment of hemorrhagic shock, can result in pulmonary edema in the setting of neurogenic shock.

  Bulbocavernosus Reflex

• The bulbocavernosus reflex refers to contraction of the anal sphincter in response to a squeeze on the glans penis in a male, the clitoris or the mons pubis in a female, or a pull on the urethral catheter.

• The absence of this reflex indicates spinal shock.

• The return of the bulbocavernosus reflex heralds the end of spinal shock and generally occurs within 24 hours of the initial injury.

• The presence of a complete lesion after spinal shock has resolved portends a virtually nonexistent chance of neurologic recovery.

• The bulbocavernosus reflex is not prognostic for lesions involving the conus medullaris or the cauda equina.

  RADIOGRAPHIC EVALUATION

• The lateral cervical spine radiograph is routine in the standard evaluation of trauma patients. Patients complaining of neck pain should undergo complete radiographic evaluation of the cervical spine, including anteroposterior and odontoid views.

• Lateral radiographic examination of the entire spine is recommended in patients with spine fractures when complete clinical assessment is impaired by neurologic injury or other associated injuries.

• Despite using all the radiographic techniques available, uncertainty about cervical spinal clearance may remain. Continued protection of the neck and serial studies may ultimately demonstrate occult injuries.

• Magnetic resonance imaging may aid in assessing spinal cord or root injury as well as the degree of canal compromise.

  CLASSIFICATION

  The functional consequences of spinal cord injury are usually described by terms that refer to the severity and pattern of neurologic dysfunction: complete spinal cord injury, incomplete injury, and transient spinal cord dysfunction describe different grades of severity of neurologic injury. Names for different types of spinal cord injury syndromes, such as anterior cord syndrome, central cord syndrome, and Brown-Séquard syndrome, refer to patterns of neurologic dysfunction observed during clinical evaluation.

  GRADING OF NEUROLOGIC INJURY

  Spinal Cord Injury: Complete

• No sensation or voluntary motor function is noted caudal to the level of injury in the presence of an intact bulbocavernosus reflex. (The sacral levels are commonly quoted as being S2, S3, and S4.)

• Reflex returns below the level of the cord injury.

• The level of injury is named by the last spinal level of partial neurologic function.

• One can expect up to one to two levels of additional root return, although the prognosis for recovery is extremely poor.

  Spinal Cord Injury: Incomplete

• Some neurologic function persists caudal to the level of injury after the return of the bulbocavernosus reflex.

• As a rule, the greater the function distal to the lesion and the faster the recovery, the better is the prognosis.

• Sacral sparing is represented by perianal sensation, voluntary rectal motor function, and great toe flexor activity; it indicates at least partial continuity of white matter long tracts (corticospinal and spinothalamic) with implied continuity between the cerebral cortex and lower sacral motor neurons. It indicates incomplete cord injury, with the potential for a greater return of cord function following resolution of spinal shock.

  PATTERNS OF INCOMPLETE SPINAL CORD INJURY (TABLE 8.4)

   

  

   

   

  Brown-Séquard Syndrome

• This is a hemicord injury with ipsilateral muscle paralysis, loss of proprioception and light touch sensation, and contralateral hypesthesia to pain and temperature.

• The prognosis is good, with over 90% of patients regaining bowel and bladder function and ambulatory capacity.

  Central Cord Syndrome

• This is most common and is frequently associated with an extension injury to an osteoarthritic spine in a middle-aged person.

• It presents with flaccid paralysis of the upper extremities (more involved) and spastic paralysis of the lower extremities (less involved), with the presence of sacral sparing.

• Radiographs frequently demonstrate no fracture or dislocation because the lesion is created by a pincer effect between anterior osteophytes and posterior infolding of the ligamentum flavum.

• The prognosis is fair, with 50% to 60% of patients regaining motor and sensory function to the lower extremities, although permanent central gray matter destruction results in poor hand function.

  Anterior Cord Syndrome

• This is common and involves motor and pain/temperature loss (corticospinal and spinothalamic tracts) with preserved light touch and proprioception (dorsal columns).

• The prognosis is good if recovery is evident and progressive within 24 hours of injury. Absence of sacral sensation to temperature or pinprick after 24 hours portends a poor outcome, with functional recovery in 10% of patients according to one series.

  Posterior Cord Syndrome

• This is rare and involves loss sensation of deep pressure, deep pain, and proprioception with full voluntary power, pain, and temperature sensation.

  Conus Medu laris Syndrome

• This is seen in T12–L1 injuries and involves a loss of voluntary bowel and bladder control (S2–S4 parasympathetic control) with preserved lumbar root function.

• It may be complete or incomplete; the bulbocavernosus reflex may be permanently lost.

• It is uncommon as a pure lesion and more common with an associated lumbar root lesion (mixed conus–cauda lesion).

  NERVE ROOT LESIONS

• Isolated root lesions may occur at any level and may accompany spinal cord injury.

• This may be partial or complete and results in radicular pain, sensory dysfunction, weakness, hyporeflexia, or areflexia.

  CAUDA EQUINA SYNDROME

• This is caused by multilevel lumbosacral root compression within the lumbar spinal canal.

• Clinical manifestations include saddle anesthesia, bilateral radicular pain, numbness, weakness, hyporeflexia or areflexia, and loss of voluntary bowel or bladder function.

  GRADING SYSTEMS FOR SPINAL CORD INJURY

  Frankel Classification

  Grade A: Absent motor and sensory function

  Grade B: Absent motor function; sensation present

  Grade C: Motor function present but not useful (2/5 or 3/5); sensation present

  Grade D: Motor function present and useful (4/5); sensation present

  Grade E: Normal motor (5/5) and sensory function

  American Spinal Injury Association (ASIA) Impairment Scale

  Grade A: Complete: No motor or sensory function is preserved in sacral segments S4–S5.

  Grade B: Incomplete: Sensory but not motor function is preserved below the neurologic level and extends through the sacral segment S4–S5.

  Grade C: Incomplete: Motor function is preserved below the neurologic level; most key muscles below the neurologic level have a muscle grade <3.

  Grade D: Incomplete: Motor function is preserved below the neurologic level; most key muscles below the neurologic level have a muscle grade >3.

  Grade E: Normal: Motor and sensory function is normal.

   

  American Spinal Injury Association Neurologic Assessment

  According to ASIA definitions, the neurologic injury level is the most caudal segment of the spinal cord with normal motor and sensory function on both sides: right and left sensation and right and left motor function. For functional scoring, 10 key muscle segments corresponding to innervation by C5, C6, C7, C8, T1, L2, L3, L4, L5, and S1 are each given a functional score of 0 to 5 out of 5. For sensory scoring, both right and left sides are graded for a total of 100 points. For the 28 sensory dermatomes on each side of the body, sensory levels are scored on a zero- to two-point scale, yielding a maximum possible pinprick score of 112 points for a patient with normal sensation.

  TREATMENT

  Note: Specific fractures of the cervical and thoracolumbar spines will be covered in their respective chapters.

  Immobilization

  1. A rigid cervical collar is indicated until the patient is cleared radiographically and clinically. A patient with a depressed level of consciousness (e.g., from ethanol intoxication) cannot be cleared clinically.

  2. A special backboard with a head cutout must be used for children to accommodate their proportionally larger head size and prominent occiput.

  3. The patient should be removed from the backboard (by logrolling) as soon as possible to minimize pressure sore formation.

  Medical Management of Acute Spinal Cord Injury

• Intravenous methylprednisolone

  • It may improve recovery of neurologic injury.

  • The efficacy of spinal cord injury steroid protocols is controversial. While it is not considered “standard of care” in many centers, some institutions continue to employ the protocol if administered within 8 hours of injury. The increased risk of complications such as

    gastrointestinal hemorrhage, wound infection, sepsis, and pneumonia and its questionable efficacy have resulted in the trend away from use of methylprednisolone.

  • There is a loading dose of 30 mg/kg.

    • 5.4 mg/kg per hour over the next 24 hours if started within 3 hours of spinal cord injury

    • 5.4 mg/kg per hour over the next 48 hours if started within 8 hours of spinal cord injury

  • It is not indicated for pure root lesions.

• Experimental pharmacologic agents include:

  • Naloxone (opiate receptor antagonist)

  • Thyrotropin-releasing hormone

  • GM1 gangliosides: A membrane glycolipid that, when administered within 72 hours of injury, results in a significant increase in motor scores. Administer 100 mg per day for up to 32 days after injury. It is not recommended for simultaneous use with methylprednisolone.

  • Riluzole (sodium channel blocker) U.S. Food and Drug Administration (FDA)–approved for use in amyotrophic lateral sclerosis (ALS): It blocks pathologic activation of sodium channels reducing glutamate release.

    COMPLICATIONS

• Gastrointestinal: Ileus, regurgitation and aspiration, and hemorrhagic gastritis are common early complications, occurring as early as the second day after injury. Gastritis is thought to be the result of sympathetic outflow disruption with subsequent unopposed vagal tone resulting in increased gastric activity. Passage of a nasogastric tube and administration of histamine (H2) receptor antagonists should be used as prophylaxis against these potential complications.

• Urologic: Urinary tract infections are recurrent problems in the long-term management of paralyzed patients. An indwelling urinary catheter should remain in the patient during the acute, initial management only to monitor urinary output, which is generally low with neurogenic shock because of venous pooling and a low-flow state. Following this, sterile intermittent catheterization should be undertaken to minimize potential infectious sequelae.

• Pulmonary: Acute quadriplegic patients are able to inspire only using their diaphragm because their abdominal and intercostal muscles are paralyzed. Vital capacity ranges from 20% to 25% of normal, and the patient is unable to forcibly expire, cough, or clear pulmonary secretions. Management of fluid balance is essential in the patient in neurogenic shock because volume overload rapidly results in pulmonary edema with resolution of shock. Positive pressure or mechanical ventilation may be necessary for adequate pulmonary function. Without aggressive pulmonary toilet, pooling of secretions, atelectasis, and pneumonia are common and are associated with high morbidity and mortality.

• Skin: Problems associated with pressure ulceration are common in spinal cord–injured patients owing to anesthesia of the skin. Turning the patient every 2 hours, careful inspection and padding of bony prominences, and aggressive treatment of developing decubitus ulcers are essential to prevent long-term sequelae of pressure ulceration.

  CLEARING THE SPINE

• A cleared spine in a patient implies that diligent spine evaluation is complete and the patient does not have a spinal injury requiring treatment.

• The necessary elements for a complete spine evaluation are:

  1. History to assess for high-risk events and high-risk factors

  2. Physical examination to check for physical signs of spinal injury or neurologic deficit

  3. Imaging studies based on an initial evaluation

• Patients with a diagnosed cervical spine fracture have at least one of the following four characteristics: midline neck tenderness, evidence of intoxication, abnormal level of alertness, or several painful injuries elsewhere.

• Therefore, criteria for clinical clearance are:

  1. No posterior midline tenderness

  2. Full pain-free active range of motion

  3. No focal neurologic deficit

  4. Normal level of alertness

  5. No evidence of intoxication

  6. No distracting injury

• Radiographs are not necessary for patients who are alert, are not intoxicated, have isolated blunt trauma, and have no neck tenderness on physical examination.

• The process of clearing the thoracolumbar spine is similar to that for clearing the cervical spine. Only anteroposterior and lateral view radiographs are necessary. Patients with clear mental status, no back pain, and no other major injuries do not need radiographs of the entire spine to exclude a spinal fracture.