Spinal cord injury remains one of the most devastating of all survivable traumatic injuries. Each year, more than 11,000 new spinal cord injuries occur in the USA. Most of the injured are between 16 and 30 years of age at the time of injury, and males are much more likely than females to be injured. From the time of injury to death, the average cost of care of one patient exceeds $500,000, and the annual cost for acute and chronic care of spinal cord-injured patients is estimated to be $4 billion.
In the past, management of spinal cord injury focused on conservative care. The finding that pharmacologic treatment with intravenous methylprednisolone resulted in modest improvements in the National Acute Spinal Cord Injury Studies has provided new hope that future pharmacologic therapies may further diminish neurologic deficits. Recently, significant advances have also been made in the safety and efficacy of surgical decompression, stabilization, and fixation of the spine, paving the way for potentially repairing the damage resulting from the spinal injury. It is likely that future treatments will combine pharmacologic and surgical approaches to improve the outcome of this devastating injury.
In general, injury to the spinal cord follows compression or severe angulation of the vertebral spine. In rare instances, severe hypotension will lead to cord infarction, or axial distraction of elements of the vertebral column will result in a stretch injury of the cord. Most cord injuries follow subluxation with or without rotation of adjacent vertebral bodies that compress the cord between dislocated bone. Less often, axial compression of the spine will crush or wedge a vertebral body, and either bone or intervertebral disk fragments can be extruded into the spinal canal and compress the spinal cord. Another injury, seen usually in older patients with degenerative arthritis and stenosis of the cervical spine, involves neck hyperextension with infolding of the ligamentum flavum located in the spinal canal posterior to the cord. The spinal cord is trapped between arthritic bony spurs anteriorly and the ligamentum flavum posteriorly, producing a characteristic injury known as the central cord syndrome.
Early after spinal cord injury, there is a temporary loss of function. However, the initial trauma initiates a cascade of injury mechanisms that includes accumulation of excitatory amino acids, neurotransmitters, vasoactive eicosanoids, oxygen free radicals, and by-products of peroxidation. Activation of programmed cell death pathways occurs. Loss of the “blood-cord barrier” causes edema and increased tissue pressure that, along with cord hemorrhage, limit the blood supply, with the result that cell ischemia may further damage the cord. The distribution of cord edema, hemorrhage, and infarction dictates the neurologic symptoms and signs elicited at the time of evaluation.
Symptoms, Signs, and Syndromes of Spinal cord injury
In complete spinal injuries, there is no voluntary nervous function below the injury site. There is an initial phase of spinal shock, a loss of all reflexes below the injured segment, including bulbocavernosus, cremasteric, anal contraction to perianal stimulation, and deep tendon reflexes. This phenomenon may be temporary because of ionic and blood flow changes at the injury site. In incomplete spinal injuries, some function is present below the injury site, accounting for a much more favorable overall prognosis. Cord function may improve rapidly as spinal shock clears, or function may improve slowly in the months or years after injury.
The sites of damage within the cord and nerve root will determine what function is lost and what remains:
Anterior Cord Syndrome
This disorder results from damage to spinothalamic tracts and corticospinal tracts with relatively intact dorsal columns and preservation of touch and position sense, often related to injury to the spinal artery.
Central Cord Syndrome
Injury to the central portions of the cervical spinal cord often follows a brief concussive injury. Because distal leg and sacral motor and sensory fibers are located most peripherally in the cervical cord, the perianal sensation and some lower extremity movement and sensation may be preserved.
Nerve Root Injury
This can occur at the level of vertebral body dislocation. Direct root compression may be relieved by reduction of the dislocation or by removal of fractured bone or disrupted disk.
Conus Medullaris Syndrome
Injuries at the thoracolumbar region may cause injury to nerve cells of the tip of the spinal cord, descending corticospinal fibers, and lumbosacral nerve roots.
Cauda Equina Syndrome
This syndrome may arise from bony dislocation or disk extrusions in the lumbar regions, with compression of lumbosacral nerve roots below the conus medullaris. Bowel dysfunction as well as leg numbness and weakness occur commonly in this syndrome.
Evaluation and initial treatment must be started at the scene of the injury. Early recognition of a spine or spinal cord injury will dictate preventive measures to preserve remaining neurologic function. Patients suspected to have spinal cord injuries must be immobilized with rigid cervical collars and backboards. At the receiving medical facility, care must be taken to treat hypoventilation, hypoxia, and hypercapnia. Hypotension accompanied by bradycardia may be present. This results from the loss of sympathetic innervation to the heart in injuries to the cervical cord and is known as neurogenic shock. The loss of sympathetic innervation may also lead to paralytic ileus with abdominal sequestration of fluid, bladder distention, and hypothermia.
Until x-rays show otherwise, the examiner should assume that any comatose patient has an unstable spine fracture. Concern about combined injury must not delay resuscitation of hypotension and hypoventilation. Complaints of numbness and weakness should be noted carefully. Severe headache, particularly occipital pain, is common with odontoid fracture or hangman’s fracture (bilateral fracture of the C2). Palpation of the spine by sliding the hands under the patient with minimal spine movement can reveal focal bone tenderness or deformity. To assess weakness, the patient is asked to move hands and feet spontaneously and against resistance. Deep tendon reflexes must be evaluated in arms and legs; depression or absence of these reflexes will help localize the level of injury. An intact bulbocavernosus reflex (anal sphincter contraction to penile or clitoral compression or downward pressure on the bladder trigone by a Foley catheter balloon when the catheter is gently pulled) indicates that sacral motor and sensory pathways are present; absence of the bulbocavernosus reflex is consistent with spinal shock or with sacral nerve root injury. Sensory testing of the extremities, anterior trunk, neck, and face should be done to define a sensory level below which sensation is absent or decreased. Sensation in the sacral region should always be noted as sparing at this level may provide evidence of an incomplete injury.
When the patient must be transferred to an x-ray table or bed, the transfer should be done with a fireman’s carry, with at least three people on each side of the patient, with a fourth person, who directs the move, keeping the head in a neutral position by gentle axial traction (4–7 kg) applied with one hand on the chin and the other on the occiput.
Along with the physical examination, x-rays are essential for the evaluation of spine injuries. The lateral film is the most informative. Paravertebral or prevertebral soft tissue swelling usually indicates hemorrhage into these areas from fractures or ligamentous disruption. Anterioposterior spine films of the thoracic region and other levels permit assessment of lateral displacement of the vertebral bodies or widening or disruption of the pedicles. Oblique views in the cervical and lumbar regions will demonstrate facet fractures or dislocations. Frontal and lateral tomography can further identify bony abnormalities, but this procedure requires movement of the patient onto special tables for study.
MRI gives excellent views of the spine, disks, and spinal cord and is the diagnostic procedure of choice in patients with spinal cord injuries. Increased T2 signal in the spinal cord indicates injury to the cord. CT scanning provides superior visualization of the bony spine and paraspinal soft tissues that often provides additional insights regarding the management of spinal injury. Instillation of intrathecal metrizamide can outline the spinal cord and demonstrate cord compression.
A detailed neurologic examination of motor and sensory function allows for the classification of a spinal cord injury and differentiation from other pathologic entities. Often, the principal diagnostic obstacle in the setting of trauma is the inability to assess a patient due to altered mental status from associated brain injury or intoxication. Other complicating factors in the differential diagnosis include peripheral nerve injuries secondary to fractures of the extremities. The possibility of factitious symptoms should also be considered, especially when there is a question of psychiatric illness or secondary gain. This diagnosis can be addressed by detailed serial neurologic examinations. The potential for other related traumatic injuries must be considered, as nearly 60% of patients with spinal cord injury have other organ system injuries and 10% have additional spinal fractures.
Treatment of Spinal cord injury
Injuries of bony and neural elements of the spine often coexist, and the treatment of both should be coordinated to ensure the best possible outcome. Anatomical transection of the spinal cord almost never occurs in humans. Thus, strict adherence to the following principles is imperative to protect surviving spinal tissue: First, the injury must be recognized. Second, care must be exercised to prevent further damage (“secondary” injury) and to detect deteriorating neurologic function. Third, the patient must be maintained in optimal condition. Fourth, evaluation and rehabilitation of the patient must be actively pursued to maximize the function of surviving but dysfunctional nervous tissue. These principles must be followed in order to diminish the economic, social, and emotional cost of spinal cord injury.
Emergency resuscitation of the spinal cord-injured patient parallels that of any major trauma, with the modification that alignment of the spine must be scrupulously maintained. Based on evidence from the NASCIS-3 studies, adult patients with acute, nonpenetrating spinal injury can be treated with methylprednisolone immediately after recognition of spinal cord injury. Patients should be given 30 mg/kg of methylprednisolone intravenously within 8 hours. Those patients that received the initial bolus of methylprednisolone between 3 and 8 hours after injury should receive a 48-hour infusion instead of the standard 24-hour regimen used for patients treated within 3 hours.
Maintenance of adequate ventilation is critical. Patients with upper cervical cord injuries rely primarily on diaphragmatic activity for breathing. If paralytic ileus with abdominal distention occurs—or if the patient becomes fatigued—initially adequate ventilation may deteriorate. The patient will become hypoxic, requiring intubation and mechanical ventilation. Because of the loss of spinal cord sympathetic pathways, blood pressure may be low and may contribute to secondary injury. A mean arterial blood pressure between 85 and 90 mm Hg should be maintained for the first 7 days to improve perfusion of the injured cord. If urinary output is inadequate after catheterization, patients with mild hypotension will respond to low doses of pressors such as ephedrine, but these should be used only after unsuspected sources of hemorrhage in the chest or abdomen have been excluded.
Unstable cervical fractures should be managed initially with external immobilization. Skeletal fixation with Gardner-Wells tongs or halo traction can be achieved in most emergency rooms, or halter traction can be used temporarily. Thoracic and lumbar fractures are managed by keeping in a neutral position, “logrolling” as necessary for skin care or pulmonary management. Oscillating beds also improve skin and pulmonary care.
Operative management of spinal cord injury must take into account two major considerations: decompression and stability. Realignment of the spinal canal can be achieved by proper application of traction, postural adjustment, and spine manipulation done by experienced physicians. Surgical exploration for bony realignment may be necessary in some patients.
The primary causes of death after spinal injury are potentially avoidable. Renal failure following repeated urinary tract infections is best prevented by carefully performed intermittent bladder catheterization, which often can be done by the patient. Decubitus ulcers form easily over bony prominences in anesthetic areas and can be prevented with intermittent turning of patients and rotary beds.
The neurologic examination and age of the patient are the most critical prognostic factors for short-term and long-term recovery. In the acute trauma setting, spinal cord injury mortality is 20%. Recovery is more likely with limited lesions and in younger patients. Of the incomplete cord syndromes, the central cord syndrome and the Brown-Séquard’s syndrome have relatively good prognoses, while patients with anterior cord syndrome improve less. Excluding the first 18 months, patients’ 25-year survival rate is 70–80%. The most frequent causes of death include respiratory and cardiac disease, as well as a tenfold increased risk of suicide.
The team approach provided by centers that specialize in the spinal injury has been very successful and has shown that hospital stays can be shortened, complications can be reduced, and costs lowered. Rehabilitation also requires emotional support and patient education for the activities of daily living and job retraining. Exciting new insights into molecular mechanisms involved in spinal injury hold great promise for improved pharmacologic treatments. Emerging surgical procedures that incorporate advances in bioengineering and functional neurosurgery suggest that restorative neurosurgery will also have an increasing role in improving the functional abilities of patients with spinal injuries. It is likely that the evolving multidisciplinary approach will lead to improved treatment, recovery, and outcome for patients with spinal injuries.