Acute spinal cord injury (SCI) occurs with trauma and certain procedures in which the spinal cord or vasculature is at risk. Acute SCI is assessed by level of injury, degree of neurologic impairment, spinal instability, and time since injury. It is associated with complications from pulmonary, cardiac, and neurologic dysfunction. This evolves to chronic spinal cord injury with different complications, including mass reflex and reflex hypertension. Optimal management of acute SCI depends on early recognition and minimization of mechanical and vascular compromise.
Keywordsacute spinal cord injury, autonomic hyperreflexia, chronic spinal cord injury, complications, surgery
A 32-year-old man presents to the emergency department following a motorcycle accident in which he was thrown to the roadside. He is mildly obtunded, smells of alcohol, and is difficult to examine neurologically, but he appears to have loss of sensation and motor activity below the C5 dermatome. Lateral neck films fail to identify bony injury or subluxation. Vital signs reveal hypotension (90/40 mm Hg), bradycardia (50 beats per minute), respiratory difficulty, and an oral temperature of 36.2°C. He is taken to the operating room emergently for repair of an open tibial fracture.
Spinal cord injury (SCI) is defined as injury to the spinal cord with neurologic dysfunction, with or without spinal column disruption. Anesthesia care is often required shortly after injury for resuscitation or surgical intervention. Later, anesthesia care may be required for surgery in patients with chronic SCI. Care may also be needed for patients who have recently sustained iatrogenic SCI (e.g., corrective surgery for scoliosis, aortic reconstructive surgery). Acute SCI occurs most frequently with trauma. Most of the problems accompanying SCI are a result of the neurologic loss, and they evolve over time.
Early recognition of SCI is important if devastating late complications are to be reduced or prevented. Acutely, the spinal cord distal to the level of injury is nonfunctional (e.g., areflexia, muscle flaccidity). Loss of thoracic sympathetic outflow leads to the spinal shock syndrome; this is characterized by hypotension and bradycardia due to unopposed vagal parasympathetic tone. After several days to 8 weeks, spinal reflexes in the uninjured cord become functional, but it is isolated from higher neural influence (i.e., cephalad spinal cord, brainstem, brain). This leads to uncontrolled spinal reflexes, muscle spasticity, and, ultimately, contractures. Such changes distinguish acute from chronic SCI and explain the attendant neurophysiologic differences between acute and chronic phases of injury.
All patients with multiple trauma should be evaluated for acute SCI, especially those with neck complaints or neurologic abnormalities; those who are comatose, with hypotension and absent reflexes; and any trauma patient with apparent hypovolemic shock without the expected compensatory tachycardia. Most traumatic acute SCI occurs in the more flexible cervical and thoracolumbar regions, but especially in the cervical spine. Radiographic films of the lateral cervical spine (C1–C7) and anteroposterior open-mouth (“swimmer’s view”) films usually confirm any bony injury. However, an unstable cervical spine may be missed in as many as 30% of cases. Thus clinical symptoms and computed tomography or magnetic resonance imaging may be required to identify all cervical injuries. Acute SCI can also occur without ligamentous or bony injury, especially in children; this is called spinal cord injury without radiographic abnormality (SCIWORA).
SCI is evaluated according to the following parameters:
Level of injury
Time since injury
Presence of spinal instability
Degree and type of neurologic impairment
Associated injuries (especially head injury) and medical problems
The level of injury is usually related to the mechanism of injury and the site of trauma. It is inferred by the neurologic examination and confirmed by any of the aforementioned radiographic procedures. The SCI level defines the potential complications and has implications for management. Up to 20% of patients (80% when cervical) have more than one level of injury.
The time since injury is usually apparent from the trauma event itself or the onset of neurologic findings. Early recognition of acute SCI is important, because early treatment may reduce the degree of irreversible injury. As time progresses, the spectrum of residual injury changes (see later).
Recognition of spinal instability (especially in the cervical spine) is important for patient positioning and movement, including during airway management and tracheal intubation. However, spine injury can occur without bony or ligamentous instability (e.g., spinal hematomas and abscesses; intraoperative injuries; trauma in children). Finally, the degree and type of neurologic impairment define the potential neurologic sequelae.
Certain surgical procedures are associated with a recognized risk of acute SCI. The neurologic risk in spinal column correction procedures is approximately 1% to 4%; however, the risk approaches 75% for the correction of severe kyphosis and is high with the removal of spinal cord tumors. Surgery involving the thoracic aorta also has a high risk (see Chapter 79 ). In surgical patients, early detection of the injury by intraoperative monitoring (sensory and motor evoked potentials) may allow correction before the injurious process (often ischemia) causes irreversible injury.
Acute SCI should be suspected in all trauma victims. Major trauma victims have a 2.6% risk of acute SCI, and patients with head trauma have a 4% to 5% risk of associated cervical spine injury. Traumatic acute SCI is thought to occur in 12 to 53 persons per million yearly, more often in males (4:1 predominance), and most commonly at C4 to C6. The second most commonly injured spine region is T11 to L2. The most frequent cause is motor vehicle accidents, often associated with alcohol or drug consumption. Falls in elderly persons and diving accidents are among the other important causes. Of patients with cervical spine injuries, about 25% become quadriplegic, and 40% have no residual neurologic impairment. That leaves about 35% with some degree of residual neurologic impairment.
Patients with acute SCI who show no resolution of neurologic impairment progress to chronic SCI. In obtunded patients, a careful history and neurologic examination may be needed to distinguish chronic SCI from cerebral injury. A better understanding of the mechanisms of SCI and its management has reduced overall mortality rate from 80% (World War I era) to less than 2% by the early 1980s.
The complications of SCI depend on the level of injury and the particular syndrome of injury, defined by the zone of injury in the spinal cord. The greatest number of complications occur with neurologically complete SCI (comparable to spinal cord transection). This is characterized by initial loss of all neurologic function at and below the level of injury. With high spinal cord injury (C4–C6), pulmonary function studies usually reveal reduced total lung capacity, vital capacity, expiratory reserve volume, and forced expiratory volume and increased residual lung volume. Vital capacity is an excellent measure of pulmonary compromise; patients with a vital capacity less than 15 mL/kg often require tracheal intubation and ventilatory support.
A variety of factors contribute to ventilatory compromise, which occurs in 67% of acute SCI patients within the first few days after injury ( Box 77.1 ). Acute SCI patients ventilate better when supine, because the abdominal contents tent the diaphragm, allowing for better mechanical action (except when distended bowel or stomach hinders diaphragmatic movement). Retained airway secretions and atelectasis are common. Ventilation may improve with chronic SCI due to strengthening of the chest wall and abdomen by intercostal and abdominal muscle contractures.