Pathophysiologic factors

Spinal cord injury can have catastrophic results. A typical injury to the cord results in edema, hemorrhage, and involvement of sensory, motor, and sympathetic changes that may result in spinal shock. Injuries are more likely to damage the spinal cord when they involve C3 and vertebrae below it. Injuries involving the C1 and C2 vertebrae are less likely to impinge on and damage the spinal cord; patients who survive the precipitating event have a good chance of retaining neurologic function. However, injuries severe enough to damage C1 and C2 vertebrae often have a high mortality rate, either because of associated traumatic brain injury or injury to the airway.

Respiratory considerations

A lesion at a vertebra above T7 may alter respiratory function. Vital capacity, expiratory reserve volume, and forced expiratory volume typically are decreased. The resulting respiratory physiologic characteristics depend on three factors: intercostal muscle function, the diaphragmatic function, and the use of accessory muscles of respiration.

Neurons exiting the cord at C3, C4, and C5 provide innervation of the diaphragm, so a spinal cord injury at C3 results in paralysis of the diaphragm; if the injury is not recognized and treated immediately, patients with such lesions asphyxiate. With a C5 lesion, a patient may have signs of partial diaphragmatic paralysis. By comparison, a C6 lesion enables the patient to maintain ventilation because innervation of the diaphragm is intact. Even so, the patient will have some compromised respiratory function, with sternal retraction and paradoxical breathing. This problem of respiratory compromise is due to intercostal paralysis; the patient can still have a compromised cough and an inability to clear secretions.

Spinal cord lesions are not always static. They may be complete or incomplete, such as a Brown-Séquard syndrome. A spinal cord lesion may involve a spreading hematoma that then leads to increased edema and ischemia of the neural tissue. Ondine curse, “central” sleep apnea, can be caused by a lesion involving the anterolateral portion of C2 through C4 spinal cord segments. Patients who have traumatic injury to the spinal cord with associated neurologic deficit have an increased risk of developing deep venous thrombosis and pulmonary embolic events due to thrombus, or from a fat embolus, the latter associated with other bone-related injuries. Other pulmonary disorders associated with spinal cord injury are neurogenic pulmonary edema, aspiration pneumonia, and acute respiratory distress syndrome.

Cardiovascular considerations

After spinal cord injury, blood pressure and heart rate increase, sometimes dramatically, because of the associated sympathetic storm. Over time, parasympathetic activity increases, manifested by bradycardia, sinus node pauses, sick sinus syndrome, supraventricular arrhythmias, ventricular ectopy, and possibly ST-segment changes, based on the individual’s coronary anatomy.

Depending on the level and severity of injury, spinal shock may occur and last up to 6 weeks as a result of a loss of vascular tone and of the vasopressor reflex. Injury to the spinal cord from the level of the T1 to L2 damages the sympathetic nervous system (see Chapter 40) and may result in orthostatic hypotension and, potentially, bradycardia. The bradycardia results from the loss of cardiac acceleration fibers. Prompt treatment of spinal shock with intravascular fluids and vasoactive agents (see Chapter 88) to maintain a mean arterial pressure of 65 mm Hg to 75 mm Hg can potentially improve neurologic outcome.

Gastrointestinal considerations

Many patients with spinal cord injury subsequently develop paralytic ileus, resulting in gastric distention impinging on diaphragmatic excursion, and decreasing functional reserve capacity of the lungs, requiring prolonged preoxygenation prior to induction of anesthesia for any surgical procedures. The gastric distention and delayed gastric emptying place these patients at increased risk of regurgitating and aspirating gastric contents during induction of anesthesia.