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.

Metabolic considerations

On initial presentation, patients with spinal cord injury often require emergency airway management. Succinylcholine is preferred by many in the emergency department or operating room to manage patients with acute spinal cord injury. When these same patients subsequently return to the operating room for additional surgical procedures, the use of succinylcholine can lead to a tremendous potassium release, which may cause ventricular fibrillation and cardiac arrest. With denervation of muscle, there is an increase in the number of nicotinic receptors: some from the muscle membrane where, previously, there were no nictonic receptors and also from the appearance of new isoforms of these nicotinic receptors. All of these receptors respond to succinylcholine with release of potassium from a larger area of muscle membrane than would normally occur, and hence, hyperkalemia results. The change in the number and type of receptors occurs as early as 3 days after injury and may be ongoing for up to 6 months. The marked hyperkalemic response has been reported to occur as early as 5 days after injury, but the hyperkalemia also occurs in patients who have an associated ongoing infectious process.

Patients with an injury to the spinal cord at between T1 and L2, with sufficient damage to the sympathetic nervous system, lose the ability to thermoregulate. Hypothermia can lead to vasoconstriction, metabolic acidosis from peripheral vasoconstriction and myocardial ischemia from coronary artery vasoconstriction. Conversely, patients with spinal cord lesions above C7 have an inability to sweat, which can be manifested by hyperthermia.

In patients with longstanding paralysis, bone reabsorption can lead to hypercalcemia. Patients with impaired ventilatory drive can present with respiratory acidosis, with or without a compensating alkalosis.

Airway management mandates stabilization of the neck while intubating the trachea in an expeditious manner for the reasons mentioned previously. Chest physiotherapy, deep vein thrombosis prophylaxis (beginning 2-3 days after the injury to avoid hemorrhage at the site of injury), decompression of the stomach, administration of stress-related ulcer prophylaxis, and monitoring gas exchange are all considerations.