Neurogenic Shock and Spinal Injury

This condition should NOT be confused with spinal shock. Neurogenic shock is a true form of shock and described as a hemodynamic disruption (reduced heart rate and blood pressure) as a result of a spinal injury. Since spinal injuries result in this condition, the anesthetic implications will cover both neurogenic shock and spinal injury in general.

Hemodynamic instability - Liberal crystalloid and blood administration should be used to correct hemodynamic drops - especially in cervical and/or thoracic injuries where sympathectomy causes widespread vasodilation. Standard drugs such as phenylephrine and ephedrine are also acceptable if not otherwise contraindicated.

Spinal clearance - always get a spinal clearance. Even if the patient is cleared, take precautions to limit the possibilities of injury while moving the patient or manipulating the airway.

Fiberoptic intubation - if there's any question of cervical instability, maintain the head and neck in a neutral position at all times and utilize fiberoptic intubation to secure the airway.

Cervical collars/braces - these do not always provide optimal stabilization. DO NOT assume the patients C-spine is stable.

Tracheobronchial suctioning - associated with bradycardia and cardiac arrest! This should only be done after optimal oxygenation.

Avoid nitrous oxide - In the event that there is diffuse trauma along with the spinal injury, air entrainment in closed spaces could expand/migrate with the use of nitrous.

Monitor and supplement O2 EARLY – muscle weakness, sympathectomy, etc. all contribute to arterial hypoxemia, which is very common after spinal cord injury. Cervical injury (especially C3-C5) - associated with hypoxemia due to disruption of diaphragm innervation. Hypoxemia is an early sign of cervical injury.

Rocurronium/Vecuronium - these are the nondepolarizing neuromuscular blockers (NDNMB) of choice. As a general rule, RSI with Rocurronium is the most common approach to avoid the potential for hyperkalemia associated with Succinylcholine. Succinylcholine may be used for the first 24 hours after the injury, but should be avoided thereafter.

Prolonged ventilation - These patients may require prolonged mechanical ventilation depending on the spinal levels affected and severity of the injury.

C-spine precautions - During transport, always use the C-collar or brace.

Smooth transitions - Ensure the patient is deep enough before intubation. If not contraindicated, deep extubation is sometimes preferred to prevent bucking/coughing. Coughing and/or bucking in these transitions may cause disruption of the surgical site and/or damage to the spine.

Poikilothermia - This is the inability to regulate one’s body temperature and is common in spinal cord injuries. Be ready to monitor and maintain normothermia.

The one finding that separates it from septic shock - Both are distributive, both look warm and vasodilated, and both are hypotensive. Septic shock is tachycardic; neurogenic shock is bradycardic. Bradyarrhythmia, hypotension, and flushed warm skin together are the classic triad here - see the Sepsis / Septic Shock entry for the other side of that contrast.

Fluids to euvolemia, then vasopressor - Volume comes first, but once the patient is euvolemic, repeat boluses are not the answer and only add edema; the deficit is tone, not volume. Norepinephrine is the preferred agent because its combined alpha and beta activity treats the hypotension and the bradycardia together. Phenylephrine is pure alpha, and the reflex bradycardia it produces stacks on top of already unopposed vagal tone. Epinephrine is reserved for refractory hypotension and is rarely needed.

Cord perfusion target - Keep MAP 85 to 90 mmHg for the first 7 days after acute spinal cord injury to protect the cord from secondary ischemic injury. That is a higher pressure than you would settle for in other shock states, and it is the number the anesthetic is built around. Use caution with vasoconstrictors where coexisting injuries could be worsened by them.

Pretreat the vagal stimulus - Atropine or glycopyrrolate to oppose vagal tone before tracheobronchial suctioning, not after the rate drops. Isoproterenol is an option when a pure chronotropic effect is what is needed, and profound bradycardia in a high cervical injury (C1 through C5) may need temporary pacing.

Warm and pink is not the same as perfused - Vasodilated skin gives a flash capillary refill and a normal-looking extremity while the kidney and the cord are underperfused, so the look of the patient will flatter you. Follow urine output (under 0.5 mL/kg/hr signals renal hypoperfusion) and serial lactate instead.

It rides alongside spinal shock, it is not a synonym for it - Beyond the usual caution not to confuse the two: they occur together in the same patient, and neurogenic shock is the hemodynamic component of the spinal shock syndrome. They are tracked by different markers - spinal shock by the return of reflexes over hours to weeks, neurogenic shock by the vasopressor requirement, which can persist for weeks. An areflexic patient who is also hypotensive has both problems, not one or the other. See the Spinal Shock and Spinal Injury entry.

Neurogenic shock describes is a hemodynamic disruption characterized by a reduction in blood pressure and/or heart rate severe enough to impair organ function.

Neurogenic shock may last hours to weeks. The average is 1-3 weeks.

Sympathectomy, bradycardia, and increased SVR are all associated with cervical fractures. Sympathectomy causes widespread vasodilation and shock.

Cervical injury is the primary cause for hemodynamic changes. Thoracic injuries are also associated with hemodynamic changes, but to a lesser extent when compared to cervical injury.

T1-T4 injury is more especially related to bradycardia because these nerves supply sympathetic innervation to the heart.

The major cause of morbidity/mortality in these patients is a combination of alveolar hypoventilation and inability to clear secretions. Be cognizant of atelectasis and perform recruitment maneuvers where possible.

The patient should be able to generate a tidal volume > 10-15 cc/kg and/or a negative inspiratory force of 20 mmHg.

Where this sits among the shock states: shock sorts into four categories - distributive, hypovolemic, cardiogenic, and obstructive - and neurogenic shock belongs to the distributive group, the same family as septic and anaphylactic shock, because the primary lesion is vascular tone rather than pump or volume. Loss of descending sympathetic outflow with preserved vagal tone drops systemic vascular resistance and leaves a dilated, underfilled venous bed; filling pressures are low. That is the opposite of hypovolemic shock, in which systemic vascular resistance rises as the body compensates - and that difference is exactly why a hypotensive patient with warm, flushed, well-perfused skin and a slow heart rate is the one in whom to suspect cord injury.

It is a diagnosis of exclusion in trauma. ATLS holds that hemorrhage is the more common cause of hypotension, so bleeding is ruled out first; finding a vertebral fracture does not close the question, because the two coexist often enough to fool you. Incidence is roughly 19% of cervical spine injuries and 7% of thoracic injuries, and most studies use a systolic pressure under 90 mmHg with a heart rate under 80 as the working definition.