Spinal Shock and Spinal Injury

This condition should NOT be confused with neurogenic shock. Spinal shock describes arreflexia and/or parathesia below the level of injury. This condition is NOT a true form of shock. Since spinal injuries result in this condition, the anesthetic implications will cover both spinal 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 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. See "additional notes" on collars/braces.

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 SaO2 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, but should be avoided thereafter.

MEP monitoring - Ensure that the surgical case does not require MEP monitoring during the case before administering NDNMBs.

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

Maintain cervical neutrality - 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.

Tight temperature control - poikilothermia (the inability to regulate one’s body temperature) is common in spinal cord injuries, so be ready to monitor and maintain normothermia.

Areflexia and hypotension are two separate problems - Spinal shock is the reflex phenomenon and carries no hemodynamic definition of its own. When the same patient is hypotensive and bradycardic, that is neurogenic shock riding alongside it - the hemodynamic component of the same cord injury, and a distributive shock in its own right. Do not file the blood pressure under "spinal shock is not really shock" and leave it alone. See the Neurogenic Shock and Spinal Injury entry for how to treat that half.

Name the exam you are documenting - Use the ASIA (American Spinal Injury Association) impairment scale for the baseline neurologic exam, and a serial reflex exam for the trajectory. Record level and grade before induction; that is the comparison point if anything changes intraoperatively, and reflex recovery in the early phase has been linked to functional prognosis.

Rule out hemorrhage before crediting the cord - A hypotensive trauma patient is bleeding until proven otherwise. Hemorrhagic shock is tachycardic with cool, clammy, mottled skin and delayed capillary refill; the cord-injured patient is warm with a slow rate. Physical exam alone is unreliable for sorting shock states, so back it with serial lactate and urine output - under 0.5 mL/kg/hr means renal hypoperfusion and is often the first objective sign.

Not every case is trauma - Cord ischemia produces the same picture: the persistently hypotensive ICU patient, or thrombotic occlusion of the vessels supplying the cervical cord after angiography. Ischemic spinal shock is managed differently from traumatic spinal shock and carries a different outlook, so it is worth asking about mechanism when an areflexic patient has no history of impact.

Autonomic dysreflexia appears as spinal shock resolves - Once reflexes return in a patient with a lesion above T6, a noxious stimulus below the level - bladder or bowel distension, surgical stimulation - triggers uninhibited sympathetic vasoconstriction and severe hypertension, with compensatory bradycardia and vasodilation above the lesion. It does not occur in the first month after injury, so the newly injured areflexic patient is not yet at risk, but the patient returning months later is. Find and remove the trigger first, then treat with antihypertensive agents.

Not considered a true form of shock

Characterized by flaccid areflexia and/or parathesia BELOW the level of the injury WITHOUT hemodynamic changes.

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: circulatory shock sorts into four categories - distributive, hypovolemic, cardiogenic, and obstructive - and spinal shock belongs to none of them, because nothing in the term describes the circulation. The name is historical: Hall coined it in 1840, and Sherrington defined it as a transient extinction of reflexes below the level of injury. What it actually names is the acute post-injury state of flaccid paralysis, anesthesia, loss of bowel and bladder control, and absent reflexes caudal to the lesion. Definitions in the literature are not uniform - some require hypotension, some do not - which is a large part of why the term gets misapplied.

The clock you are watching is the reflex exam. Reflexes are lost in a rostrocaudal sequence and return caudorostral. Superficial reflexes can be back within about an hour; deep tendon and autonomic reflexes take weeks to months, and the duration of spinal shock is defined by that recovery. Contrary to the classic teaching that the bulbocavernosus reflex returns first, the observed order is delayed plantar reflex, bulbocavernosus reflex, cremasteric reflex, ankle jerk, Babinski sign, then knee jerk.