11.1 Spinal Cord Injury & Neuromuscular Emergencies

Spinal Cord Injury: Classification and Level-Based Deficits

Spinal cord injury (SCI) is classified by completeness and by neurologic level using the ASIA Impairment Scale (AIS), where the American Spinal Injury Association grades injuries A through E. A complete injury (AIS A) means no motor or sensory function is preserved below the level, including the lowest sacral segments (S4-S5) - the critical marker is loss of sacral sparing (perianal sensation and voluntary anal contraction). An incomplete injury (AIS B-D) preserves some function below the level, and sacral sparing is the hallmark that separates incomplete from complete.

Several incomplete syndromes recur on the exam. Central cord syndrome is the most common, typically from a hyperextension injury in an older adult with cervical spondylosis, producing weakness that is worse in the upper extremities than the lower. Anterior cord syndrome damages the anterior two-thirds of the cord: motor function plus pain and temperature are lost while proprioception and vibration (posterior columns) are preserved - it carries the worst prognosis. Brown-Sequard syndrome (cord hemisection) causes ipsilateral motor and proprioception loss with contralateral pain and temperature loss.

The diaphragm depends on C3-C5

The mnemonic "C3, 4, 5 keep the diaphragm alive" anchors respiratory risk. The phrenic nerve arises from C3-C5, so an injury at or above C4 compromises the diaphragm and intercostals, threatening ventilation and frequently mandating intubation and long-term ventilator support. A quick functional map:

Neurogenic Shock Versus Spinal Shock

These two terms are constantly confused and are high-yield. Neurogenic shock is a hemodynamic state - a form of distributive shock caused by disruption of sympathetic outflow (thoracolumbar sympathetic chain) in injuries at T6 or above. Loss of vascular tone causes vasodilation, and unopposed vagal tone produces bradycardia. The classic triad is hypotension WITH bradycardia and warm, dry, flushed skin (low systemic vascular resistance). That combination of low blood pressure and a slow heart rate distinguishes it from hypovolemic or septic shock, where compensatory tachycardia is expected. Management targets a mean arterial pressure of 85-90 mmHg for the first 5-7 days to protect cord perfusion: judicious isotonic fluids first, then vasopressors (norepinephrine), with atropine or chronotropic support for symptomatic bradycardia.

Spinal shock, by contrast, is not a blood-pressure state. It is the transient loss of ALL reflex activity, tone, and sensation below the level of injury - flaccid paralysis and areflexia - immediately after acute SCI. It resolves over days to weeks, and the return of the bulbocavernosus reflex signals its end, after which true motor/sensory prognosis can be judged.

Autonomic Dysreflexia: A Hypertensive Emergency

Autonomic dysreflexia (AD) develops in patients with injuries at or above T6, typically after spinal shock has resolved. A noxious stimulus below the level of injury triggers a massive, unopposed sympathetic discharge, causing severe hypertension (systolic often 200+), a pounding headache, and reflex bradycardia (the intact vagus responds to the high pressure). Above the lesion there is flushing, sweating, and nasal congestion; below the lesion the skin is pale and cool. Untreated AD can cause hemorrhagic stroke, seizure, or death.

The immediate nursing actions are ordered: (1) sit the patient upright to induce orthostatic lowering of blood pressure, (2) loosen constrictive clothing/devices, and (3) find and remove the trigger - a distended bladder from a kinked or blocked catheter is the number-one cause, followed by bowel impaction and skin irritation. If blood pressure stays dangerously high after the trigger is removed, a rapid-onset antihypertensive (nitrate paste, nifedipine) is added.

Guillain-Barre Syndrome and the Crises of Myasthenia

Guillain-Barre syndrome (GBS) is an acute autoimmune demyelinating polyradiculoneuropathy, often following an infection such as Campylobacter jejuni. It classically causes ascending, symmetric weakness with areflexia that can climb to involve the respiratory muscles and produce autonomic instability (labile blood pressure, arrhythmias, ileus). The CCRN priority is serial respiratory monitoring: forced vital capacity (FVC) and negative inspiratory force / maximal inspiratory pressure. An FVC falling toward 15-20 mL/kg (or a steep downward trend), or an inspiratory force weaker than about -25 to -30 cmH2O, warrants elective intubation before an emergent crash. Disease-modifying treatment is IVIG or plasmapheresis (plasma exchange); corticosteroids are NOT effective in GBS.

Myasthenia gravis (MG) is an autoimmune attack on postsynaptic acetylcholine receptors, producing fatigable weakness, ptosis, diplopia, and bulbar symptoms. Two crises must be distinguished:

Both present with respiratory muscle weakness and possible respiratory failure, so airway protection is the shared first priority. Historically an edrophonium (Tensilon) test distinguished them - improvement suggests myasthenic, worsening suggests cholinergic - but it is rarely used today; the safer approach is to secure the airway, hold the anticholinesterase if cholinergic toxicity is suspected, and treat the underlying trigger.