20.2 Acute Spinal Cord Injury, Neurogenic Shock & Autonomic Dysreflexia

Immediate Assessment

• Immobilize until the spine is cleared; log-roll and maintain in-line stabilization during airway management. Awake fiberoptic or video laryngoscopy with manual in-line stabilization is preferred in an unstable cervical spine.
• Respiratory failure depends on the level:
  • Above C3 to C5 ("C3, 4, 5 keep the diaphragm alive"): diaphragmatic paralysis requiring ventilation.
  • C5 to C8: preserved diaphragm with loss of intercostal and abdominal muscle function, so vital capacity falls, cough is weak, and secretions accumulate. Deterioration occurs over the first days as edema ascends and fatigue sets in. Follow vital capacity and negative inspiratory force, and intubate early rather than after a crisis.
  • Ventilated patients with high cervical injury often improve in the supine position, which is the opposite of most respiratory failure, because the abdominal contents push the paralyzed diaphragm upward and improve its mechanics.
• ASIA classification: examine motor and sensory levels, sacral sparing, and the bulbocavernosus reflex; complete injury (ASIA A) versus incomplete injury changes prognosis.
• Imaging: CT of the whole spine for fracture; MRI for cord signal change, ligamentous injury, and compression, especially with neurologic deficit and a normal CT.

Neurogenic Shock Versus Spinal Shock

These two terms are frequently confused.

Treatment of neurogenic shock:

1. Exclude hemorrhage first. A trauma patient can have both; hemorrhagic shock gives tachycardia and cool extremities, so bradycardia with warm skin points to neurogenic shock.
2. Volume to euvolemia, avoiding overload.
3. Vasopressors with chronotropic support: norepinephrine is commonly used; dopamine or epinephrine help when bradycardia dominates. Phenylephrine raises pressure but can worsen reflex bradycardia.
4. Atropine for symptomatic bradycardia, with temporary pacing for refractory bradyarrhythmia or arrest during suctioning.
5. Mean arterial pressure target of 85 to 90 mmHg for the first 5 to 7 days to support cord perfusion, which guidelines suggest while acknowledging limited high-quality evidence.
6. Watch for profound bradycardia or asystole during tracheal suctioning, a vagally mediated reflex in high cervical injury; pre-oxygenate and consider atropine.

Interventions With and Without Evidence

• Steroids: high-dose methylprednisolone is not recommended. The NASCIS trials' claimed benefits came from post hoc subgroups, and steroids increase pneumonia, sepsis, hyperglycemia, and gastrointestinal bleeding.
• Timing of surgical decompression: early decompression (within about 24 hours) is associated with better neurologic recovery in observational and some prospective data and is generally pursued when the patient can tolerate it.
• Thromboprophylaxis: the risk of venous thromboembolism is very high. Start low-molecular-weight heparin within about 72 hours once bleeding risk allows, plus mechanical prophylaxis. Inferior vena cava filters are not routine.
• Stress ulcer prophylaxis and bowel and bladder programs begin immediately; neurogenic bladder requires intermittent or indwelling catheterization.
• Pressure injury prevention: turning schedules and specialty surfaces from day one.
• Succinylcholine: safe within the first 24 to 48 hours, then avoided from about 48 to 72 hours after injury for up to a year or more, because upregulated extrajunctional acetylcholine receptors cause massive potassium release and cardiac arrest.
• Temperature dysregulation: poikilothermia below the lesion impairs both heat generation and dissipation.

Specific Incomplete Cord Syndromes

Autonomic Dysreflexia

Autonomic dysreflexia occurs in chronic injury at or above T6 (usually after spinal shock resolves). A noxious stimulus below the lesion triggers unopposed sympathetic outflow, because descending inhibitory pathways are interrupted.

• Presentation:
  • Severe hypertension (a rise of 20 to 40 mmHg above the patient's low baseline is significant; systolic pressures above 200 mmHg occur).
  • Reflex bradycardia from intact baroreceptor input to the vagus.
  • Above the lesion: pounding headache, flushing, sweating, and nasal congestion.
  • Below the lesion: pallor, cool skin, piloerection.
• Triggers (most to least common): bladder distension or catheter blockage, fecal impaction, pressure injury, ingrown toenail, fracture, acute abdomen, labor, and procedures such as cystoscopy.
• Complications: hypertensive encephalopathy, intracranial hemorrhage, seizures, retinal hemorrhage, pulmonary edema, and arrhythmia.
• Management, in order:
  1. Sit the patient upright and lower the legs to use orthostatic pooling.
  2. Loosen clothing and abdominal binders.
  3. Check the bladder: catheterize, or irrigate or replace a blocked catheter using lidocaine jelly.
  4. Check for fecal impaction after applying topical anesthetic, because the examination itself can worsen the episode.
  5. Antihypertensives if the pressure remains very high: a short-acting agent such as nitroglycerin paste (easily removed once the pressure falls, and avoided if a phosphodiesterase-5 inhibitor has been taken), nifedipine (immediate-release, bite-and-swallow), captopril, or an IV infusion of nicardipine or clevidipine for severe cases.
  6. Search for and remove the trigger, then continue monitoring, because recurrence is common.
• Prevention: scheduled bladder and bowel programs, skin care, pre-procedural anesthesia and prophylaxis, and patient education with a wallet card. Pregnancy and labor in women with high injury require planned regional anesthesia.