2. Epidemiology
• Incidence depends on location of
spinal cord injury
• Cervical
• Fewer than 20% of patients will present
with classical symptoms
• Thoracic
• Less than 10%
• Lumbar
• Rare
• Take-home point
• More likely with C-spine injury
• Can occur in patients with TBI as well
3. Recognition
• Spinal Cord Injury (SCI)Loss of sympathetic tone
• Classic cardiovascular signs and symptoms
• Hypotension refractory to fluid boluses
• Bradycardia
• Warm, dry skin
• Respiratory complications
• Weakness of diaphragm and chest wall muscles
impaired secretion clearance and hypoventilation
• Respiratory failure, pulmonary edema, etc.
• Take-home point
• No objective criteria for diagnosis
4. Pitfalls and Considerations
• Overall, rare entity
• Must be considered DIAGNOSIS OF EXCLUSION
• These patients are more likely to be suffering from hemorrhagic shock
• Picture is often mixed
• Patients in neurogenic shock can still present with tachycardia and other non-
classical symptoms
• Often coexists with hemorrhagic or cardiogenic shock
• No specific diagnostic criteria in terms of BP or HR
• Timeline
• Can happen WEEKS after initial spinal cord injury
5. Hemodynamic Management
• Current guidelines
• Maintain MAP > 85-90 mmHg to prevent secondary spinal cord ischemia
• Evidence is weak, and this threshold is somewhat arbitrary
• Some smaller studies claim improved neurologic outcomes after 1 year in patients
• Norepinephrine is preferred pressor agent
• .05-1 mcg/kg/min
• Combined a and b activity shown to increase spinal perfusion relative to dopamine and
phenylephrine
• Caveat: use of pressors in patients with MULTIPLE traumatic injuries may end up causing
harm
• Atropine for bradycardia
6. Glucocorticoids
• Animal studies have shown use of steroids in setting of acute SCI
reduces edema and inhibits detrimental intracellular electrolyte shifts
• National Acute Spinal Cord Injury Study III (1997)
• Methylprednisolone for 48 hrs vs. 24 hrs vs. tirilazad mesylate for 48 hours
• For patients treated between three to eight hours from injury, 48 hours of
methylprednisolone was associated with a greater motor, but not functional
recovery compared with other treatments
• No mortality difference
• Increased rate of sepsis and infection with longer duration of infusion
• Take-home point
• “no clinical evidence exists to definitely recommend”
7. Points to remember
• Presentation
• Classic = bradycardia, hypotension, and warm skin
• This classic presentation is RARE
• Often coexists with other shock types
• MUST rule out hemorrhagic shock first
• If primary survey, FAST, and CT series ALL negative for hemorrhage, think about
neurogenic etiology
• Management
• Norepinephrine, atropine, and fluids are your friends
• Consider presence of additional traumatic injuries
• MAP between 85-90 mmHg
• Steroid use still occurs, but is declining overall
8. Additional Resources
• Podcasts and Blogs
• http://ercast.libsyn.com/spinal-shock
• https://emergencymedicalminute.com/podcast-168-gsw-with-neurogenic-
shock/
• https://blogs.bmj.com/emj/2016/11/04/nuances-of-neurogenic-shock/
• Video
• https://www.youtube.com/watch?v=-Y3CbsxhlQE
9. References
• Guly, et al. The incidence of neurogenic shock in patients with isolated
spinal cord injuries. Resuscitation. 2008 Jan; 76(1): 57-62
• Ruiz, et al. Incidence and natural progression of neurogenic shock after
traumatic spinal cord injury. J Neurotrauma. 2018 Feb 1; 35(3): 461-466
• Lewin, et al. Chemical characteristics of traumatic spinal cord edema in
cats. Effects of steroids on potassium depletion. J Neurosurgery. 1974;
40(1): 65
• Jia, et al. Critical care of traumatic spinal cord injury. J Intensive Care
Medicine. 2013 Jan; 28(1): 12-23
• Bracken, et al. Methylprednisolone or tirilazad mesylate administration
after acute spinal cord injury: 1 –year follow-up. Results of the third
National Acute Spinal Cord Injury Randomized Control Trial. J Neurosurg.
1998; 89(5): 699
