Spinal Shock vs Neurogenic Shock

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August 15, 2017 by jtreb

Chalkie Studebaker is a 45yo male s/p motorcycle crash. He comes to your ED via EMS. Upon arrival, patient is in a c-collar and on a backboard, screaming, “I can’t move my legs.” ABCs are intact, GCS 15. FAST negative. Secondary survey reveals scattered contusions and abrasions on the chest/abdomen/back. Vitals BP 90/50, HR 40. Your subintern, who is expertly performing a neurological exam, glances at the patient’s vitals and says, “I’m concerned for spinal shock—should we give steroids?”

1) What’s going on? Traumatic Spinal Cord Injury

-#1 cause in the US is Motor Vehicle Accidents (48%), followed by falls (16%) and GSW/Violence (12%).

-Risk factors = Males, ~37years old, alcohol use, underlying spinal pathology


2) How are spinal cord injuries classified?  Primary vs Secondary

-Primary –> Immediate effect of trauma; compression, contusion, transection, or shearing of the spinal cord

-Secondary –>Occurs within minutes to hours after initial injury—involves spinal cord ischemia, hypoxia, inflammation, edema


3) A point of confusion: Spinal shock vs Neurogenic Shock

-These terms are often used interchangeably, which is not only incorrect but also inappropriate


Spinal shock: 

-Not a type of “shock” in the traditional sense

-The term is used to refer to the neuropraxia from incomplete spinal cord injuries that can last hours-weeks; usually resolves on its own (bulbocavernosus reflex is one of the first reflexes to return as spinal shock resolves)

-Mechanism thought to be from loss of potassium within the injured spinal cord cells = accumulates in extra-cellular space = reduced axonal transmission

-Symptoms include flaccid paralysis, bowel incontinence, priapism


Neurogenic shock: 

-A type of distributive shock

-Mechanism is due to spinal cord injury causing interruption in autonomic pathways = decrease vascular tone/altered vagal tone = vasodilation + unopposed parasympathetic stimulation = hypotension, bradycardia, poikilothermia 

-Usually occurs with injuries at T5 or above (due to sympathetic involvement)


-With respect to the shock, guidelines currently recommend MAP 85-90; utilize IVF/transfusions/vasopressors(NE) as necessary

-Bradycardia may require atropine (0.6mg IV boluses) or external pacing

-Diaphragm involvement can lead to ineffective clearance of secretions/cough–be vigilant for signs of respiratory failure


4) To use or not to use in traumatic spinal cord injury? Steroids

-Short answer: No

-Less short answer: It is currently not recommended, as of data published in 2015, to give methylprednisolone for the treatment of acute spinal cord injury. There exists no Class I or II medical evidence to support the benefit, and there is Class I, II, and III evidence that high-dose steroids are associated with harmful side effects. This is in contrast to older recommendations that viewed steroids as a potential treatment option. For more information, please see reference #3.


5) Tips to keep in mind: 

-#1 cause of hypotension in a trauma patient with possible spinal cord injury = HEMORRHAGE (hypovolemic shock is more common than neurogenic shock)

-Vagal stimuli such as NGT insertion and intubation can exacerbate neurogenic shock

-Do not confuse the terms spinal shock and neurogenic shock!



  1. Hansebout RR and Kachur E. Acute traumatic spinal cord injury. UpToDate. Accessed at http://www.uptodate.com/contents/acute-traumatic-spinal-cord-injury
  2. Nickson, Chris. March 21, 2012. “Traumatic Spinal Injury Overview, Initial Assessment and Management.” LifeInTheFastLane. Accessed from https://lifeinthefastlane.com/trauma-tribulation-016/
  3. Tintinalli JE, Stapczynski JS, Ma JO, Cline DM, Cydulka RK, and Meckler GD. 2011. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th edition. The McGraw-Hill Companies, Inc. Chapter 255.

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