Neurogenic Shock: Definition, Identification, and Management in the ED

Authors: Kira Brayan, MD (EM Resident Physician, Mount Sinai Morningside-West); Jenny Beck-Esmay, MD (Assistant Program Director, Mount Sinai Morningside-West) // Reviewed by: Jessica Pelletier, DO (EM Education Fellow, Washington University in St. Louis School of Medicine), Marina Boushra, MD (EM-CCM Attending, Cleveland Clinic Foundation); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)


A 24-year-old male with no past medical history is brought to the emergency department (ED) by emergency medical services (EMS) after falling from a roof. He reports severe back pain. The patient was decorating the roof for Christmas when he lost his footing and landed on his back. Initial vitals are T 36.8°C, HR 53 bpm, BP 88/43 mm Hg, RR 15 per minute, and  oxygen saturation 98% on room air. A fingerstick blood glucose on arrival is 97 mg/dL. A cervical collar was placed by EMS prior to arrival in the ED. The airway is clear and the patient is able to answer questions. There are clear, equal breath sounds bilaterally. On chest auscultation, the heart rate is regular but bradycardic. He has symmetric pulses in all extremities. His Skin is flushed and warm with normal capillary refill. He is awake and oriented with Glasgow Coma Scale (GCS) of 15. On neurologic exam, he has normal grip strength and 5/5 bilateral upper extremity strength. Bilateral lower extremity strength is 3/5. The remainder of the neurological exam is within normal limits. While logrolling the patient, bruising is noted to the thoracic back and midline tenderness is present over the thoracic spine at T2-T3.

What is the typical ED presentation of neurogenic shock?

What evaluation is important when diagnosing neurogenic shock?

How is neurogenic shock managed in the ED?


Shock is a state of tissue hypoxia caused by a mismatch between oxygen delivery and consumption, leading to end-organ damage.1 Shock can be broadly divided into four pathophysiologic categories (Table 1): distributive, cardiogenic, hypovolemic, and obstructive. Approximately 33-50% of patients presenting to the ED with shock are found to have distributive shock.1 The pathophysiology of distributive shock involves decreased systemic vascular resistance caused by systemic vasodilation, leading to relative intravascular volume depletion and the development of hypotension (systolic blood pressure < 90 mmHg).1

Traumatic injury to the spinal cord can result in neurogenic shock, a type of distributive shock. Traumatic injury results from two mechanisms: primary injury and secondary injury.2 Primary injury is a result of direct mechanical trauma to the spinal cord.2 The primary injury leads to secondary injury through edema and vascular compromise that can result in spinal cord ischemia.2 When the injury occurs at or above T6, the patient is at risk for neurogenic shock due to the disruption of sympathetic innervation to the heart and peripheral vessels.2 This loss of sympathetic innervation explains the hallmark symptoms of neurogenic shock, bradycardia and hypotension.2 Hypotension is secondary to the loss of vasomotor tone and resulting peripheral vasodilation.2 Loss of sympathetic innervation to the heart can prevent the compensatory tachycardia usually seen in response to hypotension and may lead to bradycardia.2

Trauma is the most common cause of neurogenic shock, occurring in 19.3% of cervical spine injuries and 7% of thoracic spine injuries.3 In trauma patients, it is important to distinguish neurogenic shock from spinal shock. Spinal shock is a temporary state that presents as loss of reflexes and flaccidity.2 The key difference is that while both result from central nervous system (CNS) trauma, spinal shock is limited to neurologic deficits and neurogenic shock is a systemic process associated with cardiovascular effects.

It is important to consider other causes of hypotension in trauma patients, including hemorrhagic shock and cardiopulmonary injuries.2 With this in mind, neurogenic shock is a diagnosis of exclusion in the setting of trauma.2 Other causes of neurogenic shock are rare and include Guillain-Barre syndrome, transverse myelitis, and spinal anesthesia.6


As with any trauma assessment, a head-to-toe examination is required, starting with the primary survey. Suspicion should be higher for neurogenic shock in hypotensive trauma patients who present with signs of distributive shock (warm extremities and flushed skin), especially if they are also bradycardic.2 While more commonly seen in cervical injuries, any spinal cord injury above T6 can result in disruption of the sympathetic chain, leading to hemodynamic compromise from neurogenic shock.6 Neurological deficits below the level of the injury, such as loss of sensation, motor function, or reflexes, may be present.4 A normal neurological examination does not exclude the diagnosis of neurogenic shock.


Once the patient has been stabilized and life threats eliminated or mitigated, further evaluation of a spinal injury requires advanced imaging, such as computed tomography (CT) (the gold standard for bony injury) or magnetic resonance imaging (MRI) (if there is concern for spinal cord or nerve root injury). Several clinical decision rules help differentiate patients who require imaging from patients who can be cleared clinically. For patients with head or neck trauma and a GCS < 15, a head CT and CT of the cervical spine are indicated.2 In trauma patients without neurologic deficits who are alert and stable, the National Emergency X-Radiography Utilization Study (NEXUS) and the Canadian Cervical Spine Rule for Radiography (CCR) help guide the decision to obtain imaging of the spine (

As for thoracolumbar (TL) spine imaging, the clinical examination was found in one study to be only 48.2% sensitive for thoracolumbar spine fractures.2 Additionally, there are no commonly accepted clinical decision rules for determining which patients require imaging.2 Therefore, the decision to obtain thoracolumbar imaging should be based on clinical presentation and risk factors, rather than physical examination alone. 2 A 2009 review found a significantly increased risk of TL fracture in blunt trauma patients who had a high-risk mechanism, painful distracting injury, new neurological abnormalities, new back pain or tenderness, cognitive impairment, or known cervical spine fracture.7 CT is useful for identifying vertebral fractures, assessing their stability, and evaluating for spinal cord impingement from bone fragments.2 However, MRI is the preferred study if there is any concern for spinal cord or nerve root injury.2


The initial strategy for the treatment of neurogenic shock prioritizes spinal immobilization and blood pressure stabilization, as both of these are critical for preventing further spinal cord damage and improving outcomes. The recommended approach to spinal immobilization is the placement of a cervical collar, blocks, and a rigid spinal board.8 Management of hypotension is important in neurogenic shock as persistent hypotension can lead to spinal cord hypoperfusion, worsening the initial injury.6 The literature recommends maintaining a mean arterial pressure (MAP) greater than 85-90 mmHg.6

The first-line treatment for hypotension in trauma patients is intravenous crystalloid fluid resuscitation.5,6 After the initial bolus, the type of shock dictates the next step. For trauma patients with concern for severe hemorrhage, the next step is blood transfusion and likely transfer to the operating room for source control.6 In non-hemorrhagic shock, once the patient has been adequately fluid resuscitated, vasopressors are needed for persistent hypotension.

There are several vasopressors used in clinical practice, although no consensus has been reached on which medication should be first line. The alpha and beta agonism of norepinephrine (at an initial dose of 8-12 mcg/minute IV) oppose peripheral vasodilation and vagal-induced bradycardia, respectively.6 Norepinephrine is the recommended vasopressor. Phenylephrine, at an initial dose of 100-200 micrograms/minute IV, is an alpha agonist that is commonly used because of its peripheral vasoconstrictive properties.6 However, phenylephrine can also worsen bradycardia due to its lack of beta activity and potential for causing reflexive bradycardia.6 A recent retrospective study found that phenylephrine and dopamine were associated with higher rates of complications compared to other vasopressors in neurogenic shock.

Bradycardia that is not improved with vasopressors can be managed with atropine and glycopyrrolate.6 Other cardiac dysrhythmias, such as third-degree atrioventricular block or supraventricular tachycardia (SVT), have also been observed in patients with neurogenic shock.10 Stable patients with tachydysrhythmias can be managed with medications, while unstable patients will require synchronized cardioversion.11  Cardiac pacing is a reasonable alternative for refractory sinus bradycardia, and overdrive pacing may be considered for SVT.10

Early surgical consultation is important as surgical decompression of the spinal cord may be required to treat neurogenic shock.6 Studies on the timing of surgical decompression generally agree that earlier surgical intervention (less than 72 hours) leads to better neurological outcomes, decreased length of hospital stay, and fewer complications.8 Steroids are not currently recommended as studies have not shown a benefit that outweighs the risk of steroid use.6 Finally, patients with neurogenic shock will require admission to the hospital for monitoring until hemodynamic changes resolve, which can take as long as 4-5 weeks.6

Pearls and Pitfalls 

-Consider neurogenic shock in hypotensive trauma patients with high-level spinal injuries who present with signs of vasodilation but do not have compensatory tachycardia.

-Focal neurologic deficit is not a defining feature of neurogenic shock and neurogenic shock can be present in the setting of a normal neurologic exam. Physical exam of the thoracolumbar spine has poor sensitivity for spine and spinal canal injury. There should be a low threshold to obtain imaging in patients presenting with symptoms of neurogenic shock

-Neurogenic shock is a diagnosis of exclusion in trauma patients. Other causes of hypotension should be considered, particularly hemorrhagic shock in trauma patients, before coming to the diagnosis of neurogenic shock

CT is the gold standard for bony spinal trauma, but MRI is necessary for suspected spinal cord injuries

-IV fluids are not adequate for hypotension caused by neurogenic shock and these patients will require vasopressors (norepinephrine is first line) to maintain adequate blood pressure.



  1. Nicks BA, Gaillard JP. Approach to Nontraumatic Shock. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. Accessed January 25, 2023.
  2. Go S. Spine Trauma. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. Accessed January 25, 2023.
  3. Committee on Trauma. “Spine and Spinal Cord Trauma.” Advanced Trauma Life Support: Student Course Manual, by Committee on Trauma, tenth ed., Chicago, Ill., American College Of Surgeons; 2018.
  4. Colwell, Christopher. “Approach to Shock in the Adult Trauma Patient.” UptoDate, 30 Sept. 2022, Accessed 30 Jan. 2023.
  5. ‌Raja, Ali. “Initial Management of Trauma in Adults.” UptoDate, 24 Jan. 2023, Accessed 5 Feb. 2023.
  6. Dave S, Cho JJ. “Neurogenic Shock.” Stat Pearls, 10 Feb. 2022. Treasure Island, FL, StatPearls Publishing; 2022.
  1. O’Connor E, Walsham J. Review article: indications for thoracolumbar imaging in blunt trauma patients: a review of current literature. Emerg Med Australas. 2009 Apr;21(2):94-101. doi: 10.1111/j.1742-6723.2009.01164.x.
  2. Sandean D. Management of acute spinal cord injury: A summary of the evidence pertaining to the acute management, operative and non-operative management. World J Orthop. 2020;11(12):573-583. Published 2020 Dec 18. doi:10.5312/wjo.v11.i12.573
  3. Inoue T, Manley GT, Patel N, Whetstone WD. Medical and surgical management after spinal cord injury: vasopressor usage, early surgerys, and complications. J Neurotrauma. 2014;31(3):284-291. doi:10.1089/neu.2013.3061
  4. Sacino A, Rosenblatt K. Critical Care Management of Acute Spinal Cord Injury-Part II: Intensive Care to Rehabilitation. J Neuroanaesth Crit Care. 2019;6(3):222-235. doi:10.1055/s-0039-1694686
  5. Brady WJ, Glass III GF. Cardiac Rhythm Disturbances. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. Accessed February 27, 2023.



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