Neurogenic Shock - StatPearls - NCBI Bookshelf

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Introduction

Neurogenic shock is a devastating consequence of spinal cord injury (SCI), also known
as vasogenic shock. Injury to the spinal cord results in a sudden loss of sympathetic
tone, which leads to the autonomic instability that is manifested in hypotension,
bradyarrhythmia, and temperature dysregulation. Spinal cord injury is not to be confused
with spinal shock, which is a reversible reduction in sensory and motor function following
spinal cord injury. Neurogenic shock is associated with cervical and high thoracic spine
injury. Neurogenic shock should be differentiated from hypovolemic shock; the latter is
often associated with tachycardia.

Early identi cation and aggressive management are vital in neurogenic shock to prevent
secondary spinal injury. This chapter is a concise overview to further aid the care for
these patients who develop neurogenic shock. [1][2][3]

Etiology

Neurogenic shock is de ned as the injury to the spinal cord with associated autonomic
dysregulation. This dysregulation is due to a loss of sympathetic tone and an unopposed
parasympathetic response. Neurogenic shock is most commonly a consequence of
traumatic spinal cord injuries. A review of the trauma database showed the incidence of
neurogenic shock in 19.3% of cervical spine injuries and 7% of thoracic spine injuries.
Other causes of neurogenic shock that are far less common include spinal anesthesia,
Guillain-Barre syndrome, autonomic nervous system toxins, transverse myelitis, and other
neuropathies. The pediatric population reports the incidence of neurogenic shock in
children with Trisomy 21, skeletal dysplasia, and tonsillopharyngitis. Neurogenic shock
remains a diagnosis of exclusion in the traumatic patient—Advance Trauma Life Support
states hemorrhagic shock is the more common cause of hypotension and once
managed appropriately, the neurogenic shock should be considered.[4]

Epidemiology

An estimated 8000 to 10,000 people experience traumatic spinal cord injury per year in
the United States of America. A review of isolated spinal cord injury from the Trauma
Audit and Research Network identi ed 490 isolated spinal cord injuries. Out of these
isolated spinal cord injuries, 64 patients developed neurogenic shock, which is 14.2% of
the isolated spinal cord injuries. However, a retrospective study at a high volume level 1
trauma center cited an incidence of the neurogenic shock of 8.8%. There are no de ned
universal hemodynamic parameters for a neurogenic shock. However, most studies use
the de nition of systolic blood pressure less than 100 mm Hg and a heart rate of less
than 80 bpm. The epidemiology of neurogenic shock is di cult to assess as it is still
unknown how hemorrhagic shock and other injuries impact the hemodynamic effects of
spinal cord injury.

Pathophysiology

Neurogenic shock is the clinical state manifested from primary and secondary spinal
cord injury. Hemodynamic changes are seen with an injury to the spinal cord above the
level of T6. The descending sympathetic tracts are disrupted most commonly from
associated fracture or dislocation of vertebrae in the cervical or upper thoracic spine.
Primary spinal cord injury occurs within minutes of the initial insult. Primary injury is
direct damage to the axons and neural membranes in the intermediolateral nucleus,
lateral grey mater, and anterior root that lead to disrupted sympathetic tone. Secondary
spinal cord injury occurs hours to days after the initial insult. Secondary injury is a result
of vascular insult, electrolyte shifts, and edema that lead to progressive central
hemorrhagic necrosis of grey matter at the injury site. At a cellular level, there is
excitotoxicity from NMDA accumulation, improper homeostasis of electrolytes,
mitochondrial injury, and reperfusion injury which all lead to controlled and uncontrolled
apoptosis. Neurogenic shock is a combination of both primary and secondary injuries
that lead to loss of sympathetic tone and thus unopposed parasympathetic response
driven by the vagus nerve. Consequently, patients suffer from instability in blood
pressure, heart rate, and temperature regulation.

History and Physical

Neurogenic shock can be a di cult diagnosis to make and requires meticulous

investigation. Neurogenic shock is most commonly associated with a blunt cervical
spine injury. Identi cation of traumatic cord injury is vital to the investigation of
neurogenic shock. Providers should ascertain the mechanism of injury, the presence of
midline spinal tenderness, a distracting injury that may take attention from a spinal area,
loss of consciousness, neurologic de cits, or intoxication that may misconstrue the
exam, as these are associated with a vertebral injury. Though neurogenic shock should
be considered only after a hemorrhagic shock has been ruled out in a traumatic patient,
the presence of vertebral fracture or dislocation raises the concern for a neurogenic
shock. Bradyarrhythmia, hypotension, ushed warm skin are the classic signs associated
with neurogenic shock. The joint committee of the American Spinal Injury Association
and the International Spinal Cord Society proposed the de nition of a neurogenic shock
to be general autonomic nervous system dysfunction that also includes symptoms such
as orthostatic hypotension, autonomic dysre exia, temperature dysregulation. A focal
neurologic de cit is not necessary for the diagnosis of neurogenic shock.

Evaluation

Before advanced imaging, the neurogenic shock was associated with spinal cord injury
without radiologic abnormality (SCIWORA). With the advent of advanced imagining such
as CT scan and Magnetic Resonance Imaging, spinal cord injury is more accurately
identi ed. The diagnosis of neurogenic shock remains a combination of radiographic
imaging, hemodynamic monitoring, and clinical exam.[3][5][6][7][8]

Treatment / Management

Initial management of neurogenic shock is focused on hemodynamic stabilization.

Hypotension should be treated rst to prevent secondary injury. The rst-line treatment
for hypotension is intravenous uid resuscitation. This is to allow appropriate
compensation for the vasogenic dilation that occurs. If hypotension persists despite
euvolemia, vasopressors and inotropes are the second lines. No single agent is
recommended. Phenylephrine is commonly used as it is a pure alpha-1 agonist that
causes peripheral vasoconstriction to counteract the loss of sympathetic tone. However,
the lack of beta-activity leads to re ex bradycardia which augments the already
unopposed vagal tone. Norepinephrine has both alpha and beta activity aiding both
hypotension and bradycardia thus the preferred agent. Epinephrine has been cited for
refractory cases of hypotension and is rarely needed. Recommend keeping the mean
arterial pressure (MAP) at 85–90 mmHg for the rst 7 days to improve spinal cord
perfusion. Caution should be used when using vasopressors as there may be co-existing
injuries exacerbated with vasoconstriction.[9][10][11][12]

Treatment for bradycardia is atropine and glycopyrrolate to oppose vagal tone especially
before suctioning. Isoproterenol is considered for a pure chronotropic effect.
Methylxanthines such as theophylline and aminophylline have been cited for refractory
cases of bradycardia.

Initial c-spine immobilization is important to prevent further spinal cord injury. Miami J or
Philadelphia collar should be used. Methylprednisolone and corticosteroids showed
promise in animal models. However, this has not been displayed in clinical trials, and
steroids raise the risk for complications such as infection and are not recommended by
multiple societies. Ultimately, surgical intervention may be required for decompression of
spinal injury and improvement of neurogenic shock. Symptoms of neurogenic shock
have been reported to persist for as long as 4 to 5 weeks.

Differential Diagnosis
All these types of shocks are associated with tachycardia, whereas neurogenic shock is
associated with bradycardia.

The term "spinal shock" denotes the acute loss of motor, sensory and re ex functions
below the level of injury, and can be associated with neurogenic shock.

Prognosis

The overall prognosis depends on the extent of spinal cord injury and response to
treatment. Those associated with neurological de cits tend to have poor outcomes.

Enhancing Healthcare Team Outcomes

The diagnosis and management of neurogenic shock are not easy, thus, the condition is
best managed by an interprofessional team that includes the emergency department
physician, neurologist, neurosurgeon, orthopedic surgeon, trauma specialist, and the
intensivist. These patients are usually monitored by neuro intensive care unit nurses.
While uid resuscitation is the initial treatment, one should use vasopressors cautiously,
since they may exacerbate any vasoconstriction. Most patients have other concomitant
injuries that also require attention. Nurses should ensure that patients have deep vein
thrombosis prophylaxis, pressure sore protection, and a foley catheter. These patients
may develop a range of complications including aspiration pneumonia, stress ulcer, and
deep vein thrombosis. Close monitoring of the patient is critical and all team members
should communicate the treatment plan with each other to ensure that the patient is
receiving optimal care.

The outlook for these patients depends on the severity of the injury, presence of
neurological de cits at the time of presentation, age, concomitant other organ injuries,
and a low Glasgow Coma Scale score.[9][13] 

Questions

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