Neurogenic shock is a devastating consequence of spinal cord injury (SCI), also known as vasogenic shock. Injury to the spinal cord results in 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. Early identification 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. 
Neurogenic shock is defined as the injury to the spinal cord with associated autonomic dysregulation. This dysregulation is due to a loss of sympathetic tone and unopposed parasympathetic response. Neurogenic shock is most commonly a consequence of traumatic spinal cord injuries. Review of 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. 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, neurogenic shock should be considered.
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 identified 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 defined universal hemodynamic parameters for neurogenic shock. However, most studies use the definition of systolic blood pressure less than 100 mmHg and heart rate less than 80 bpm. The epidemiology of neurogenic shock is difficult to assess as it is still unknown how hemorrhagic shock and other injuries impact the hemodynamic effects of spinal cord injury.
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 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 injury 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.
Neurogenic shock can be a difficult diagnosis to make and requires meticulous investigation. Neurogenic shock is most commonly associated with a blunt cervical spine injury. Identification of traumatic cord injury is vital to the investigation of neurogenic shock. Providers should ascertain mechanism of injury, the presence of midline spinal tenderness, a distracting injury that may take attention from a spinal area, loss of consciousness, neurologic deficits, or intoxication that may misconstrue exam, as these are associated with 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 neurogenic shock. Bradyarrhythmia, hypotension, flushed 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 propose the definition of neurogenic shock to be general autonomic nervous system dysfunction that also includes symptoms such as orthostatic hypotension, autonomic dysreflexia, temperature dysregulation. A focal neurologic deficit is not necessary for the diagnosis of neurogenic shock.
Before advanced imaging, 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 identified. The diagnosis of neurogenic shock remains a combination of radiographic imaging, hemodynamic monitoring, and clinical exam.
Initial management of neurogenic shock is focused on hemodynamic stabilization. Hypotension should be treated first to prevent secondary injury. The first-line treatment for hypotension is intravenous fluid 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 sympathetic tone. However, the lack of beta-activity leads to reflex 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 first 7 days to improve spinal cord perfusion. Caution should be used when using vasopressors as there may be co-existing injuries exacerbated with vasoconstriction.
Treatment for bradycardia is atropine and glycopyrrolate to oppose vagal tone especially before suctioning. Isoproterenol is considered for 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 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.
The diagnosis and management of neurogenic shock is 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 ICU nurses. While fluid resuscitation is the initial traetment, 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 DVT prophylaxis, pressure sore protection and a foley catheter. The outlook for these patients depends on the severity of the injury, presence of neurological deficits at time of presentation, age, concomitant other organ injury and a low GCS.
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