Annals of B-Pod: Neurogenic Shock

history of presenting illness

A male in his 50s presented to the emergency department (ED) via ambulance following a single motor vehicle collision. The patient was the restrained driver who crashed into a utility pole. Per emergency medical services (EMS), the patient had a decreased level of consciousness at the scene, which improved following administration of 0.5 mg of naloxone. The patient struck his head but it was unknown if he lost consciousness. On arrival to the ED, he complained of numbness throughout his arms, torso, and legs, and stated that he could not move his legs. He also endorsed shortness of breath. He denied headache, neck pain, chest pain, abdominal pain, nausea, and vomiting. He denied any use of anticoagulant agents although he was prescribed aspirin.

Past Medical History: HIV, hepatitis C, hypertension, diabetes mellitus, bipolar disorder

Past Surgical History: Abdominal hernia repair

Medications: Aspirin, atorvastatin, lisinopril, metformin, quetiapine

Allergies: Sulfa antibiotics

Vitals HR 94 BP 84/48 RR 14 SaO2 92% on reservoir mask

Physical Exam: The patient was awake, alert, and immobilized on a backboard. A small right scalp abrasion was present. A cervical collar was in place with no midline cervical tenderness. All four extremities and the pelvis were non-tender with no obvious deformities. The thoracic and lumbar spines were non-tender without step-offs or deformity. The patient had a GCS of 15. He demonstrated occasional spastic flexion of his upper extremities and could not intentionally move his upper or lower extremities. Sensation to light touch was absent below the level of the nipple. He had no response to painful stimuli in the lower extremities. Rectal tone was absent. Patellar reflexes were absent with reduced muscle tone in all four extremities. Cardiac, pulmonary, and abdominal exams were normal.


Image 1: sagittal section of patient’s ct depicting widening and offset c4-c5 vertebral bodies. osteophyte complex with canal stenosis at c4-c7.

CT C-spine: Comminuted mildly displaced fracture of left transverse foramen of C4. Widening and offset of bilateral C4-5 facet joints. Osteophyte complex with severe canal stenosis at C4-5. Moderate to severe canal stenosis at C5-7.

CTA Neck: Left greater than right vertebral artery contour irregularities at C4 concerning for focal dissection.

CT Chest: Right hemidiaphragmatic elevation.

Hospital course

While in the emergency department, the patient was hypotensive with a systolic blood pressure in the 80s without compensatory tachycardia or evidence of blood loss. A norepinephrine drip was started for treatment of presumed neurogenic shock with improve-ment of his systolic blood pressure to the 130s without additional fluid resuscitation. The patient was admitted to the neuroscience intensive care unit (NSICU) and underwent C3-T1 fusion with C3-C6 decompression on hospital day 0 (HD0). A 7-day mean arterial pressure (MAP) goal of 85 mmHg was established. This was achieved with a norepinephrine drip, midodrine, and pseudoephedrine. Eventually a phenylephrine drip replaced the norepinephrine. The patient failed multiple extubation attempts and a tracheostomy was eventually placed for prolonged ventilator weaning. His course was further complicated by Serratia pneumonia and bacteremia, followed by methicillin-resistant Staphylococcus epidermidis bacteremia. He completed two full courses of antibiotics for each respective infection. Prior to discharge to a long-term acute care facility, the patient had 4/5 strength in his deltoids and 1/5 strength in his biceps bilaterally with paralysis and loss of sensation distal to the nipple line, consistent with a C6 American Spinal Injury Association (ASIA) A spinal cord injury.


Shock is defined as the failure of circulation to provide adequate oxygenation to meet cellular demand. To better identify and man-age this compromised physiologic state, shock is subcategorized into four overlapping mechanistic models: hypovolemic, cardiogenic, obstructive, and distributive.[1] Neurogenic shock is a subset of distributive shock caused by a spinal cord injury (SCI) with associated loss of sympathetic innervation to the heart and systemic vasculature. With the sympathetic trunks damaged, the uninjured vagus nerve provides unopposed parasympathetic innervation to the heart. Clinically this causes hypotension and bradycardia, which are the hallmark features of neurogenic shock.[2]

Table 1: american spinal injury association (asia) scale classifications system.

It is important to note that neurogenic shock is distinct from spinal shock, which is the loss of sensation, motor function, and reflexes distal to a spinal cord injury that develops within 24 hours of the initial insult. The name derives from the return of some degree of function over time as the “shock” of acute cellular and metabolic derangements dissipates.[2] All further discussions of shock in this article will refer to neurogenic shock.

Although no universal objective parameters exist to formally define neurogenic shock, it is generally defined as a cervical or upper thoracic SCI with associated systolic blood pressure less than 90-100 mmHg and a heart rate less than 60-80 beats/minute. Because the T1 to T5 thoracic paraspinal ganglion provides sympathetic innervation to the heart, it is classically taught that cord injuries distal to this level should not cause neurogenic shock.[3] The incidence of neurogenic shock is indeed greater with higher SCIs. Approximately 25% of patients with cervical injuries and between 5-20% of patients with thoracic injuries develop neurogenic shock.[4] Contrary to classic teaching, lower thoracic and even lumbar SCIs have precipitated cases of neurogenic shock.[2] Bradycardia is not a universal finding early in neurogenic shock, often developing in the first few hours after injury in some animal models and over four days after injury in some humans.[5]

In the clinical arena, neurogenic shock can present with variable vital sign abnormalities on a widely variable timeline, making the diagnosis challenging. While neurogenic shock may seem easy to identify in patients who present with isolated SCIs, the traumatic context inherent to neurogenic shock places the burden on the emergency physician to rule out multiple other etiologies that may be contributing to the patient’s inadequate perfusion.[6] Hypovolemia from blood loss, obstructive physiology secondary to cardiac tamponade or tension pneumothorax, and cardiogenic shock from cardiac contusion can all coexist in a patient simultaneously suffering from neurogenic shock. It is therefore critical to keep neurogenic shock in mind, particularly when evaluating and treating hypotensive patients who present after traumatic injuries.[3]

Three patterns of neurological deficits on physical exam comprise 90% of incomplete spinal cord injuries.[7] It is useful to review these patterns, as neurogenic shock is more commonly occurs in patients who present with these physical exam findings. The first is central cord syndrome, which typically is the result of a hyperextension injury. This causes the ligamentum flavum to exert pressure on the central aspect of the spinal cord. The crossing fibers of the pain-mediating spinothalamic tract and the medial descending fibers of the corticospinal tract that mediate motor control of the upper extremities are damaged with this type of injury. This classically results in decreased pain, temperature, and motor function in the upper extremities. Patients may present with abnormal upper extremity movement or arm pain only. The second pattern of deficits is anterior cord syndrome. This frequently occurs following a flexion injury that causes disruption of the anterior spinal artery that supplies the spinothalamic and corticospinal tracts. This results in bilateral loss of motor function and pain sensation below the level of injury but spares light touch sensation. The third and rarest of the incomplete cord injuries is Brown-Sequard syndrome. This is caused by complete hemisection of the cord, and is more likely to be seen in penetrating trauma. This injury causes ipsilateral loss of motor function, light touch sensation, and pain sensation at and below the level of the lesion. This injury also causes contralateral loss of pain sensation slightly below the level of the lesion due to the ascending pain fibers that have already crossed the anterior commissure further down in the cord.[8]

With other sources of shock being managed or ruled out with ultra-sound and cross sectional imaging, it is prudent to initiate appropriate treatment for neurogenic shock and the complications of SCI as quickly as possible. Patients with a high SCI often require emergent airway intervention secondary to hypersecretion, atelectasis, bronchospasm, and respiratory failure. All of these complications can develop immediately after the injury or in a delayed fashion necessitating close observation and frequent reassessment. Because the phrenic nerve derives from the C3-C5 nerve roots, it makes sense that the risk of respiratory failure declines with lower cord injuries: 40% for C1-C4 injuries, 23% for C5-C8 injuries, and approximately 10% for thoracic injuries.[4] Respiratory failure can occur with thoracolumbar injuries due to loss of innervation to the intercostal and abdominal muscles that contribute to both inspiration and active expiration. Loss of active expiration can eliminate a patient’s ability to generate an effective cough, leading to additional delayed respiratory complications.[9] Therefore, emergency physicians should consider early intubation for patients with cervical spine injuries, especially those above C5. For patients who appear to be breathing without difficulty, monitoring ventilation with end-tidal CO2 can help physicians detect impending respiratory failure requiring intubation should the patient become increasingly hypercarbic. As with all forms of shock, blood pressure support is the primary focus of management in neurogenic shock in order to improve systemic circulation and oxygen delivery.[1] This is even more important in neurogenic shock to maximize the patient’s potential neurologic recovery. It is helpful to review the pathophysiology of spinal cord injuries to understand why aggressive blood pressure management is paramount.

table 2: associated mechanism, symptoms, and prognosis of incomplete spinal cord injuries.

Spinal cord injuries typically occur in two phases. The first phase of injury is the primary insult, involving some form of pathologic flexion, extension, rotation, or compression of the spinal cord with a resulting cord injury. Immediate spinal protection with a cervical collar and spinal board is used to prevent additional injury to the cord in the setting of an unstable spine fracture. Although there is no strong evidence to guide the timeline of surgical intervention, urgent stabilization and decompression of the primary injury may lead to improved neurologic outcomes compared to delayed surgical intervention.[3]

The second phase of injury is caused by the subsequent inflammatory response that results in edema, vascular congestion, cytokine release, and cellular dysfunction.[3] Hypotension from neurogenic shock results in decreased perfusion to the spinal cord and creates a local inflammatory response that worsens cellular dysfunction.[4] Injuries to the thoracic cord are most susceptible to secondary in-jury from hypotension given the high reliance on watershed perfusion in this area. This pathophysiological relationship serves as the theory behind a 1997 publication in the Journal of Neurosurgery, which concluded that a mean arterial pressure (MAP) greater than 85 mmHg for seven days is associated with improved neurological recovery in patients presenting with acute complete spinal cord injury. The MAP goal of 85 was arbitrarily chosen and no control group was used for comparison in this study. The seven day duration of MAP maintenance was chosen base on experimental cord injury studies which demonstrated that peak vascular congestion and edema occur in the three to day day range after injury.[10] Although this publication continues to serve as the basis behind blood pressure management in patients with spinal cord injuries, no subsequent publications have set out to refine this blood pres-sure goal or treatment duration.[11]

Volume expansion with crystalloid resuscitation is first line treatment to maintain a MAP over 85 until the patient appears clinically euvolemic. Since the underlying etiology of hypotension in neurogenic shock is decreased systemic vascular resistance (SVR) secondary to loss of vasomotor tone, vasoactive agents are frequently required to further augment blood pressure. Vasoactive agents with both alpha and beta agonist properties, such as norepinephrine, are typically started first.[3] Alpha selective agonists, such as phenylephrine, are less ideal given the reflex bradycardia that often accompanies its use. Additional tools in the vasoactive arsenal include the mixed alpha and beta agonist pseudoephedrine and the alpha-selective agonist midodrine, both of which are orally administered and may facilitate weaning of intravenous vasopressors.[12]

While vasopressor administration is standard of care for MAP maintenance in SCI, some of the current literature challenges its use. One recent study theorizes that perfusion through the microvasculature of the damaged spinal cord may actually be decreased by the vasoconstriction and increased resistance to flow caused by these medications. These authors argue that more aggressive volume expansion has the benefit of improving both blood pressure and flow without the risk of vasoconstriction.[4] This debate remains largely theoretical and is unresolved, leaving clinicians with flexibility when attempting to maintain MAP above the accepted standard of 85 mmHg.

Two additional interventions that may be considered in patients with SCI include glucocorticoid administration and therapeutic hypothermia. It is important to note that neither of these treatments is considered standard of care at this time. Glucocorticoids theoretically protect the at-risk cell membranes of damaged neurons by inhibiting lipid peroxidation caused by oxygen free radicals generated during SCI. The current clinical data on glucocorticoid use in SCI are mixed. Most studies have shown that steroids—methylprednisolone in particular—have little benefit in SCI. The potential downsides of steroid administration are significant and include increased infection rates, bleeding, and steroid myopathy. The decision to initiate steroids in an otherwise healthy patient with a new SCI should be made in conjunction with the spine surgery team which will be managing the patient’s long-term care.[3] Previous cardiac arrest research has demonstrated neuroprotective effects with therapeutic hypothermia by decreasing metabolic demand and prolonging recoverable ischemia time.[13,14] This raises the question of whether therapeutic hypothermia may have similar effects in the setting of spinal cord injury, especially in incomplete injuries with evidence of remaining cord function. While novel, this strategy currently lacks sufficient evidence to guide its use and should not be initiated before discussion with the spine surgery and intensive care teams.[3]

Patients with SCI and neurogenic shock are at significant risk for developing cardiovascular and respiratory complications. Patients with SCIs who are treated at Level I trauma centers with specific protocols in place for these injuries demonstrate better neurologic outcomes and lower rates of complications and mortality compared to similar patients treated at less specialized centers of care.[3,11] These patients should be admitted to an intensive care unit due to the risk of cardiovascular and respiratory instability, particularly in cervical and complete cord injuries.[8] Cord injuries that result in paralyzed abdominal musculature severely impair adequate clearance of airway secretions and make an effective cough difficult if not impossible. As a result, acute respiratory failure complicated by pneumonia is the leading cause of mortality in this patient population. Survival rates decrease significantly if mechanical ventilation is required compared to patients with similar SCIs who do not require ventilatory support.3 Standard endotracheal suctioning only reliably clears secretions from the right mainstem bronchus and may induce bradycardia and cardiac arrest in these patients due to ongoing cardiovascular instability.[3,11] Cough-assist devices, bronchodilators, and mucolytics can help to minimize the risk of developing pneumonia, but bronchoscopy may be necessary to clear secretions.[9] Patients with a high level SCI often eventually require tracheostomy for long-term ventilator weaning and airway clearance.


Spinal cord injuries are devastating injuries and often occur in otherwise healthy individuals whose lives will be forever changed. Emergency physicians are often the first providers that come into contact with these patients, and aggressive resuscitation and minimization of secondary injury in the ED is extremely important. With early recognition of neurogenic shock and appropriate intervention, emergency physicians can truly make a difference in these patients’ lives and give them the best chance at a meaningful recovery.

authored by nicholas jensen, m.d.

posted by matthew scanlon, m.d.

Peer Reviewed as part of the Winter 2019 Annals of B Pod Issue


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