Identify patterns of neurological deficits in spinal cord injury
Describe the management of spinal cord injury
Recognize neurogenic shock
Describe the pathophysiology and management of neurogenic shock
You arrive on scene at a shopping mall with a BLS crew to find a 78-year-old woman lying at the bottom of a staircase. A bystander says he saw the woman lose her balance and fall backward down the stairs. As you approach, the woman complains of numbness in her hands and feet and says she hasn’t been able to move. She also complains of feeling light-headed.
You direct your partner to hold manual c-spine stabilization while you perform a rapid trauma exam and check vitals. The trauma exam is significant for a contusion over the occiput and point tenderness over the cervical spine. She has diminished sensation in her distal upper and lower extremities. Her grip strength is diminished, and she is unable to move either foot or wiggle her toes. Her skin is warm and pink. Vital signs are significant for blood pressure of 60/30, heart rate of 52, and respirations of 22. While you direct the BLS crew to apply a cervical collar and package the patient for transport, you wonder what is causing her hypotension and bradycardia.
Spinal Cord Injury
Spinal cord injury (SCI) is devastating to patients. Given the lifelong disability associated with these injuries and fear that neurological injury may be exacerbated during transport, immobilization of the spine using cervical collars and backboards has long been ingrained into EMS training and protocols. However, recent research highlighting the potential harms and uncertain benefit of backboards has triggered a shift from the historical “backboard everyone” approach to a more selective protocol of spinal protection.1 With this more nuanced approach, it has become even more important for EMS providers to understand the mechanisms and management of spinal cord injury.
SCI can be caused by a variety of traumatic mechanisms. Motor vehicle collisions are the most common, accounting for 48% of all SCIs.2 Falls account for 16% and are the most common cause in patients over 60.2,3 Violence and sporting accidents are other common causes.2
Injury to the spinal cord can occur as a result of vertebral fractures or dislocation, direct damage to the cord from penetrating trauma (e.g., shootings or stabbings), or tearing of the ligaments that support the spine.4 Unstable fractures are of particular concern to EMS because they have the potential to cause or worsen SCI if the spine is not protected during transport.5 While unstable fractures can occur after blunt trauma, they are exceedingly rare in patients with penetrating injuries.6 Spinal fractures can also result in bleeding within the epidural space of the spinal cord, much like how there can be an epidural hematoma in the brain. Bleeding within the epidural space of the spinal cord can result in neurological deficits similar to those observed in direct SCI. Patients on anticoagulants are at increased risk for spinal epidural hematoma after trauma.
After the initial insult to the spinal cord, a series of changes at the cellular level result in additional damage to neurons in the spinal cord. These cellular insults, termed the secondary mechanisms of SCI, can be exacerbated by hypoxemia or hypotension.3,7 Early identification and treatment of hypotension and hypoxemia in patients with SCI is therefore important to avoid secondary damage to the spinal cord.
The majority of SCIs occur at the level of the cervical spine.7 The cervical spine is vulnerable to injury because there are few surrounding structures to provide support. In addition, the joints between cervical vertebrae require less force to dislocate than the joints in the thoracic and lumber spine.3 Because the cervical spine is inherently less stable and more likely to be injured than the thoracic or lumbar, it is particularly important to immobilize.
Many disorders of the spine can predispose patients to SCI after traumatic injury. Osteoporosis increases the risk for SCI and may reduce the mechanism required to produce it.4 Rheumatoid arthritis can cause destruction of the cervical joints, predisposing patients to severe SCI from low-mechanism injuries.8 A variety of other degenerative spinal conditions, including cervical spondylosis and ankylosing spondylitis, also increase the risk for SCI after trauma.
Spinal Cord Anatomy
The spinal cord is a conduit that conveys motor commands from the brain to the muscles and sensations from the peripheral sensory receptors to the brain. It begins at the end of the brain stem, passes through the foramen magnum, and continues down through the spine to the lumbar vertebrae. The spinal cord ends around the level of the L1 vertebra and turns into the cauda equina, a bundle of spinal nerves that carries information from the spinal cord to the pelvic organs and lower limbs. Spinal nerves exit from each level of the spinal cord and split up into different nerves to send signals to muscles and receive information from sensory receptors. The spinal nerves are named after their corresponding vertebrae, so the spinal nerve that exits at the C5 vertebra is called the C5 spinal nerve.
There are some important nerves that travel within the spinal cord and can impair respirations or cause hemodynamic instability if damaged. The nerve that controls the diaphragm exits the spinal cord at the level of C3–C5. Therefore, injuries above C5 can impair breathing (the rhyme “C3 through C5 keeps the diaphragm alive” is a helpful memory tool). In addition, neurons for the sympathetic nervous system also travel through the spinal cord. These neurons leave the spinal cord at the T1–L2 levels and eventually travel to innervate the heart, blood vessels, bronchi, and other organs. Therefore, injury to the spinal cord can interrupt the sympathetic nervous system, resulting in a form of shock.
The level of injury within the spinal cord can be estimated from the pattern of muscle weakness and sensory deficits observed in the patient. Landmarks for identifying the level of SCI include the clavicles, which are at the C4 level; nipple line, which is at the T4 level; and umbilicus, which is at the T10 level.9 For example, if the patient has lost sensation below the nipple line, you know the spinal cord is injured at the T4 level. If the patient has no sensation at the clavicles, you should suspect an injury at or above the C4 level and maintain a high degree of suspicion for diaphragmatic weakness and respiratory failure. There can be overlap between levels, so the injury level and its pattern of sensory deficits may vary slightly.
Spinal Cord Syndromes
Sensory and motor neurons travel down different parts of the spinal cord. Therefore, injuries to only certain areas of the spinal cord can cause unique patterns of motor and sensory deficits. These different patterns of deficits are called spinal cord syndromes. They include:
Complete transection—When the entire spinal cord is affected. These patients have complete loss of sensation and paralysis below the level of the injury.
Brown-Séquard (hemicord) syndrome—When half the spinal cord is affected. Patients present with paralysis on one side of the body and loss of sensation on the other.
Anterior cord syndrome—When the anterior portion of the spinal cord is affected. Patients present with paralysis and loss of pain sensation below the level of injury but have preserved sensation of proprioception and vibration.
Central cord syndrome—When there is damage to the center of the spinal cord. This syndrome typically occurs in older adults with degenerative conditions of the cervical spine. Patients present with weakness of the upper extremities that’s worse than the lower extremities.
For EMS providers, it is not important to memorize the specific patterns of neurological deficits associated with each of these syndromes. Rather, it is more important to be aware that patients may have one of these syndromes rather than a complete transection, resulting in a pattern of neurologic deficits that is different than in a complete transection. For this reason, EMS providers should not discount the possibility of SCI in patients with sensory deficits or weakness on only one side of the body (i.e., Brown-Séquard syndrome) or weakness of the upper extremities but not the lower (i.e., central cord syndrome).
Assessment of the patient with suspected spinal cord injury includes determining the mechanism of injury, performing a physical exam of the spine, and evaluating for neurological deficits.
Evaluating the mechanism of injury is helpful for gauging the likelihood the patient has suffered a spinal injury. Falls from height, particularly when patients land on their heels, cause axial loading of the spine that can lead to SCI.10 Diving injuries, which cause axial loading on the head, are also at high risk for causing SCI. The deceleration forces in motor vehicle collisions can cause flexion and hyperextension injuries to the cervical spine.10 Motor vehicle collisions at high risk for serious injury include head-on and side-impact collisions, ejection from a vehicle, and pedestrians struck by a vehicle.
Consider the mechanism of injury in the context of the patient’s underlying medical history. For example, a patient with osteoporosis could experience a spine fracture from a mechanism that would not injure the spine of an otherwise healthy patient.
All patients with suspected SCI after trauma should be fully examined with a rapid trauma assessment so as not to miss any injuries. Palpation of the spine is an important component. To palpate the spine, log-roll the patient while maintaining manual c-spine stabilization. Palpate the entire spine to identify point tenderness over spinous processes, gaps between vertebrae, and step-offs. Point tenderness along the spine is concerning for spinal injury, while gaps between vertebrae or step-offs should raise suspicion for vertebral dislocation or fracture.
The initial neurological exam to screen for SCI involves testing whether motor strength and sensation are intact in the upper and lower extremities. First ask the patient if they’re experiencing any numbness or tingling, which are both signs of SCI. Next, gently touch the patient’s distal upper and lower extremities to test sensation. Motor strength in the upper extremities can be tested by asking the patient to grasp your fingers, while strength in the lower extremities can be tested by asking the patient to plantar-flex their feet. Sensory deficits and motor weakness or paralysis are highly suspicious for SCI. It also is helpful to ascertain whether the patient was ambulatory on scene prior to EMS arrival, since the ability to ambulate decreases the likelihood of SCI.
Assessment of the patient with suspected spine injury can be hindered by painful distracting injuries and altered mental status. Painful distracting injuries can make detection of point spine tenderness difficult. Altered mental status, whether caused by head injury or intoxication, prevents accurate identification of neurological deficits, making it difficult to rule out SCI in these patients. Since both head injuries and alcohol use are associated with cervical spine injuries, there should be heightened suspicion for SCI in these patients.7
Approaches to spinal protection vary widely, and EMS providers should follow their local protocols. However, there are some principles that guide the general approach to spinal protection.
Given the potential harms of backboards, many EMS agencies have curtailed their use. Some restrict the use of backboards to patients at high risk for SCI, since the benefit of spinal immobilization in these patients may outweigh the risks. Other agencies do not use backboards for any patients. Backboards generally should not be used for patients with penetrating trauma.6,13
Spinal protection can be achieved without the use of a backboard by using the “cot and collar” method. This involves applying a cervical collar and securing the patient to the ambulance cot with seat belts. With this method the cot acts as a padded backboard, with the seat belts preventing excessive movement of the spine.1 Towel rolls or head blocks can be used to further secure the cervical spine.
If the cot and collar method is used, the patient must be safely moved from where they are found to the ambulance cot. The first step upon arriving on scene is to apply a cervical collar to the patient and initiate manual c-spine stabilization. Patients who are alert, able to follow instructions, and able to ambulate may be allowed to self-extricate and sit down on the cot. Studies of simulated extrications have demonstrated that allowing patients to self-extricate after being given clear instructions to avoid unnecessary movement of the head is associated with less movement of the cervical spine than conventional extrication methods.14,15 If patients are unable to self-extricate, a scoop stretcher or backboard can be used to help move them to the cot. The scoop stretcher may be favored for patients found lying supine because its application causes less movement of the spine than application of a backboard.16
In addition to protecting the spine, EMS providers should evaluate for and treat any compromise to airway or breathing. As discussed above, any SCI above the level of C5 can impair ventilations by causing paralysis of the diaphragm.
Neurogenic shock is a form of distributive shock that occurs in 20% of cases of cervical SCI.17 It is caused by disruption of sympathetic output from the spinal cord. The loss of sympathetic tone results in a loss of peripheral vasoconstriction, leading to hypotension and warm skin. Without sympathetic innervation to the heart, there is unopposed vagal activity, leading to bradycardia. Together, the cardinal signs of neurogenic shock are hypotension, bradycardia, and warm skin in patients with suspected SCI.
It is important to understand the distinction between neurogenic shock and spinal shock, since the terms are often confused. Spinal shock refers to flaccid paralysis and loss of spinal reflexes that occurs after SCI.18 Spinal shock is a temporary state, and spinal reflexes and motor function may return once spinal shock resolves. Although patients with spinal shock may also develop neurogenic shock, the terms are not interchangeable.
Types of Shock in Trauma
EMS providers must initially consider the full range of possible causes of shock in trauma before concluding their patient is suffering from neurogenic shock. Hypovolemic shock is the most common cause of shock in trauma. The body responds to hypovolemic shock by activating the sympathetic nervous system, resulting in increased heart rate and vasoconstriction. Patients with hypovolemic shock therefore present with varying degrees of pale, cool skin, tachycardia, and hypotension.
Obstructive shock can be present if there is cardiac tamponade or tension pneumothorax and would present with signs of tension pneumothorax (e.g., diminished lung sounds and JVD) and/or signs of cardiac tamponade (e.g., JVD and decreased heart sounds) in addition to hypotension and tachycardia. Neurogenic shock presents differently from hypovolemic and obstructive shock. Because sympathetic tone is lost in neurogenic shock, there will be vasodilation and bradycardia. The vasodilation results in warm, well-perfused skin in addition to hypotension.
Because hemorrhage is the most common cause of shock in trauma, suspect it whenever neurogenic shock is considered. Patients with SCI have high rates of internal injuries because the forces required to cause SCI are often powerful enough to cause organ injury and internal bleeding.10 It is also rare for patients to present with the classic findings of neurogenic shock—bradycardia and hypotension—in the prehospital setting.19 Therefore, although it is important for EMS providers to consider neurogenic shock, it may be challenging to accurately detect.
Treatment of Neurogenic Shock
It is important to recognize and treat shock in patients with spinal cord injury because hypotension and hypoxemia can cause secondary injury after SCI, worsening the initial insult to the spinal cord.3 After appropriately managing the airway and ensuring adequate ventilations, neurogenic shock should initially be managed with IV fluid boluses.
In most cases of neurogenic shock, fluid resuscitation alone is sufficient to resolve hypotension.10 Some patients require vasopressors to maintain adequate perfusion, but hypovolemia should be excluded prior to administering them. Given that it’s difficult to exonerate hypovolemia as a contributor to shock in the prehospital setting, vasopressors may have a limited role in the prehospital treatment of suspected neurogenic shock. There is no consensus blood pressure goal for treatment of neurogenic shock, though there is weak evidence to support maintaining a mean arterial pressure of greater than 85 to avoid secondary injury to the spinal cord.19,20
As the BLS crew begins to package your patient, you consider what might explain her shock. Given the combination of hypotension, bradycardia, and warm skin in the setting of neurological deficits concerning for SCI, you decide neurogenic shock is the most likely cause. You also consider hypovolemic shock from internal bleeding, given that she experienced a traumatic mechanism. Obstructive shock from either cardiac tamponade or tension pneumothorax is less likely given that lung sounds are clear bilaterally, there is no JVD, and heart sounds are not muffled. Because the patient is in shock, you establish two large-bore IVs and provide a 500-mL IV fluid bolus. You also place the patient on the cardiac monitor, which reveals sinus bradycardia.
Meanwhile, the BLS crew has carefully protected the patient’s spine by applying a cervical collar and holding manual stabilization. Following local protocol, they use a scoop stretcher to move the patient from the floor to the cot, then remove it and secure her. You load the patient into the ambulance and begin transport to a local trauma center. You recheck vitals, and her blood pressure has increased to 100/50 with the IV fluid bolus. After notifying the trauma center to prepare for the patient, you continue to carefully monitor her throughout transport.
1. White CC 4th, Domeier RM, Millin MG; Standards and Clinical Practice Committee, National Association of EMS Physicians. EMS spinal precautions and the use of the long backboard—Resource document to the position statement of the National Association of EMS Physicians and the American College of Surgeons Committee on Trauma. Prehosp Emerg Care, 2014 Apr–Jun; 18(2): 306–14.
2. Devivo MJ. Epidemiology of traumatic spinal cord injury: Trends and future implications. Spinal Cord, 2012 May; 50(5): 365–72.
11. Burton JH, Dunn MG, Harmon NR, et al. A statewide, prehospital emergency medical service selective patient spine immobilization protocol. J Trauma, 2006 Jul; 61(1): 161–7.
12. Maarouf A, McQuown CM, Frey JA, et al. Iatrogenic spinal cord injury in a trauma patient with ankylosing spondylitis. Prehosp Emerg Care, 2017 May–Jun; 21(3): 390–4.
13. Velopulos CG, Shihab HM, Lottenberg L, et al. Prehospital spine immobilization/spinal motion restriction in penetrating trauma: A practice management guidelines from the Eastern Association for the Surgery of Trauma (EAST). J Trauma Acute Care Surg, 2018 May; 84(5): 736–44.
14. Dixon M, O’Halloran J, Cummins NM. Biomechanical analysis of spinal immoblisation during prehospital extrication: a proof of concept study. Emerg Med J, 2014 Sep; 31(9): 745–9.
15. Cowley A, Hague A, Durge N. Cervical spine immobilization during extrication of the awake patient: A narrative review. Eur J Emerg Med, 2017 Jun; 24(3): 158–61.
16. Krell JM, McCoy MS, Sparto PJ, et al. Comparison of the Ferno scoop stretcher with the long backboard for spinal immobilization. Prehosp Emerg Care, 2006 Jan–Mar; 10(1): 46–51.
17. Guly HR, Bouamra O, Lecky FE; Trauma Audit and Research Network. The incidence of neurogenic shock in patients with isolated spinal cord injury in the emergency department. Resuscitation, 2008 Jan; 76(1): 57–62.
18. Go S. “Spine Trauma.” In: Tintinalli JE, Stapczynski JS, Ma OJ, et al., eds. Tintinalli’s Emergency Medicine, 8th ed. McGraw-Hill Education, 2016.
20. Casha S, Christie S. A systematic review of intensive cardiopulmonary management after spinal cord injury. J Neurotrauma, 2011 Aug; 28(8): 1,479–95.
Sidebar: SCI Pearls and Pitfalls
Burning, numbness, or tingling may be the initial presenting symptom of SCI. The presence of any of these symptoms should raise suspicion for SCI even in the absence of motor or sensory deficits.
Rheumatoid arthritis, ankylosing spondylitis, and osteoporosis can lead to vertebral fractures after low-mechanism trauma. Have an elevated index of suspicion for vertebral fractures and SCI in patients with degenerative conditions that affect the spine.
Spinal cord injury does not always present with bilateral motor and sensory deficits. Patients with Brown-Séquard syndrome or other forms of incomplete SCI may have weakness or sensory deficits on only one side of the body. Patients with central cord syndrome may have weakness in the bilateral upper extremities but intact strength in the lower extremities.
Sidebar: Recognizing the Harms of Backboards
Harms associated with backboards include causing pain and pressure sores as well as impairing ventilations. Because backboards force the naturally curved spine to conform to a flat surface, they are known to cause neck and low back pain.1 There is even a case report of a patient with ankylosing spondylitis, a form of arthritis that can cause an abnormal curvature of the spine, developing a vertebral fracture and SCI after being secured to a backboard.12 Backboards can also cause pressure ulcers, with early stages developing within 30 minutes of the patient being placed on a backboard.1 In addition, the straps used to secure patients to a backboard can restrict ventilations.1 It is also time-consuming to immobilize a patient to a backboard, and time is of the essence in trauma.
Alexander Ordoobadi, NREMT-I, is a medical student at Harvard Medical School. He volunteers as a medic with the Bethesda-Chevy Chase Rescue Squad in Montgomery County, Md. He can be reached at email@example.com.
Sean M. Kivlehan, MD, MPH, NREMT-P, is director of the International Emergency Medicine Fellowship at Brigham and Women’s Hospital and faculty at Harvard Medical School. He was a New York City paramedic for 10 years and is a member of the EMS World Editorial Advisory Board. He can be reached at firstname.lastname@example.org.