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Spinal Cord Injury

| Source: ems1.com

An injury to the spinal cord could result in a catastrophic permanent disability to the patient. Approximately 10,000 new cases of spinal cord injury (SCI) occur each year in the United States with most occurring in men between the ages of 16 and 30. The etiology of the majority of cases is associated with motor vehicle crashes followed by penetrating trauma; falls, especially in the elderly; and sports and recreational activities. Elderly patients are more prone to suffering from SCI from minor trauma due to degenerative vertebral disorders. In addition, elderly patients have become more active over the years; thus, the incidence of SCI in the elderly is on the rise.

In order to effectively assess for a spinal cord injury, you must first understand the basic anatomy and physiology of the spinal cord. Once you have achieved this understanding, assessment for such an injury makes much more sense when applied clinically to a patient.

The Spinal Cord

The spinal cord is a continuation of the brainstem. It is housed within the bony vertebral column in an area referred to as the spinal canal. The spinal cord has 31 pairs of spinal nerves that exit at various levels and are responsible for transmitting motor and sensory information. The spinal cord originates at the cervicomedullary junction, which is just below the foramen magnum. The true portion of the cord terminates at the lower margin of the first lumbar vertebra (L1). The most inferior portion of the spinal cord, known as the conus medullaris, continues and narrows to a point at the lumbosacral enlargement. A group of segmental spinal nerves, known as the cauda equina, exit through the lumbar and sacral vertebrae as spinal nerves. Thus, an injury below the level of the second lumbar vertebrae (L2) is not necessarily considered a spinal cord injury since it only involves segmental spinal nerves. Like the brain, the spinal cord is covered by the dura mater, arachnoid and pia mater meningeal layers, which extend from the brain to approximately the second sacral vertebrae. The meningeal layers provide protection for the spinal cord.

The spinal cord is comprised of central nervous system tissue similar to brain tissue. It requires a constant supply of oxygen and glucose for normal cellular metabolism. One anterior and two paired posterior spinal arteries continuously supply the spinal cord with blood. The anterior spinal artery supplies two-thirds of the cord with blood in the anterior segment and extends the full length of the spinal cord. The posterior spinal artery supplies the remaining one-third of the posterior segment of the cord with blood. An injury to either the anterior or posterior artery from laceration or compression can lead to ischemia and tissue necrosis with resultant neurologic dysfunction.

The cord is separated into a right and left half by the anterior medial fissure and the posterior medial sulcus. A cross section of the cord reveals a gray “H” pattern surrounded by white matter. The gray matter contained within the “H” pattern contains cell bodies of neurons. The white matter contains ascending and descending nerve tracts. Ascending axons carry sensory impulses to the brain for interpretation; whereas, the descending axons carry motor impulses that control movement. An injury or disruption to any of these tracts will produce a loss of neurologic function such as loss of movement or sensory function below the point of spinal cord injury.

Spinal Cord Injuries

The spinal cord can be injured by a variety of mechanisms including flexion, rotation, compression, hyperextension, lateral bending, distraction and penetrating wounds. An actual complete physical transaction of the cord, where the cord is physically torn into two pieces, is relatively rare. A physiologic or functional transaction, where the cord remains intact but the neurons are dead and nonfunctional across a complete section of the cord, is much more common.

Injury is referred to as primary or secondary. Primary injury is caused by the initial direct injury to the cord from compression, tearing, stretching or laceration. EMS management cannot reverse any of the effects of primary injury. Once the primary injury has occurred, a cascade of events can lead to ischemia of the white and gray matter leading to a secondary spinal cord injury. Hypoxia, hypoglycemia, hypotension, hyperthermia and improper spinal immobilization can all lead to an exacerbated secondary injury. This is where EMS and proper prehospital emergency management plays a significant role in reducing the morbidity associated with a spinal cord injury.

Prehospital Emergency Management

If a significant mechanism of injury has occurred, the patient is unreliable and cannot effectively participate in a spinal clearance protocol assessment. In addition, if the patient has any complaint of pain or tenderness in any location along the length of the spine, or the patient presents with any motor or sensory deficit in the neurologic assessment, the patient must be completely immobilized onto a spine board. An unreliable patient is one who is in an acute stress reaction, is intoxicated by drugs or alcohol, suffered a head injury, has a language barrier, cannot communicate, or has a distracting injury such as an extremity fracture. Improper or lack of immobilization can convert a stable vertebral fracture into an unstable fracture, move fractured bony fragments, or cause dislocated vertebrae to encroach on the cord and lead to secondary injury.

Establish and maintain a patent airway. Assess the tidal volume and rate of respiration. If either the tidal volume or rate is inadequate, provide positive pressure ventilation with supplemental oxygen connected to the ventilation device. If the respirations are adequate, administer oxygen based on the SpO2 reading and patient signs and symptoms of hypoxia or respiratory distress. If the SpO2 is less than 95 percent on room air or the patient is exhibiting signs of hypoxia, administer oxygen via a nonrebreather mask at 15 lpm. An inadequate airway, inadequate ventilation, or poor oxygenation can lead to hypoxia, hypercarbia and acidosis, all of which contribute to secondary spinal cord injury.

Reverse any hypotension through the initiation of an intravenous infusion of normal saline or Lactated ringers with a large bore catheter and macrodrip tubing. Maintain a systolic blood pressure of at least 90 mmHg. The vasogenic component of spinal shock usually produces a systolic blood pressure of approximately 80 mmHg or so. If the fluid infusion is not increasing the pressure or profound signs of hypoperfusion are present, consider a vasopressor agent such as dopamine. Begin at 5 mcg/kg/minute and titrate up quickly. At lower doses, dopamine primarily has a beta effect. Once a dose of 10 mcg/kg/minute is achieved, predominantly alpha stimulation occurs with systemic vasoconstriction.

Assess the blood glucose level. If the blood glucose level (BGL) is less than 60 mg/dL with signs and symptoms of hypoglycemia, or if the BGL is less than 50 mg/Dl with no signs of hypoglycemia, administer 50 percent Dextrose. The standard dose is 25 grams; however, many systems are now administering 12.5 grams and reassessing the patient and BGL prior to administering the second 12.5 gram dose. Always be sure to follow your local protocol.

EMS plays a significant role in attempting to reduce secondary injury of the spinal cord through proper assessment and management. If there is any doubt based on your clinical assessment whether the patient has suffered a vertebral or spinal cord injury, err on the side that benefits the patient and provide complete immobilization.

Joseph J. Mistovich, M.Ed, NREMT-P, is the chairperson of the Department of Health Professions and a professor at Youngstown State University in Ohio. He has more than 23 years of experience as an educator in EMS and multidisciplinary healthcare. He received a Master of Education degree from Kent State University, a Bachelor of Science in Applied Science degree and an Associate in Applied Science degree in EMS both from Youngstown State University. He has authored numerous EMS textbooks and EMS journal articles. He is a frequent speaker at state and national conferences. To contact Joseph, email joseph.mistovich@ems1.com.

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