1) Understand the pathophysiology of spinal cord injury (SCI)
2) Describe the neuroanatomical relationship and effect of SCI for the lungs, skin, bowel, bladder, cardiovascular system
3) Examine the medical management of the most serious and common complications after SCI
4) Differentiate the sensory, motor, and reflex function for different types and levels of SCI
5) Identify and structure rehabilitation interventions for incomplete and complete SCI
6) Recognize adjustment issues of individuals with SCI and their families
CASE A, PART I
Jane Roberts is a 45-year-old African-American woman who entered the Emergency Department via ambulance with a self-inflicted gunshot wound to the neck at C2–3. She was intubated in the field and placed on a respirator when admitted to the hospital. Her blood pressure, 98/62, and heart rate, 60, were low and continued to fall. Radiographs show a projectile near C2, a vertebral fracture of C2, and a bony fragment within the spinal canal. She has a history of depression and mild obesity but takes no medications for these conditions. Ms. Roberts presented in the Emergency Department with no volitional movement in any of the extremities. The plantar reflex was present, but deep tendon reflexes (DTRs) in all extremities were absent. She is not married, works in a parts-assembly factory, and lives alone in a two-story home.
What Is Spinal Cord Injury?
The spinal cord is protected by the surrounding bone of the vertebrae, but in severe trauma, the vertebrae fracture or dislocate. In fact, fracture, dislocation, and/or subluxation of the vertebrae are the most common causes of spinal cord injury (SCI). The damaged bony segments impinge the spinal cord and immediately cause a lesion. This direct damage to the spinal cord is called the primary injury. It is important to note that the spinal cord is almost never completely severed; some spinal cord tissue is usually spared. Commonly, the fractured or dislocated bone compresses the cord or only partially pierces it. In most cases, the primary injury begins in the gray matter of the cord, when the blood vessels shear and rupture, directly damaging neurons. There is frank hemorrhage at the injury site and small petechial hemorrhages away from the injury over the next couple of hours. White matter axons may also be directly lesioned with the primary injury. These initial events set off a complex secondary cascade that cause the lesion to expand in size, over a long distance and over a very long period of time.
The secondary injury events stem from a toxic environment created by the initial injury.1 The opening of the blood–brain barrier allows red blood cells to flood the gray matter, and the iron and hemoglobin they contain are toxic to neurons that were not initially damaged by the trauma. As these bystander neurons die, they release neurotoxins and glutamate that go ...