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wagner6e_ch19_chapter_summary.docx

Uploaded: A year ago
Contributor: Kim
Category: Nursing
Type: Other
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Filename:   wagner6e_ch19_chapter_summary.docx (22.46 kB)
Page Count: 2
Credit Cost: 1
Views: 33
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Transcript
Chapter 19: Acute Spinal Cord Injury Chapter Summary The spine is composed of 33 individual and fused vertebrae. The spinal nerves join complex networks after leaving the cord to innervate parts of the body. The spinal cord consists of an outer region of white matter and an inner region of gray matter that transmits motor activity from the brain to the body and serves as a ‘relay’ station for sensory messages from the body to the brain. Damage to specific regions of the cord may produce alterations in either sympathetic or parasympathetic function. Complete SCI results in paraplegia or tetraplegia, with loss of motor and sensory function below the level of injury. Incomplete SCI results in variable degrees of loss of motor and sensory function because there is partial interruption of motor and sensory pathways. SCI can occur as a result of traumatic injuries (e.g., motor vehicle crashes, falls) or nontraumatic injuries (e.g., degenerative changes of the vertebrae, space-occupying lesions, cord infarction). SCI can be classified on the basis of the extent of cord damage (complete or incomplete) and level of injury (location of cord injury relative to the corresponding vertebrae,—e.g., cervical, thoracic, or lumbar). Mechanisms of SCI include primary injury and secondary injury. Primary injury occurs as direct injury at the time of the insult. There are four major mechanisms of primary injury—hyperflexion, hyperextension, flexion–rotation, and compression—and one less common mechanism, distraction injury. Secondary injury develops as a result of vascular injury to the cord from disruption of perfusion and ischemia. Damage occurs over time due to complex biochemical processes that may last days to weeks postinjury. Damage to a UMN pathway results in loss of cerebral control over reflex activity below the lesion level and may produce spastic paralysis. Damage to LMN may result in flaccid paralysis. There are three broad categories of complications associated with SCI related to alterations in mobility, perfusion, and reflex activity. Pneumonia and septicemia are the most frequent causes of death in patients with SCI. Patients with SCIs, especially cervical injuries, have a high incidence of pulmonary complications, including pneumonia, atelectasis, and respiratory failure, and are at great risk for developing decreased cardiac output related to orthostatic hypotension, spinal and neurogenic shock, venous pooling, emboli, and bradycardia. The degree of bladder and bowel dysfunction depends on the location and completeness of the SCI. Autonomic dysreflexia (AD) is a potentially life-threatening complication that involves an exaggerated sympathetic response and occurs in patients with SCI at or above the T6 level. AD may occur anytime after spinal shock resolves. The diagnosis of spinal cord injury (SCI) begins with a detailed history of events surrounding the incident, radiographic studies of the spine, and an assessment of sensory and motor function. Serial neurologic exams are performed hourly for at least the first 24 hours after SCI. Physical and neurologic examination consists of assessment of motor, sensory, and reflexes. Timely spinal cord alignment and stabilization maximize cord recovery, minimize additional damage, and prevent late deformity.

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