Nursing Concepts NRSG 3040
Weber State University
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This 6 page Class Notes was uploaded by Floy Dietrich Jr. on Wednesday October 28, 2015. The Class Notes belongs to NRSG 3040 at Weber State University taught by Staff in Fall. Since its upload, it has received 29 views. For similar materials see /class/230776/nrsg-3040-weber-state-university in Nursing and Health Sciences at Weber State University.
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Date Created: 10/28/15
ng 3040 Spinal Cord Patho Spinal cord anatomy and topographical pathophysiology The spinal cord is divided into 31 segments each with a pair of anterior motor and dorsal sensory spinal nerve roots On each side the anterior and dorsal nerve roots combine to form the spinal nerve as it exits from the vertebral column through the neuroforamina Extends from the base of the skull and terminates near the lower margin of the L1 vertebral body Thereafter the spinal canal contains the lumbar sacral and coccygeal spinal nerves comprising the cauda equina Pathology of the spinal cord mainly produces symptoms and signs due to the involvement of 3 main areas of the spinal cord Dorsal columns Spinothalamic tracts Corticospinal motor tracts Note Spinal injuries below L1 therefore do not muse spinal cord injury but may cause segmental spinal nerve andor cauda equina injuries Spinal injuries proximal to L1 above the termination of the spinal cord often precipitate a combination of spinal cord lesion and segmental root or spinal nerve injury Dorsal columns Contain sensory tracts for Crude touchpressure blunt sharp Two point discrimination paper clip Vibration timing fork Position sense proprioception Most discriminating test for injury is proprioception or position testing Lateral spinothalamic tracts Contain sensory tracts for Pain blunt sharp Temperature hot cold Light touch cotton strand Most discriminating test for injury is pain blunt sharp Anterior spinothalamic tract Contains sensory tracts for Touch Qtip and blunt sharp Pressure Qtip Anterolateral corticospinal tracts Carry descending motor pathway bers movement and strength Injury to Dorsal columns Pt will complain of Unpleasant deep sensations and buzzing paresthesias or negative sensations of quotdeadnessquot Parts of the neuro exam eg stroking the foot to elicit the plantar response or bending the digits to test position sense are unusually pain il or uncomfortable unpleasant vibrating paresthesias like touching a vibrator Injury to the lateral spinothalamic tract NOTE pain and temperature fibers enter spinal cord ascend a few spinal segments before crossing to travel up the contralateral lateral spinothalamic tract Contralateral pain and temperature sensory deficit There will be a difference of a few spinal dermatome levels between the level of detectable sensory deficit and the true level of spinal pathology Injury or disease of the central cord Can affect the paintemperature sensory bers crossing the midline Produces a unilateral or bilateral band of paintemperature sensory deficit affecting a few dermatomes just below the level of the spinal cord lesion Lateral corticospinal tract pathology affecting the upper motor neuron fibers traveling in the corticospinal tract produces an ipsilateral motor deficit Anterior cord syndrome characterized by a loss of motor mction and paintemperature sensation below the level of the lesion preserved posterior column mction position sense and vibration sense typically seen following hyper exion injuries with impingement of bone or herniated disc tissue directly on the anterior spinal cord or due to mechanical compression of the anterior spinal artery and secondary infarction of the anterior spinal cord or rarely due to aortic dissection interrupting the blood supply to the anterior spinal arteries Central cord syndrome most commonly associated with hyperextension injuries in elderly patients with cervical spondylosis and a narrow cervical canal gt bilateral arm weakness gtgt lower limb weakness with paresis more dense distally than proximally variable sensory impairment pain and temperature sensory loss gtgt propioceptive sensory loss and bladder dysfunction mnemonic MUD motor gt sensory upper gt lower and distal gt proximal the degree and lomtion of the neurological deficits depends on the exact lomtion and size of the lesion bilateral quotburning handsquot paresthesias may be an early symptom and may precede any neurological signs or may occur in isolation without any neurological deficits may also be chronic and slowly progressive in its timecourse seen in chronic cervical spondylosis compressing the spinal cord and in tumors of the central spinal cord Posterior cord syndrome characterized by proprioceptive sensory loss preservation of pain and temperature sensory function preservation of motor function usually due to posterior spinal artery occlusion chronic atherosclerosis and impaired collateral circulation tumors or discs compressing the posterior spinal cord or vitamin B12 deficiency BrownSequard syndrome lateral cord syndrome due to a lesion involving half of the spinal cord ipsilateral loss of motor mction and proprioceptive sensory mction contralateral loss of paintemperature sensation most commonly due to traumatic hemisection of the spinal cord eg stabbing knife thrust rarely due to radiation injury or air embolism associated with scuba diving can also occur secondary to spinal tumors or other local pathology compressing the lateral spinal cord partial BrownSequard syndromes are more common gt varying degrees of paresis and analgesia Cauda equina syndrome slow progressive loss often asymmetric or unilateral often due to chronic disc herniation spinal stenosis may be due to spinal tumors less severe back pain may produce severe radicular symptoms sensory loss affects all sensory modalities lumbar gt sacral sensory loss may affect penisclitoris and pubic area and be asymmetrical sensory loss may follow a specific dermatomal pattern muscle weakness lumbar gt sacral muscle weakness mainly affects glutei hamstrings gastrocnemius and soleus muscles muscle atrophy and fasiculations common tendon re ex loss knee gt ankle bladder involvement late accid bladder Management of Spinal Cord Injury Spinal cord injuries may be primary or secondary Primary spinal cord injury arises from mechanical disruption transection or distraction of neural elements This usually occurs with fracture andor dislocation of the spine Penetrating injuries from bullets or other weapons may also cause primary spinal cord injury More commonly displaced bony fragments precipitate penetrating spinal cord or segmental spinal nerve injuries Extradural pathology may also precipitate a primary spinal cord injury Spinal epidural hematomas or abscesses cause acute cord compression and injury Spinal cord compression from metastatic disease is a common oncologic emergency Vascular injury to the spinal cord caused by arterial disruption arterial thrombosis or hypoper ision om shock are the major causes of secondary spinal cord injury Anoxia or hypoxia effects will compound the extent of spinal cord injury Spinal cord injury as with acute stroke is a dynamic process In all acute cord syndromes the lll extent of injury may not be apparent initially Incomplete cord lesions may evolve into more complete lesions More commonly the injury level rises one or two spinal levels over the subsequent hours to days after the initial event A complex cascade of pathophysiologic events relating to ee radicals vasogenic edema and altered blood ow accounts for this clinical deterioration ABCBSS NOTE Neurogenic shock is characterized by severe autonomic dys mction resulting in hypotension relative bradymrdia peripheral vasodilation and hypothermia It does not usually occur with spinal cord injury below T6 Ifthe patient is shocky rule out hypovolemia rst Beyond that is minimizing the damage CORD PROTOCOL Methylprednisolone Solu Medrol Start within 8 hours of injury for bene t the earlier the better max bene t at 3 hours 30 mgkg body weight administered as an IV bolus over 15 minutes 45minute pause 23hour continuous infusion of 54 mgkg per hour Exclusion Criteria Cauda equina Gunshot wounds Life Threatening Morbidity Pregnancy Narcotic Addiction Maintenance steroids lt 13 years ofage Why it works Speculated there are 2 main effects Immunosuppression blocking vigorous in ammatory responses at the site of injury may worsen its impact Block the formation of ee radicals that worsen injury Nontrauma causes with alterations in nervous system mction CreutzfeldJakob syndrome and its 3 variants Characterized by a rapidly progressive dementia Diagnosis of TSE can be reliably made only postmortem The neuropathological hallmarks of TSEs are spongiform change astrocytic gliosis neuronal loss and PrP positive plaques
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