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Spinal C ord Injury. Etiology of Traumatic Spinal Cord Injury. MVA- most common cause Other: falls, violence, sport injuries SCI typically occurs from indirect injury from vertebral bones compressing cord SCI frequently occur with head injuries - PowerPoint PPT Presentation
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Etiology of Traumatic Spinal Cord InjuryMVA- most common causeOther: falls, violence, sport injuriesSCI typically occurs from indirect injury from
vertebral bones compressing cord SCI frequently occur with head injuriesCord injury may be caused by direct trauma
from knives, bullets, etc
Etiology of Traumatic Spinal Cord Injury78% people with SCI are maleTypically young men – 16-30Number of older adults rising (>61 yr)Greater complicationsLife Expectancy 5 years less than same age
without injury90% go home
Pathophysiologyanatomy of the spine
PathophysiologyNormal Spinal Cord
Spinal cord begins at the foramen magnum in the cranium
Cord ends at the L1-L2 vertebra level
Spinal nerves continue to the last sacral vertebra
PathophysiologyNormal Spinal Cord
Vertebral Column
8 Cervical12 Thoracic5- Lumbar5- Sacral
Protection of Spinal Cord from Injury
Bones- vertebral column
Discs- between vertebra
Internal and external ligaments
Dura
Protection of Spinal Cord from Injury
Internal and external ligaments
DuraMeningesCSF in
subarachnoid space allow for movement within spinal canal
Nervous System and the Spinal Cord
ANS can be affected by SCI
Sympathetic chains on both sides of the spinal column
Parasympathetic nervous system is the cranial-sacral branch
Normal Spinal Cord
Normal spinal cord
DermatonesSkin innervated by
sensory spinal nerves
Normal Spinal Cord
Reflex Arc Where sensory and
motor nerves arise from cord
Sensory fibers enter posterior
Motor fibers leave from anterior
Once outside cord join form spinal nerve
reflex movement
Normal Spinal CordWhite tracts send
messages to and from the brain
Pyramidal- Voluntary movements
Posterior column (Dorsal)- touch, proprioception, and vibration sense
Lateral spinothalamic tract- pain and temperature sensation (only tract that crosses within the cord)
voluntary movement
Spinal Cord Injury- SCICompressionInterruption of blood supplyTractionPenetrating Trauma
Spinal Cord InjuryPrimary
Initial mechanism of injurySecondary
Ongoing progressive damage Ischemia Hypoxia Microhemorrhage Edema
Spinal Cord InjuryHemorrhage and edema occur in the cord
post injury, causing more damage to cord
Extension of the cord injury from cord edema can occur over the first few days- watch the phrenic nerve!
Initially SCI experience spinal shock- depression of all cord & ANS function below injury. Lasts from few min to wks
Classifications of SCI1. Mechanism of Injury2. Skeletal and Neurologic Level3. Completeness (degree) of Injury
Classifications of SCIMechanism of Injury1. Mechanism of Injury
FlexionHyperextensionFlexion RotationCompression
Classifications of SCIMechanism of Injury
Flexion (hyperflexion)Most common because
of natural protection position.
Generally cause neck to be unstable because stretching of ligaments
Classifications of SCIMechanism of Injury
HyperextentionCaused by chin hitting a
surface area, such as dashboard or bathtub
Usually causes central cord syndrome symptoms
Classifications of SCIMechanism of Injury
CompressionCaused by force from
above, as hit on headOr from below as
landing on buttUsually affects the
lumbar region
Classifications of SCIMechanism of Injury
Flexion/RoatationMost unstableResults in tearing of
ligamentous structures that normally stabilize the spine
Usually results in serious neurologic deficits
Classification of SCI- Level of InjurySpinal cord levelWhen referring to
spinal cord level, it is the reflex arc level not the vertebral or bone level.
Note that the thoracic, lumbar & sacral reflex arcs are higher than where the spinal nerves actually leave through the opening of there respective vertebral bone
Classification of SCI- Level of Injury
Spinal cord injuries are described by the level of the injury– the cord segment or dermatome level
Such as C6; L4 spinal cord injury
Classifications of SCICompleteness (Degree) of Injury
CompleteIncomplete
Central cord syndromeAnterior Cord syndromeBrown-Sequard SyndromePosterior Cord SyndromeCauda Equina and Conus Medullaris
Classification of SCI Completeness (degree) of InjuryComplete (transection)After spinal shock: Motor deficits- spastic
paralysis below level of injury
Sensory- loss of all sensation perception
Autonomic deficits- vasomotor failure and spastic bladder
Classification of SCI Completeness (degree) of InjuryIncompleteCentral Cord Syndrome
Injury to the center of the cord by edema and hemorrhage
Weakness in both upper extremities- legs are spared
Varied loss of sensation
Classification of SCI Completeness (degree) of InjuryIncomplete
Brown-Séquard Syndrome
Hemisection of cordIpsilateral paralysisIpsilateral superficial
sensation, vibration and proprioception loss
Contralateral loss of pain and temperature perception
Classification of SCI Completeness (degree) of InjuryincompleteAnterior Cord Syndrome
Injury to anterior cord Loss of voluntary motor
(Pyramidal track) below Loss of pain and
temperature perceptionRetains posterior column
function
Classification of SCI Completeness (degree) of InjuryincompletePosterior Cord Syndrome
Least frequent syndromeInjury to the posterior
columns results in proprioceptive loss (dorsal columns)
Pain, temperature, touch are preserved. Motor function is preserved to varying degrees.
Classification of SCI Completeness (degree) of InjuryincompleteConus Medullaris
Syndrome Injury to the sacral cord
(conus) and lumbar nerve roots within the spinal canal, usually results in are-flexic bladder and bowel, and lower limbs (in low-level lesions)
Cauda Equina Syndrome Injury to the lumbosacral
nerve roots within the neural canal, results in areflexic bladder, bowel, lower limbs
Common Manifestations/ComplicationsTerms used to describe motor deficitsPrefix: para- meaning two extremities; tetra-
or quadra- all four extremitiesSuffix –paresis meaning weakness; -plegia
meaning paralysisQuadraparesis means what?
Common Manifestations/Complications
C1-3 usually fatal- Loss of phrenic
innervation ventilator dependent
No B/B controlSpastic paralysisElectric w/c with
chin/mouth control
Common Manifestations/Complications
C6- weak graspHas shoulder/biceps to
transfer & push w/cNo bowel/bladder
control.
Considered level of independence
Common Manifestations/Complications
T1-6- full use of upper extremity
TransferDrive car with hand
controls and do ADL’sNo bowel/bladder
control
Clinical Manifestations of SCISkin: pressure ulcers
Neuro: pain; sensory loss; upper/lower motor deficits; autonomic dysreflexia
Cardio: dysrhythmias; spinal shock; loss of sympathetic nervous system control over blood vessels (vasomotor control)- decreased venous return, orthostatic hypotension, poikilothermic (takes on temp of room)
Clinical Manifestations of SCIRespiratory: decrease chest expansion; cough
reflex & vital capacity; diaphragm function-phrenic nerve
GI: stress ulcers; paralytic ileus; bowel- impaction & incontinence
GU: upper/lower motor bladder; impotence; sexual dysfunction
Musculoskeletal: joint contractures; bone demineralization; osteoporosis; muscle spasms; muscle atrophy; pathologic fractures; para/tetraplegia
Spinal and Neurogenic shockSpinal Shock
Decreased reflexes and loss of sensation below the level of injury
Motor loss- flaccid paralysis below level injurySensory loss- loss touch, pressure, temperature
pain and proprioception perception below injury
Lasts days to months
Spinal and Neurogenic ShockNeurogenic shockDue to loss of vasomotor tone
SNS loss results in parasympathetic dominance with vasomotor failure
Loss of SNS innervation causes peripheral pooling and decreased cardiac output
Hypotension and Bradycardia Orthostatic hypotension and poor
temperature control (poikilothermic- takes on temp of environment)
How do you know spinal shock is over?
Clonus is one of the first signs
Hyperreflexia of footTest by flexing leg at
knee & quickly dorsiflex the foot
Rhythmic oscillations of foot against hand
clonus
Common Manifestation/ComplicationsUpper and Lower Motor Deficits
Upper motor deficits result in spastic paralysis
Lower motor deficits result in flaccid paralysis and muscle atrophy
Diagnostic Studies for SCI
X-ray of spinal columnCT/MRIBlood gases
Collaborative CareEmergency Care at Scene, ER & ICU
Transport with cervical collar
Assess ABC’s; O2; tracheotomy/vent
IV for life lineNG to suctionFoley
Therapeutic Interventions MedicationsIV methylprednisolone (Solu-Medrol)
within 8 hrs to decrease cord edema
Therapeutic InterventionsMedications To control or to prevent complications of
SCI and immobility:Vasopressors to maintain perfusionHistamine H2 blockers to prevent stress ulcersAnticoagulantsStool softenersAntispastomotics
Therapeutic InterventionsStabilization/immobilizationTraction with Gardner-Wells tongs
Therapeutic InterventionsExternal tractionHalo device For patients who do not
have motor deficits Experience less
immobility complications
Therapeutic InterventionsCasts; splints; collars; braces
Therapeutic InterventionsSpecial Beds for SCITo decrease immobility
complicationsRotorest is a common
one used- rotates 23 hrs a day
Therapeutic InterventionsSurgery for SCI
Manipulation to correct dislocation or to unlock vertebrae
Decompression laminectomy
Spinal fusionWiring or rods to hold
vertebrae together
Nursing Management AssessmentHealth HistoryDescription of how and when injury occurredOther illnesses or disease processesAbility to move, breathe, and associated
injury such as a head injury, fractures
Nursing Management AssessmentPHYSICAL EXAM
LOC and pupils- may have indirect SCI from head injury
Respiratory status- phrenic nerve (diaphragm) and intercostals; lung sounds
Vital signsMotorSensoryBowel and bladder function
Nursing ManagementAssessmentMotor Assessment Upper Extremity
Movement, strength and symmetry
Hand grips
Flex and extend arm at elbow- with and without resistance
Nursing Management Assessment Motor Assessment Lower Extremity
Flex and extend leg at knee with and without resistance
Planter and dorsi flexion of foot
Nursing Management AssessmentMotor assessment- ClonusClonus- hyperreflexiaFlex knee and quickly
dorsiflex the foot with your hand
If has return of reflex function the foot will have repetitive movements against you hand
Spinal shock is over
Nursing Management AssessmentSensory assessment
With the sharp and dull ends of a paperclip have the individual, with their eyes closed identify
Use the dermatome as reference to identify level
C6 thumb; T4 nipple; T10 naval
Nursing Problems/Interventions
1.Impaired mobility2.Impaired gas exchange3. Impaired skin integrity4. Constipation5. Impaired urinary elimination6. Risk for autonomic dysreflexia7. Ineffective coping
1. Impaired Physical MobilityLog roll as a single unit; provide assistance
as needed to keep alignment; teach patient Care traction, collars, splints, braces,
assistive devices for ADL’sFlaccid paralysis- use high top tennis shoes
or splints to prevent contractures. Remove at least every 2 hrs for ROM (active ROM best)
1. Impaired Physical MobilitySpastic Paralysis- Assess for clonus
Prevent spasms by avoiding; sudden movements or jarring of the bed; internal stimulus (full bladder/skin breakdown; use of footboard; staying in one position too long; fatigue
Treat spasms by decreasing causes; hot or cold packs; passive stretching; antispasmotic medications
Assess skin break down thrombophlebitis; remove TED hose at least every shift
1. Impaired Physical MobilityPrevent/treat orthostatic hypotension
Abdominal binder, calf compressors, TED hose when individual gets up
Assess BP, especially when risingAssist Physical Therapy with tilt table as
individual gradually gets use to being in an upright position
1. Impaired Physical MobilityUse of transfer board
2. Impaired Gas ExchangePhrenic nerve (C3-5) controls the diaphragm
bilaterally. If nerve is nonfunctioning then individual is ventilator dependent.
Thoracic nerves control the intercostals muscles for breathing and abdominal muscles aide in breathing and coughing
2. Impaired Gas ExchangeAssess respiratory rate, rhythm, depth, and
breath soundsMonitor vital capacity, respiratory effort,
ABG’s, O2 saturationAssess for signs of impending extension of
SCI up cord to phrenic nerve level (C3-5)Assess need for ventilatory assistance,
tracheotomy, ventilator Quad cough (assistive cough) as needed
3. Impaired Skin IntegrityChange position frequentlyRemoval of TED hose every 8 hoursNutritional statusProtection from extremes in temperature
3. Impaired Skin IntegrityInspect skin at least 2x/day especially over
boney prominences Avoid shearing and friction to soft tissue
with transfers
4. ConstipationBowel rely more on bulk than on nervesStimulate bowels at the same time each day.
Best after a meal when normal peristalsis occurs
Individual may progress from Dulcolax suppository to glycerin then to gloved finger for digital stimulation
Assess bowel sounds prior to giving food for the first time– paralytic illus!
5. Impaired Urinary EliminationBladder function SCI
Upper/Lower MotorBladder reflex arc-
sacral 2,3,4
5. Impaired Urinary EliminationFlaccid bladder (lower motor neuron lesion)
No reflex from S2,3,4Automatic empting of bladder Urine fills the bladder and dribbles outNeed foley or freq intermittent self catherization
Spastic bladder (upper motor neuron lesion) Reflex arc but no connection to or from brain Reflex fires at will Bladder training- trigger points to stimulate empting;
self catherization
5. Impaired Urinary EliminationUse bladder scan to see amount of urine
in bladder Goal- residual <100ml/20% bladder
capacitySome individuals may need suprapubic
catheterAssess effectiveness of medication
Urecholine to stimulate bladder contractionUrinary antiseptic
6. Risk for Autonomic DysreflexiaSCI above T6 Results in loss of normal compensatory
mechanisms when sympathetic nervous system is stimulated
Life threatening- if goes unchecked BP can result in cerebral hemorrhage
Vasodilatation symptoms above SCIVasoconstriction symptoms below SCIThe cause of SNS stimulation
6. Risk for Autonomic Dysreflexia
Elevate head of bed- causes orthostatic hypotension
Identify cause/alleviate- if full bladder- cath; if skin- remove pressure, if full bowel- empty, etc
Remove support hose/abdominal binderMonitor blood pressure- can get > 300 SGive PRN medication to lower BPIf above not effective– call physician
7. Ineffective Coping
Grief and DepressionSexuality
7. Ineffective CopingGrief and Depression
Assess thoughts on ‘quality of life’; body image; role changes
Physical and psychological supportMost common SCI is 15-30 yeas old and
generally a risk taker– this greatly affects their perception of life and rehabilitation
7. Ineffective CopingSexualityAssess readiness/knowledge/your ability
Male sexual function- reflexogenic (S2,3,4) erections; psychogenic erections (psychological stimulation) Ejaculation/fertility may be affected
Female- hormones more than nerves regarding fertility. C-section because of chance for autonomic dysreflexia during labor. Lack of sensation/movement affects sexual performance
Suggestions: empty bladder before sex; withhold fluids and antispasmodics; certain positions may increase spasms; explore new erogenous zones; penile implants
Home CareAssess psychological, physical resources,
need for rehabilitation (in-house or outpatient); need for community resources
Home evaluation
What’s new in SCI treatment?Superman breatherYouTube - Superman breather – USAYouTube - Superman breather – USA
Kevin Everetthypothermia treatment for SCIStanding TallTravis Roy- 11 Seconds
Stem Cell treatment for SCILipitor for SCI
NCLEX questions/ case study
Case study- Jim Valdez1. Why does Jim have flaccid paralysis on
admission to ICU?2. What symptoms indicate that he is in spinal
shock? What was done about these symptoms?3. How will we know when he is out of spinal
shock?4. How does progressive mobilization assist
with orthostatic hypotension? What else can be done?
5. What are realistic functional goals for Jim?