Neuromuscular Flashcards
Cerebral Palsy pathophysiology
not caused by problem in muscles or nerves. caused by faulty development or damage to motor areas of the brain
r/t anoxic brain event causing brain damage prior to birth, during birth, or in the first 2 years of life when brain is rapidly developing
CP classified by
motor abnormalities (type and severity)
associated impairments (seizures, cognitive, communication, behavior)
anatomic and radiologic findings
causation and timing
congenital causes of CP
maternal infections
jaundice
Rh incompatibility
stroke
what to watch for in CP?
skin breakdown, pressure ulcers, missed milestones, abnormal reflexes and tone
missed motor milestones in CP
not sitting unsupported by 7 months
failure to smile by 6-8 weeks
feeding difficulties (gagging, chocking, tongue thrust after 6 months)
extreme irritability or crying
Abnormal muscle tone in CP
persistence of primitive reflexes past 6 months (moro, tonic neck, grasp reflex)
floppy or limp body posture
stiff or rigid arms or legs
motor abnormalities in CP
early sign is hand preference in the first 18 m abnormal crawl (only uses one side of the body or only arms to crawl) uncoordinated or involuntary movements facial grimacing writhing movements poor suck tongue thrust ataxia
hypotonic body tone in CP
present at birth and may persist to 1 year then replaced by hypertonic muscles
hypertonic body tone in CP
resistance to passive ROM
hips higher than trunk when prone
spine deformities r/t opisthotonic posture
contractures
clinical manifestations associated with spastic CP
seizures
contractures
incontinence ADHD
non-ambulation leads to constipation, orthopedic problems, skin breakdown, and respiratory infections
associated impairments with CP
feeding difficulties manifests as FTT, poor suck, tongue twist
affects chewing, swallowing and talking
- nurses can help improve function by helping child blow bubbles, pen wheels, and chewing gum under supervision
therapeutic management of CP
PT/OT and speech
assistive devices for mobility and ADL’s
computers
surgery ( to release tendons, and improve function)
med management of CP
used to manage associated symptoms antipyretics stimulants ( ADHD) botox ( paralysis of overactive muscles) skeletal muscle relaxants ( dantrolene, baclofen, methocarbamol) anxiolytics bowel regimen
home management of CP
helping family cope with a child with chronic illness education about inclusion at school use of assistive devices and exercise proper med administration prevent skin breakdown and respiratory infections nutrition (increase calories and rest) play and recreation safety needs
nursing care of CP
assessment and early identification reinforce therapeutic plan address home care needs routine skin assessments immunizations safety precautions (wearing helmets when needed, home adaption, modified care seats)
Duchenne Muscular Dystrophy causes
x-linked disorder
males only
absence of dystrophin leads to muscle degeneration
early clinical manifestations of Duchenne MD
onest between 3-5 yr
positive gower sign (ask child to stand from kneeling position if they have to walk hands up legs to stand it is positive)
kids will meet milestones normally until 3-5yr and will regress
rapid PROGRESSIVE muscular degeneration after normal development
waddling gate
lordosis
kids waste from inside out
progressive clinical manifestations of duchenne MD
pseudohypertrophy muscular atrophy ability to ambulate generally lost by 10-12 yr facial and respiratory muscle atrophy cardiac and respiratory failure mild to moderate cognitive impairment median age 22 yr with mechanical ventilation fatal disease child will die no cure
Duchenne MD dx by
clinical manifestations
muscle bx
EMG
Therapeutic goals of MD
to maintain function in the unaffected muscles as long as possible with bracing, range of motion, performing ADL’s and surgery to release contractures
spina bifida
malformation of spine where lamina of vertebrae fails to close
causes of spina bifida
inadequate consumption of folic acid before conception and during the first trimester
neural tube closes at 4 weeks
folic acid found in green leafy veggies, multi-vitamins
diagnosis of spina bifida
most diagnosed post-natally, but can be dx in prenatal ( 16-18 weeks gestation)
spina bifida occulta
only in vertebrae spinal cord and meninges are normal
no neuro problems
spina bifida cystica 2 types
meningocele ( external sac encases meninges and spinal fluid, no associated neurological deficit)
myelomenigocele (external sac encases meninges and spinal fluid, and nerves, most common in lumbar or lumbosacral area, location and size of the lesion determines the degree of neuro deficit, the higher the lesion the worse it is)
clinical manifestations of myelomeningocele SB
sac like protrusion evident at birth hydrocephalus varying degrees of sensory and neurological dysfunction poor muscle tone in bladder and rectum flexion of extension contractures
treatment of myelomeningocele SB
closure of sac withing 24-72 hours if possible, within 12-18 hours to prevent infection and preserve nerve roots
done by neurosurgery and plastics
prior to surgery cover area with sterile warm saline get to nicu asap, prone position
preop nursing care of myelomeningocele SB
prevent infection
cover sac with mosit sterile NS gauze , no diaper
keep genitalia clean, may need to catheterize
position prone
avoid rectal temps because of poor sphincter tone
nursing care of myelomeningocele SB
VS, weight, I and O, assess pain, observe incision, leave prone
feed when awake and parent is holding
orthopedic interventions to improve locomotion and prevent deformities post op (ROM)
treatment of urinary incontinence by intermittent cathing (prevent UTI’s) can learn to self cath at age 6
urinary diversions
treatment of bowel incontinence with myelomeningocele SB
bowel training
prevent constipation (laxatives, digital stimulation, and enemas)
dietary modifications
antegrade continence enema procedure
why are SB kids at risk for developing a latex allergy?
surgery at an early age can cause latex allergy, kids kids in latex free environment
