exam 4 Flashcards
management of soft tissue injury
RICE
most common broken bone in childhood
distal forearm
fracture in infants
huge red flag for abuse
their bones are harder to fracture
types of fractures
simple/closed
open/compound
comminuted
complicated
growth plate injuries
growth plates are the weakest of long bones.
injury here may affect future bone growth
treatment may include open reduction and internal fixation
bone healing times
the younger you are the quicker it will heal
neonates: 2-3 weeks
early childhood: 4 weeks
later childhood: 6-8 weeks
adolescents: 8-12 weeks
goals of fracture management
reduction and immobilization
restoring function
preventing deformity
diagnosing fracture
xray
history
assessing compartment syndrome: the 6 Ps
pain
pallor
pulselessness
paresthesia
paralysis
pressure
spica cast
Used for pelvic to keep legs in position
bar is to keep legs at a certain position/in place
dont use bar to move pt!
why is traction used in children
relieve fatigue of muscles
position bone ends
immobilize
prevent deformity
reduce muscle spasms
distraction of fracture
process of separating opposing bone to encourage regeneration of new bone in created space
external fixation devices are commonly used
developmental dysplasia of the hip (DDH)
misplaced hip.
Congenital
more common in girls
s/s of DDH
infants:
restricted adduction of hip
unequal gluteal folds
positive ortolani test result
positive barlow test
hip joint laxity
toddlers: walking/standing may appear off
management of DDH
from birth to 6 months: plavik harness for hip adduction and flexion. prevent harness from scratching baby-use clothes
ages 6-24 months- typically not recognized until standing/walking. need closed reduction and spica cast
as child gets older (past age 4), correction gets difficult. Need operative reduction, tenotomy, osteotomy
club foot
deformity of the foot and ankle
multiple different types: talipes varus most common
correct deformity
ponseti method (serial casting)- every couple weeks cast is changed and made straighter each time
osteogenesis imperfecta
brittle bones that fracture easy due to faulty bone mineralization or abnormal bone architecture.
med- IV pamidronate Q3 months to promote increased bone density/prevent fractures
handle these pts/babies gentle!!
they should avoid contact sports
prevent osteoporosis, malalignment, weakness, contractures
legg-calve-perthes disease
Aseptic necrosis of femoral head due to disturbed circulation to femoral head.
typically only occurs in one hip but could be bilateral
most common in white boys age 4-8
dx by MRI and XRAY
legg-calve-perthes disease manifestations
pain and limp is most evident
may also have limited ROM, soreness, stiffness
legg-calve-perthes disease management
goal is to keep head of femur in acetabulum.
femoral head collapses due to blood supply loss, it does not stay where it needs to be.
containment can be done with various appliances and devices
no weight bearing initially, rest
NSAIDs
surgery may be needed
slipped capital femoral epiphysis (coxa vara)
femoral head slips off spontaneously in a posterior-inferior direction
develops shortly before puberty
bilateral half of the time
treated by surgery
scholiosis
inward curvature of spine
most common spinal deformity
could be congenital or develop in childhood
typically idiopathic cause
generally noticeable after growth spurt
dx by XRAY and assymetry
treated by brace is not severe or surgery - rods and fusion, if severe
osteomyelitis
infection of bone
most commonly caused by staph
s/s begin abruptly, resemble arthritis and leukemia
bone scans for dx. bone cultures done for abx
ABX and good nutrition (protein) needed!
Pain management is important
may get sent with picc line for long term abx
cerebral palsy
non-progressive brain disorder affecting movement/motor skills.
causes growth and development issues as well as intellectual disabilities.
most common motor disability with childhood.
could occur prenatally or postnatal
multiple types
severity ranges person to person
causes of prenatal cerebral palsy
hypoxia
radiation
infection
causes of postnasal cerebral palsy
CNS infection
head trauma
hypoxia
spastic CP
Most common type
We see contractures. Really jerky and stiff movements due to hypotonia muscles. Muscles are flexed
Foot drop may. Sometimes will walk on tip toes if can walk, scissor legs, newborn refluxes stay throughout life
s/s of CP
pain
sleep disorders
difficulty taking PO if spasticity
communication difficulties
intellectual disabilities
hearing/vision problems
seizures
GERD
constipation/incontinence
contractures
scoliosis
diagnosis of CP
MRI and CT to role out brain damage
dx via clinical manifestations
milestones not met is common, but dont assume this is case when they arnt met
treatment of CP
give muscle relaxers and botox
most common med: Baclofen
speech therapy, OT, PT
laxatives for constipation
maximize coordinate movement, decrease pain, prevent complications
surgeries- G tube, nissen fund, spinal fusions, etc….
educate on importance of immunizations, support family
neural tube defects- spina bifida
meningocele- involves only meninges
myelomenigocele- involves meninges and spinal cord
sac could be intact or ruptured
dx by manifestations. could also be dx in utero with prenatal care
surgery will be done in 12-18 hours for best prognosis. ruptured sac is prioritized due to high infection risk
nursing care at birth for spina bifida
apply sterile dressing soaked in NS
assess/prevent infection
prevent pressure on back. keep them on stomach or side
what are spina bifida babies commonly allergic too
latex
spinal muscular atrophy (SMA)
1 genetic disorder that is lethal in children under 2 years of age
Degenerative disorder causing weakness and atrophy of skeletal muscles
3 types. The worst is wernig hoffman disease
NO CURE. care is supportive: mobility, nutrition, respiratory, developmental
dx by genetic analysis
wernig-hoffman disease (SMA)
begins in utero or by 6 months of age
Baby cannot lift head, has trouble sucking/swallowing, loss of DTR, fasciculations of tongue, weak resp muscles
death occurs due to resp compromose
Duchenne muscular dystrophy (DMD)
Due to absence of the protein dystophin, which causes muscle deterioration over time
typically dx btwn ages 3 and 7
no cure
corticosteroid meds given for clinical trial
these patients can live until they are 30, but will eventually develop cardio and resp issues
DMD s/s
Pelvic weakness, waddle, clumsy, lordosis, calf muscles look tight but its just fatty buildup
gowers maneuver- use hands pushing on thighs to get up because they are so weak
goals for treatment for DMD
maintain function, prevent contractures
resp care
cardiac assessment
family support
blood flow thru heart
vena cava- right atrium- tricuspid valve- right vent- pulmonary valve- pulmonary artery- lungs- pulmonary vein- left atrium- mitral valve- left ventricle- aortic valve- aorta
right side of heart
goes to pulmonary
only needs to pump to lungs so easy going
left side of heart
goes to body
work horse of the heart
L to R shunt heart
Blood from left side going to lungs, but o2 also going to body so sats are fine
pulmonary over load occurs
acryanotic
types of congenital heart diseases
Patent ductus arteriosus
atrial septal defect
ventricular septal defect
tetrolgy of fallot
transposition of the great arteries (TGA)
hypoplastic left heart syndrome (HLHS)
Patent ductus arteriosus (PDA)
L to R shunt
pulmonary overload
sats are normal, lungs are congested
if not treated can lead to CHF
systolic murmur may be heard
how to treat PDA
indomethacin (prostaglandin inhibitor) can be successful in premies and some newborns
coil occlusion in cath lab
surgery may be needed if cant repair in cath lab- a clip on ductus would be needed which would be done through left thoracotomy
Atrial Septal Defect (ASD)
left to right shunt
their is a whole in the septum which divides the atrium of heart
usually asymptomatic. referred to by murmur
exercise intolerance may be seen
unrepaired adults could have atrial dysrhythmias, emboli, etc
ASD treatment
depends on size
could be closed in cath lab
surgical repair- pericardial patch. this is much more invasive and is open chest surgery. Surgical repair typically happens between age 2-5 unless symptomatic
Ventricular Septal Defect (VSD)
Whole in septum between ventricles.
Left to right shunting.
can result in CHF, enlarged LV
size varies. it may close spontaneously if small
THIS IS FREQUENTLY ASSOCIATED WITH OTHER CARDIAC DEFECTS
what septal defect is worse
ventricular because left ventricle is very powerful
VSD treatment
complete surgical repair is procedure of choice. This is almost always the case
could be closed in the cath lab, but this is not common
s/s of pulmonary congestion
tachypnea
may be sweaty due to breathing so fast
cough, wheezing, grunting
resp distress
poor feeding/growing
decreased exercise tolerance
pulmonary edema
R to L shunt
decreased blood flow to the lungs, body not getting good o2
Tetrology of Fallot
4 aspects:
VSD
right ventricular outflow tract obstruction (blocking blood from getting out of RV to get to lungs)
overriding aorta (misplaced)
RV hypertrophy (pumping hard due to obsruction)
when do tet spells occur
crying, feeding
they exhibit blue skin
what to do in a tet spell
***knee to chest position- prevents blood from circulating to lower body, changes pressure in heart
calm child
100% o2
morphine
IV fluids
repair of TET
complete repair:
patch VSD
resect stenosis
enlarge RV
palliative shunt
transportation of great arteries
aorta comes off right ventricle
pulmonary artery comes off left ventricle
death will occur without repair
what to do with TGA- repair
we want PDA to stay open- use prostaglandins.
if it closes prior to finding out about this, we need to get a whole in the heart
surgery will then be needed to place the arteries in the right place
obstructive congenital heart diseases
coarctoin of the aotra
pulmonary stenosis
aortic stenosis
Coarc of the aorta
a kink/blockage of the aorta that interrupts bloodflow to the body. typically on the aorta arch
coarc of aorta s/s
BP will be drastic changes from upper body to lower body because blood flow isn’t good to lower extremities due to coaction, but very high in upper extremities due to high pressure
CHF may occur when PDA closes
treatment of coarc of the aorta
surgical repair- cut out coarction and sew aorta back together
balloon angioplasty may be done
manage HTN
evaluate upper and lower BP after surgery to evaluate if worked
Kawasaki disease
vasculitis of small/medium sized blood vessels (coronary highest risk)
usually seen in children ages 5 and under- unknown causes, noncongenital
s/s of Kawasaki disease
high persistant fever for 5 days
swelling of conjuctiva
inflamed mouth
rash
swollen red hands and feet
cervical lymphaenopathy
Kawasaki treatment
IVIG to reduce incidence of cardiac abnormalities
aspirin
IVF
mouth care
hypopituitarism
deficient secretion of pituitary hormones: GROWTH HORMONES, TSH, corticotropin, gonadotropin
inhibits somatic growth and development of secondary sex characteristics
GH deficiency clinical manifestations
normal growth for the first year, then slowed growth curve after first year
appear overweight due to short size
stim testing
kid will fast, we will give clonidine or glucagon to excrete GH, drawl blood frequently (15-30 mins) to see how much hormone is excreted, if it is not as much as we anticipated, than we know they have a deficiency
diagnosing GH deficiency under age 3
do a skeletal survey (take a Xray of most of body) to decide what bones look like from a developmental standpoint
diagnosing GH deficiency over age 3
we would take a x-ray of their left hand. They are looking at the growth plates. They will compare to bones of other ages.
what are we looking for in a hand xray for GH
advancing bone age (older than chronological age)=less time to help them
or
younger bone age than chronological age = more time we can help them
or
normal bone age for chronological age
Growth Hormone replacement
we cant help if growth plates are closed
GH replacement is done at home and is synthetic. There is not a lot of side effects. Daily injections, done sub cut. It is very successful. It is best to do these GH at night because that is when kids grow.
Changes typically take a few months. Feet grow first. An appetite increase also occurs
therapy is ended when growth rates are less than a inch/year. this is around age 14 for girls and 16 for boys, but could be different depending on bone age
pituitary hyperfunction
excess GH before closure of growth plates
patients may get VERY tall.
weight is typically normal
treatment depends on cause. it is most commonly due to tumor
acromegaly
excess GH after growth plate closure
bones cant grow anymore since plates are closed so it typically causes facial overgrowth
this doesnt occur until late adolecents after growth plates are closed
psychosocial support will be needed
precocious puberty
sexual development before age of 9 in boys and 8 of girls
if its younger than 7 in white girls and 6 in african american girls we need to fix the underlying cause
types of precocious puberty
central (CPP)- most common, caused by gonodotropin
peripheral- caused by any other hormone than gonodotropin
management of precocious puberty
leuprolide (lupron)
med that slows pubertal growth, but does not reverse it.
If girls have started their periods than we dont give this
diabetes mellitus 1
Born with a predisposition of this than a autoimmune process kicks in causing the pancreas to make no insulin
not revirsable
teach carb counting
type II DM
more common in adults but can happen in kids
caused by insulin resistance, revirsable
