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Exam 2

Terms in this set (258)

primitive reflexes
Moro
Babinski
root
suck
palmar/plantar
tonic neck/fencing
step
protective reflexes
neck righting
parachute: side, forward, & backward
neck righting
keeping head upright when tilted
parachuting
extending arm out to brace fall
alertness
wakeful state
can respond to stimuli
cognition
ability to process stimuli & have verbal or motor response
earliest indicator of improving or deteriorating neurologic status
LOC change
LOC states
full consciousness
confusion
obtunded
stupor
coma
confusion
disorientation
alert but responds inappropriately
obtunded
limited responses to environment
falls asleep unless stimulated
stupor
only responds to vigorous stimulation
coma
cannot be aroused, even w/ painful stimuli
pediatric GCS scores
15 = normal
7 or below = coma
3 = brain death (lowest possible score)
craniosynostosis
premature closure of cranial sutures
head & neck assessments w/ movement should be avoided in?
pts w/ trauma or suspected cervical injury
neck ROM alteration can indicate?
CNS infection
age to obtain head circumference
<3 yr
doll's eye maneuver
turning head
eyes move other way
cranial nerve assessment
sunset eyes can indicate?
↑ ICP
if a pt has fixed & dilated pupils, what do you do?
notify MD immediately
decorticate
rigid flexion
toward body
decerebrate
rigid extension
away from body
ICP
force exerted by:
brain tissue
CSF
blood
cerebral perfusion pressure
pressure needed to ensure adequate O2 & nutrients get delivered t obrain
↑ ICP reduces what?
brain arterial blood flow (↓ O2 & nutrients)
early ↑ ICP signs
HA
diplopia
vomit
dizzy
sunset eyes
small LOC change
sluggish pupils
unequal pupils
small ↓ P & R
diplopia
double vision
additional infant early ↑ ICP signs
bulging/tense fontanel
irritable
wide sutures
↑ head circ
dilated scalp veins
high pitch cry
late ↑ ICP signs
↓ LOC
sz
D&D posture
fixed & dilated pupils

Cushing triad:
↓ HR
Cheyne-Stokes resp
wide pulse pressure
posterior fontanels close at
2-3 mo
anterior fontanel close at
12-18 mo
Electroencephalogram (EEG)
records brain's electrical activity:
brain function
seizures
seizures are associated with?
CNS structure defects
brain injury
infection
toxins
brain tumor
electrolyte imbalance
epilepsy
chronic disorder
recurrent unprovoked sz
2ndary to brain abnormality
refractory/intractable
sz despite 2+ med trials
status epilepticus
prolonged continuous 15 min sz
or
intermittent sz 15 min w/o full recovery between sz
aura
start of sz
symptoms person may feel at beginning of sz
automatism
automatic movements:
licking lips
rubbing hands
walking
running
epilepsy based on 3 features
where sz begins
awareness level during sz
other sz features
why is where sz begins important?
onset affects sz med choice, Sx possibilities, outlook, & causes
seizure affecting 1 hemisphere
focal sz
seizure affecting both hemispheres
generalized sz
focal sz classifications
focal aware
focal impaired awareness
focal motor
focal non-motor
focal to bilateral tonic-clonic
focal to bilateral tonic-clonic sz
sz starts on 1 side of brain
crosses corpus collasum
both sides have tonic-clonic movements
generalized sz classifications
generalized motor
generalized non-motor
atonic/drop seizure
loss of muscle tone
head drop
fall risk
tonic seizure
only stiffening
remain conscious
generalized seizure pts have?
no memory of sz

may have:
cyanosis
↑ saliva (not swallowing)
lose bladder/bowel control
epilepsy 4 Tx options
meds
diet
epileptic Sx
vagus nerve stim (VNS)
epilepsy Tx of choice
monotherapy
antiepileptic med SE
rash
ataxia
vision change
mood/behavior change
sleepiness
keto diet
↑ fat
↓ carb
adequate protein
need supplements
need dietician
sluggish or hypoglycemic at diet start

reduce 50% of sz in 50% of pts
modified Atkins diet
↑ fat
↑ protein
↓ carb
less restrictive, similar results to keto
VNS
more effective over time
dysphonia, throat/neck pain, & cough can occur during stimulation
epileptic Sx who it is used in, & types
pts w/ refractory focal sz

focal resection
functional hemispheretomy
corpus callostomy
febrile sz
not caused by CNS
9 mo - 5 yr
simple: once in 24 hr, no CNS infection
complex: recur in 24 hr, ↑ risk to develop epilepsy
neonatal sz
AKA neonatal compulsions
occur in first 28 days
usually subtle signs that are overlooked
seizure precautions
bag & mask at bed
wall suction & yankauer
padded rails
side rails up when asleep & resting
during a sz, the nurse should
ease child to floor
side lying position
suction mouth
document observations
sz observation documentation
time sz w/ clock
aura
motor affects
LOC changes
postictal state
postictal state
behavior after sz
status epilepticus management
CAB
check glucose
O2
IV lorazepam (Ativan)
rectal diazepam
IM/nose/buccal midazolam
preferred status epilepticus med, & why
IV lorazepam (Ativan)
2-5 min onset
12+ hr half life
meningitis
meninges inflammation
meninges
lining surrounding brain & spinal cord
bacterial vs viral (aseptic) meningitis
bacterial more serious
viral self limiting 3-10 days
encephalitis
acute brain inflammation
Reye's Syndrome
acute encephalopathy (cerebral dysfunction) caused by toxic, inflammatory, or anoxic injurt

aspirin
bacterial meningitis risk factors
recent sinus or ear infection
VP shunt
cochlear implant
skull fracture
neurosurgery
immunosuppression
bacterial meningitis Dx test
CSF culture & sensitivity
obtained via lumbar puncture
bacterial meningitis s/s
nuchal rigidity
Kernig sign (hamstring)
Brudzinski (head flex)
opisthotonic position
infant calm laying, not held
infant poor feeding
infant weak cry
photophobia
HA
vomit
sz
meningitis nursing interventions
droplet iso 24 hr
specimen collection
IV fluids
Abx
antipyretics
anti-inflammatory
supportive therapy
calm/quiet environment
encephalitis s/s
fever
HA
irritability
bulging fontanel
flaccid or spastic paralysis
altered mental status
meningial irritation s/s
encephalitis management
prevent cerebral edema
encephalitis risk factors
recent travel
outdoor activities
animal contact
Reye's Syndrome s/s
fever
very impaired consciousness
disordered hepatic function
Reye's Syndrome has?
elevated liver enzymes & serum ammonia
Reye's Syndrome nursing management focus
respiratory & neurologic status
hydrocephalus
excess CSF in ventricles & subarachnoid
hydrocephalus is caused by?
communicating: impaired CSF absorption in subarachnoid
non-communicating: CSF flow obstruction in ventricles, CSF doesn't circulate around spinal cord & subarachnoid
hydrocephalus therapeutic management
obstruction removal
ventriculoperitoneal VP shunt
atrioventricular AV shunt

acetazolamide/Diamox
furosemide/Lasix
shunt problems
infection
malfunction (includes obstruction)
shunt infection Tx
10-14 day abx
EVD place
shunt pre-op management
do not stretch or strain neck muscles (supporting enlarged head)
small feeding/frequent burping (prevent vomit)
shunt post-op management
flat position
gradual elevation over 1-2 days
EVD & thing to know
external ventricular drain
replace CSF loss equally w/ 0.9% NS
neurogenic bladder
impaired bladder control due to brain or nerve issue
spastic neurogenic bladder
hyper-reflexive
frequent urine release
incomplete emptying
hypotonic neurogenic bladder
flaccid, weak, & stretched out
hold a lot of urine
continuous dribbling
both types of neurogenic bladder can?
cause urinary stasis & retention

UTI & bladder reflux risk
neural tube defect
serious birth defect
neural tube fails to close
most common CNS defect
spina bifida
spina bifida occulta
vertebrae incomplete closure
lumbosacral area
hair patch
no protrustion
spina bifida cystica
visible defect
external saclike protrustion
meningocele
sac encases CSF & meninges
no neural elements
myelomeningocele
sac encases CSF, meninges, & nerves
spina bifida goals & Tx
prevent infection
minimize further function loss

Sx closure ASAP
in utero fetal Sx on myelomeningocele
latex allergy is very common in?
spina bifida pts
cerebral palsy
abnormal motor pattern & postures
cerebral palsy cause
nonprogressive, abnormal brain function
CP common neurologic comorbidities
sz
hydrocephalus
CP primary concern & Tx
spasticity
oral or intrathecal baclofen to decrease tone
CP nursing management
promote mobility
maintain skin integrity
promote nutrition
most common head injury
concussion
concussion
mild TBI
disruption or malfunction of brain electrical activities
concussion s/s
HA
noise/light sensitive
dazed
vision probs
fatigue
N/V
LOC
amnesia of event
distractibility
irritability
difficulty concentrating
concussion Dx
CT & MRI do not show anything
linear skull fracture
simple break
relatively straight line
most common skull Fx
depressed skull fracture
bone locally broken & pushed inward
causes brain pressure
Sx often req
compound skull fracture
skin lacteration & bone splintering
can be linear or depressed
contusion
visible tearing of cerebral tissue
contusion s/s
altered LOC
intracranial hematoma
epidural hematoma
blood accumulation in space between skull & dura matter
subdural hematoma
blood accumulation in space between dura & anarachnoid membrane
more common than epidural
tentorial herniation
↑ ICP causes cerebrum to herniate through tentorium cerebri
subdural hematoma s/s
↑ ICP s/s
HA
confusion
↑ head circumference
shaken baby syndrome often causes?
subdural hematoma
head injury nursing management
CSF drainage (EVD)
osmotic diuretic Mannitol
HOB elevated 15-30
what do you avoid in head injury pts?
turning side to side
causes jugular compression
Mannitol
osmotic diuretic
IV
30-60 min onset
1 hr peak
6 hr duration

rapidly excreted by kidneys
Mannitol SE
dizzy
HA
hypotension
rash
nausea
anorexia
dry mouth
thirst
diuresis
F&E imbalances
musculoskeletal AHRQ pediatric quality indicator
pressure ulcer rate
preventable
50% related to equipment & devices
pressure ulcer best practice
1. assess skin at admission & daily
2. PU risk assess at admission & daily
3. reposition q 1-2 hr
4. daily rounds: nutrition, hydration, & need for pressure distribution assessments
pressure ulcers do not?
blanch
prolonged device use ↑ the risk of?
pressure ulcers
cold therapy
20-30 min on
off 1 hr
repeat

discontinue if numbness
towel to prevent thermal injury
brace/orthotic
support body weight
correct/prevent deformities
control involuntary movements
internal fixation
stabilizes fractured bony parts by direct fixation to one another w/ hardware
external fixation
holding fractured fragments together with a compression device attached to pins outside skin
traction
use of pulling forces (weights/pulleys) to treat muscle & skeletal disorders
pin care
q shift
weekly after first 48-72 hr
chlorhex 2mg/ml in alcohol
cleaning cast
clean skin just under cast & between digits w/ cotton swabs or alcohol
no lotion
no powder
surgery AHRQ quality indicator
postoperative sepsis
most common clubfoot
talipes equinavarus
talipes equinavarus Tx
serial casting
new cast q 1-2 wks
8-12 wk duration
developmental dysplasia of hip
abnormalities including dislocation, subluxation, & dysplasia
femoral head & acetabulum have abnormal relationship
usually unilateral
75% L hip
girls > boys
DDH s/s
unequal gluteal folds
limited hip abduction
apparent femur shortening
+ Ortolani sign
+ Barlow sign
Ortolani sign
abducting thighs makes clunk noise
DDH
Barlow sign
adducting thighs makes clunk noise
DDH
DDH standard Tx
Pavlik Harness
3-6 mo
worn 24/7
prevents hip extension & adduction
DDH Tx if standard fails or child too old
traction then spica cast
oseteogenic imperfecta
brittle bone disease
inherited, connective tissue disorder
low bone mass
↑ bone fragility
joint hypermobility
collagen type 1 gene defect
osteogenic imperfecta primarily affects? can also affect?
bones

teeth, ligaments, & sclera
osteogenic imperfecta s/s
osteoporosis
multiple fractures
thin, soft skin
short
blue sclera
discolored teeth
weak muscles
altered joint flexibility
osteogenesis imperfecta Tx
cast/brace/splint
PT muscle strength
hearing/dental exam
↑ Vit C, D, & calcium (needed for collagen)
what pts need special diaper changes? explain
osteogenesis imperfecta pts
don't lift by ankles
muscular dystrophy
X linked recessive
muscle fiber degeneration
muscle wasting
onset 3-7 yr
most common muscular dystrophy
Duchenne's (pseudohypertrophic)
MD s/s
weak
clumsy, fall
muscle wasting
pseudohypertorphy
lordosis
Gower sign
MD pts lose what abilities at what ages?
walk by 9 yr
hand use by 16 yr
death by 20-25 yr
what slows MD progression?
prednisone
MD Dx
family Hx
↑ creatine kinase
↑ aspartate aminotransferase (AST)
electromyogram (EMG)
muscle biopsy
MD management
prevent obesity
release contractures Sx
trach & vent
passive ROM
brace/wheelchair/PT
growth plate AKA
epiphyseal plate
weakest part of bone
epiphyseal (growth) plate
fracture at epiphyseal (growth) plate
Salter-Harris fracture
most common childhood fractures
forearm & wrist
birth trauma common fractures
midclavicular
humerus
femur
suspicious fractures in children
spiral (twisting motion)
femur
rib
humerus
at what age is having a fracture likely a sign of abuse?
before walking
what 2 common things ↑ fracture risk?
soda drinking
screen time
is complete or incomplete fracture more common in peds?
incomplete, because ossification hasn't finished
close fracture AKA
simple fracture
open fracture AKA
compound fracture
what fracture often needs external fixation?
comminuted fracture
many small bone pieces
what reduces risk of compartment syndrome in fractures?
splint for 1-2 days to allow swelling to occur
a nurse can't do which 2 fracture things at the same time?
hold pt during bone alignment, & monitor pt
reduction
realigns displaced ends of bone, or removes fragments

closed: manual manipulation or traction
open: Sx alignment
immobilization
allows healing to occur by allowing new bone growth
casting
traction
splinting
blood flow reduction to affected area due to inflammation
compartment syndrome
compartment syndrome s/s
pallor
puslelessness
pain
paresthesia
paralysis
malunion
undesired healing alignment or delayed healing
retardation of bone growth is caused by?
Salter-Harris fracture
fracture post op neurovascular assessment schedule
every time VS are taken
then q 2 hr for 24 hr
slipped capital femoral epiphysis (SCFE)
fem head displaced from fem neck
unknown cause
SCFE risk factors
obesity
recent growth spurt
hypothyroidism
hypogonadism
SCFE s/s
pain in hip, knee, groin, or medial thigh
no hip motion
stable vs unstable SCFE
stable: can walk
unstable: can't walk
SCFE categories
acute: <3 wk
chronic: >3 wk
acute-on-chronic: additional slippage in pt w/ chronic
SCFE Tx
epiphysis fixation w/ screws or pins
Legg Calve Perthes Disease
self limiting avascular necrosis of femoral head
uni or bilateral
femoral ephiphysis blood supply interruption
Legg Calve Perthes Disease may be preceded by?
mild traumatic injury or breech birth
Legg Calve Perthes Disease stages
1 necrosis
2 revascularization
3 bone healing
4 remodeling
Stage 1: necrosis
avascular 3-6 mo
asymptomatic
Stage 2: revascularization
mild pain
limp relieved by rest
favors affected hip
xray shows new bone deposits
necrosed bone is reabsorbed
Stage 3: bone healing
reossification
↓ pain
Stage 4: remodeling
disease process over
no pain
↑ joint function
Legg Calve Perthes Disease Tx
keep fem head in socket until ossification completes

initial Tx: traction
Petrie casting
soft tissue release Sx
Toronto & Scottish Rite bracing
Scoliosis
lateral S or C spine curvature
+/- spine & ribs rotational deformity
what spine curvature is considered abnormal?
>10°
Scoliosis curves can be?
congenital
idiopathic
neuromuscular
neuromuscular scoliosis
pt w/ condition that impairs control of spine supporting muscles
idiopathic scoliosis
no known cause
R thoracic & L lumbar deformity most common
rib hump
asymmetric vertebral column
mild scoliosis & Tx
10-20°
exercises
moderate scoliosis & Tx
20-40°
Boston brace 23 hr/day
severe scoliosis & Tx
>40°
spinal fusion Sx
antero-posterior plastic shell for several months post Sx
spinal fusion pt education
cannot bend/twist torso
teach ADL w/ restrictive body mechanics
activity restrictions for 6 mo
what activities can a spinal fusion pt do during the 6 mo of activity restrictions?
walk
gentle swimming
juvenile idiopathic arthritis (JIA) diagnosis requirements
inflammation of 1+ joints
lasts 6+ wks
Dx prior to 16 yr
JIA causes what?
↓ mobility
pain
swelling
JIA affects what structures?
joints
surrounding tissues
heart
lungs
liver
eyes (uveitis/middle layer)
JIA patho
synovium chronic inflammation
joint effusion, eventual erosion
joint cartilage fibrosis
JIA types
oligoarthritis (1-4 joints)
polyarthritis (5+ joints)
systemic arthritis (high fever, swollen, painful joints, & rash. affects internal organs & joints)
most common type of JIA
oligoarthritis
JIA s/s
fever
rash
lymphadenopathy
splenomegaly
hepatomegaly
slow growth
uneven extremities
pain
stiffness
loss of motion
swelling
JIA labs
anemia
leukocytosis
↑ Rheumatoid factor
↑ RBC sediment rate
↑ C reactive protein
↑ antinuclear antibody
JIA Tx
NSAIDs
DMARDs
bDMARDs
steroids
DMARDs
disease-modifying antirheumatic drugs
methotrexate
sulfasalazine
prevent JIA disease progression
bDMARDs
biologic disease-modifying antirheumatic drugs
etanercept
infliximab
JIA steroids
pridnisone
methylprednisolone
not used long term
Guillain-Barre syndrome
AKA infectious polyneuritis
acute inflammatory peripheral neuropathy
rapid onset of symmetric motor weakness
progressive ascending flaccid paralysis
demyelinization of affected neurons
Guillain-Barre s/s
infants:
hypotonia
irritable
feeding difficulties
resp distress

older kids:
numbness
pain
paresthesia
↓ DTR
Guillain-Barre lab
CSF protein twice normal high level
GBS therapy
IVIG 2-5 days
pain management
PT
dentinogenesis imperfecta
hereditary
incomplete/improper dentin development
most common peds metabolic disease
DM
T1DM
autoimmune destruction of pancreas islet 𝛃 cells that produce insulin
T2DM
insulin resistance
when are T1DM pts symptomatic?
after 90% of islet cells are destroyed
T1DM s/s
PPP
weight loss
DKA at Dx time
fatigue Hx
enuresis (bed wetting) after toilet trained
T2DM s/s
obesity
↑ waist circ
Dx during puberty onset
blurred vision
fatigue Hx
acanthosis nigricans
T2DM risk factors
obesity
high calorie foods
little exercise
↑ BMI parent
poverty
T1DM Dx
classic symptoms & glucose level
A1C >6.5%
islet cell antibodies
low C-peptide levels
DM glucose Dx levels
random 200+
2 hr GTT 200+
fasting 126+
T2DM Dx
random 200+
fasting 126+
HBA1C >6.5%
↑ triglycerides
↑ LDL
↑ BP
if child has severe hyperglycemia or DKA, what is given?
insulin, to gain glycemic control
oral glycemic drug requirement
must have some remaining pancreatic 𝛃 cell function
(T2DM only)
DM most serious SE
hypoglycemia
T2DM Tx of choice
metformin/glucophage
A1C <8.5%
4 therapies for T1DM
glucose monitoring
basal-bolus regimen
nutrition
exercise
normal child blood glucose level
70-110 mg/dl
what can toddler/preschooler w/ DM participate in?
choose finger
clean finger
pick injection spot
hold still
what can school age w/ DM participate in?
does finger poke
does accucheck
pushes syringe plunger
does ketone test

(does not inject self, only pushes plunger)
what can adolescent w/ DM participate in?
record BG
calculate dose
draws up insulin
injects self
pick appropriate foods
knows when to test for ketones
basal-bolus regimen
basal: long acting 1x/day
bolus: fast acting w/ food or to correct high BG
insulin pump
continuous SQ
fast acting for both basall & bolus dosing
fast/rapid insulin
aspart (Novolog)
lispro (Humalog)
glulisine (Apidra)
regular/short insulin
Humulin R
Novolin R
intermediate insulin
NPH
long insulin
detemir (Levemir)
glargine (Lantus)
when is insulin given?
fast acting: right before eating
other: 30 min prior to eating

infants & toddlers after eating because you never know how much they will eat
1 CHO = ?
15g of CHO
what do children w/ DM need in their diet?
high fiber
no sugary drinks (unless hypoglycemia Tx)
how does exercise impact DM?
↑ glucose control
↓ cardiovascular risks
weight management
exercise glucose control
check BG before & after
eat 15-30g of CHO for every hour of exercise before exercising
DM sick day rules
BG q 2-3 hr
ketones q4 hr
insulin dose may ↑
notify MD if dehydrated
does illness cause hypo or hyperglycemia?
either
does stress cause hypo or hyperglycemia?
either
hypoglycemia s/s
tremors
nervous
sweating
HA
confused
behavior changes
palpitations
irritable
can't concentrate
unconscious hypoglycemia Tx
glucagon injection or glucose paste on gums
hyperglycemia s/s
dehydration
weak
fatigue
HA
abd pain
N/V
blurred vision
shock
hyperglycemia management
↑ fluids
additional insulin
monitor for DKA
DKA s/s
polyuria
polydipsia
acetone breath
Kussmaul resp
hyperglycemia
glycosuria
ketonuria
hypotension
LOC change
anorexia
weight loss
abd pain
N/V
tachycardia
dehydration s/s
DKA blood values
glucose >250 mg/dL
serum ketones
acidosis
DKA management
rehydration isotonic fluid bolus
IV insulin 0.1 unit/kg/hr
frequent BG check
frequent ketonuria check
cardiac monitoring
why is DKA pt on cardiac monitoring?
pt is at risk for hypokalemia (arrhythmias)
DKA pt's blood glucose should not fall faster than?
100 mg/dl/hr
fast correction of hyperglycemia can cause?
cerebral edema
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