Pediatric Nursing Part 1 Flashcards
Preterm
birth btwn 20 - 37 weeks
- responsible for almost 2/3 of infant deaths
- ->5x the risk of SIDS
LBW
< 2500g (2.5kg); diminished prognosis
VLBW
<1500G (1.5kg); poor prognosis
SGA
< 10%ile
responsible for 20-30% of preterm births
PROM
Vertex-heel length of preterm
17-19 inches
Classic Preterm Position
Frog-like
Moro, Tonic neck, Babinski reflexes
present and normal
Next to establishing respirations, most critical element to NB survival
heat regulation
Caloric needs of a NB
120-150 cal/kg/day
Intraventricular Hemorrhage (IVH) Incidence
(Most common in preterm);
increased risk w/ low birth rate
(VLBW=50%)
s/s of IVH
Intraventricular Hemorrhage A. high pitched cry B. signs of increasing intracranial pressure C. irritability and convulsions D. focal cerebral signs E. pressure on vital centers F. anemia G. other unexplained findings
Preterm ABG’s pH
7.3 – 7.4
Preterm ABG’s PCO2
35-45
Preterm ABG’s PO2
50-80
Preterm ABG’s HCO3
19-22
Respiratory Distress Syndrome (RDS) onset
Onset around 2 hours after birth; worsens 48-72 hrs.
Closure of foramen oval occurs
1-2hrs after birth
Permanent closure occurs w/in several months
Effect of O2 on ductus arteriosus
O2–>constriction of ductus arteriosus
Functional closure-Ductus Arteriosus
15h after birth
Fibrosis- 3wks
–>reversal of bld flow through descending aorta
NB BP is lowest
3 hrs after birth
NB BP plateus
BP increases and plateaus 4-6d post birth
BP Full Term NB
60-80/40-50
NB Blood Volume
80-85 ml/Kg
WBC NB
10,000-30,000/ mm3
can carry 20-30% more O2 than maternal blood
Fetal Hmg
Phenomena in which fetal hct levels decrease progressively w/in 1st week
Physiological Anemia Of Infancy
Connects the Umbilical Vein & IVC
Ductus Venosus
Shunts blood into the IVC to prevent blood overload of the fetal liver
Ductus Venosus
Closure forces perfusion of the liver
Ductus Venosus
Opening between the Right and Left Atria in the fetal heart
Foramen Ovale
Shunts blood from the RA to LA, bypassing the fetal lungs
Foramen Ovale
-only a small amt of blood reaches lungs –>nutrition only
Opening between fetal pulmonary artery and aorta
Ductus Arteriosus
causes closure of Ductus Arteriosus
d/t increased systemic press & plum bld flow
Closure of Ductus Venosus –>
liver perfusion
2 Failure of Transitions
PPHN
PDA
PPHN aka
Persistant Pulmonary HTN
Persistance of Fetal Circulation
PDA
Patent Ductus Arteriosus
Ductus Arteriosus doesn’t close
PDA seen more often in
Preterms
S/S PDA
Initially Asymptomatic
Pulmonary Congestion
Respiratory Distress
Decreased Growth
Dx PDA
Murmur
Cardiac Cath- Increased Pulmonary Artery Oxygenation
Tx PDA in Preterm w/ RDS
Tx RDS
RDS resolves –>DA closes
Tx PDA
Indomethicin (IV)
VATS
Indomethicin
Prostaglandin inhibitor
–> DA closure 50-70% of the T
SE of indomethicin
Bleeding
GI
Decreases bone marrow production
VATS
visual assisted thoracoptic sx
–>ligate PDA w/ scope
Known causes of Congenital Heart Defects (CHD)
Infection (1st Trimester) (Mom) Alc Abuse/ Poor Nutrition (Mom) AMA (40+ yo) IDM (Infants of Diabetic Mom) Incidence increases with other defects
CHD Infant Hx (NB)
Poor feeding Tachycardia Decreased Pulses Increased Respiratory Rate Respiratory Distress s/s Cyanosis Decreased Growth Pattern
Cry & Cyanosis Worsens
cardiac
Cry & Cyanosis Improves
Respiratory
NB HR>160 when sleeping–>
Call MD
Measure pressures and oxygenation sats in chambers and vessels
Cardiac Cath
–> Structural defects
Picture inside heart, holes & narrowing
Echo
EKG Aortic Stenosis
Left Ventricular Hypertrophy
Cath- Aortic Stenosis
delayed emptying
increased L ventricle pressure
Tx Aortic Stenosis
Valve Replacement
Coarctation of Aorta
Narrowing of segment of aorta
May be pre/ post ductal
Relative to Ductus Arteriosus
S/S of Pre-ductal Coarctation of Aorta
Bounding Pulses, HA, Nose bleeds
S/S of Post-ductal Coarctation of Aorta
decreased pulses, decreased lower extremity Pulse Ox
CXR- NB
Rib Notching
LV Failure
Coarctation of Aorta
Coarctation of Aorta Cath
Increased LV Pressure
Tx Coarctation of Aorta
Surgery- Graphing
Hole between the ventricles
–>blood shunts from LV to RV–> Increased Pulmonary Circulation
VSD
VSD
Ventral Septal Defect
–>RV failure –> LV failure–> Heart Failure
Increased Pressure in Pulmonary Artery (usually asc w/ VSD)–>
Sx NOW!!!!!
Dx VSD
Cath: Increased RV O2 & Pressure
High Degree of Shunting w/ VSD
Increased fluid in lungs
URI
Pneumonia
Tx VSD
60% Self-resolving
Monitor for Pulmonary HTN
Synthetic patch/ Tent
Atrial Septal Defect
hole btwn RA& LA
Not self-resolving (Sx/Tenting)
s/s=respiratory (Volume overload)
Contributing Factors of Transient Tachypnea of the Newborn (TTNB)
C-Section
Precipitous delivery
“artificial lung’
ECMO
Last resort- Risk for bleeds, requires anticoagulant therapy
When administering surfactant, the nurse must
Turn and rotate baby–> cover lung
Risk Asc w/ Mechanical Ventilation
pulmonary air leaks/ pneumothorax
Drawback of PEEP
can cause vascular shunting in the pulmonary beds leading to persistent pulmonary hypertension and worsening RDS
baby that requires O2 at 36 wks post conception
Broncho-Pulmonary Dysplasia (BPD)
CANNOT WEIN OFF O2
Broncho-Pulmonary Dysplasia (BPD)
aka chronic lung disease; 5-50% of babies with RDS ventilation therapy
Broncho-Pulmonary Dysplasia (BPD)
Caused by therapies to treat RDS
Broncho-Pulmonary Dysplasia (BPD)
Chest Xray –>cardiomegaly, lung hyperinflation, and infiltrates
Noted difficulty weaning/ increased ventilator requirements
Broncho-Pulmonary Dysplasia (BPD)
decreased lung compliance & pulmonary function 2ndary to fibrosis, atelectasis, increased pulmonary resistance, & over distention of the lungs
Broncho-Pulmonary Dysplasia (BPD)
Dexamethasone
decrease bronchospasm, edema, & inflammation of pulmonary tissue →improved gas exchange
*BPD tx
BPD Prognosis
vary; prone to respiratory illnesses w/in 1st 2yrs
ROP
Retinopathy of the Premature
Abnormal growth of blood vessels in the baby’s eye
ROP
Incidence of ROP
weight below 900g – 90% chance
<30 wks GA*, w/ unstable clinical course
born premature→ low oxygen→ vasoconstriction→ baby gets better, O2 levels return and the blood vessels begin proliferate → too rapid growth→ abnormal growth–>Scar –>contraction → pressure on retina→ potential retinal detachment
ROP
Tx ROP
Once on PO food –>Vitamin E
Maintain PaO2 level 60-80
Laser, cryotherapy, Bevacizumab injections
acute inflammatory disease of the bowel
preterm/ babies who suffered asphyxia
(NEC)
(NEC)
Necrotizing Enterocolitis
Three factors–>development of NEC
- intestinal ischemia
- colonization by pathologic bacteria
- substrate w/in intestinal lumen (formula w/in intestinal lumen)
- abd distention
- increase in gastric residuals
- Bloody stools (+ hemocult); gross blood is rare
NEC
Onset NEC
4-7 after initiation of feedings
X-ray NEC
intestines are sausage shaped; bubble appearance, gas pockets
Tx NEC
- Make NPO
- NG Tube suction
- Iv antibiotics
- TPN feedings
When reinitiating food (NEC)
Reinitiate → fresh breast milk best, then frozen breast milk
Bleeding of IVH originates in
germinal matrix (where blood vessels form) d/t sudden change in cerebral blood flow (ie during vaginal delivery) & also occurs with asphyxia
Grades (4) of bleeding (IVH) based in
bleeding—NOT prognosis
IVH typically begins
SEE 7-10DAYS AFTER
Bulging fontanels = Late Sign
IVH
change in color
V/S
temperature instability
respiration impacts (vague); Bulging fontanels (LATE SIGN)
IVH
Dx IVH
U/S (7-10d unless other vague s/s)
CT Scan ($$)
LP/ subdural tap–>blood
Tx: IVH
PREVENTION***
Relief of ICP-(intra-ventricular tap (may be serial) <damaging than shunt
May resolve spontaneously
Level I – Nursery
Sm. Hospitals refer high risk pts
Level II - Nursery
Specialized care: kent
Level III - Nursery
Highest level of care: Christina/ AI DuPont
2 predominant types of cellular characteristics r/t SGA
Symmetrical (Hypoplasia)
Asymmetrical (late IUGR)
Asymmetrical (late IUGR)
normal # of cells
reduced CP
Late in pregnancy
Symmetrical (Hypoplasia)-
deficient # of cells
norm CP
of early growth deficit
Sm organs/ sm organs wt
Maternal Factors –> SGA
HTN (chronic or preg) Heart/ lung disease Drug use Malnutrition/ Low socioeconomic Anemia Living at high altitudes
Placental Factors–>SGA
Placental insufficient
Abnormal cord insertion
Single umbilical artery
Fetal Factors–>SGA
Intrauterine infection
Multiple gestation
Congenital deformities
Most Common Fetal Factor –>SGA
Intrauterine infection
Sutures: widely spaced d/t inadequate bone growth
Fontanels: large
SGA
Leading cause of death SGA
Asphyxia
Pregnant nurses should not care for this baby
Immunologic problems
Dx SGA
Decreased maternal weight
Fundal Ht Less than expected (McDonald’s Rule)
Both Decreased–>U/S
Common Metabolic Problems of SGA
Hypoglycemia
Hypocalcemia
Hyperbilirubinemia
Type II Respiratory Distress Syndrome (Retained lung fluid)
TTNB
Factors Contributing to TTNB
C/Section
Breech birth
Factors Contributing to TTNB
C/Section
Breech birth
maternal history (diabetes→ effects synthesis of phospholipids)
Easily oxygenate
Respiratory failure is rare
Usually Term
Transient tachypnea of Newborn
DO NOT use a bag and mask
Must immediately intubated
Diaphragmatic hernia:
Diaphragmatic hernia: (POSITION)
Place on effected side→ upper lung expand fully
Diaphragmatic hernia: (POSITION)
Place on effected side→ upper lung expand fully
Similar to RDS
resolves by ~24h; self-limiting; no risk of reoccurrence
TTNB
Barrel shaped chest Tachypnea Respiratory distress Cyanosis High oxygen concentration to relieve cyanosis
Meconium Aspiration Syndrome (MAS)
GA* MAS
Term, post-term, SGA
Contributing Factors MAS
Intrauterine stress
IUGR
Postmaturity
Breech delivery
complications d/t MAS
Pneumothorax
Pulmonary air leaks
Hypoxic damage to vital organs (brain, kidneys, liver)
CXR–>Over-aeration
Air trapping
MAS
CXR:
Ground glass appearance
Under-aeration
RDS
MAS Clinical Course
Respiratory support
Mortality high if develop severe respiratory distress
Clinical Course RDS
Progressive hypoxia & hypercapnea
Admin surfactant
Respiratory support
Contributing factors Pneumonia
Prematurity MAS PROM Maternal Fever or UTI Prolonged labor
GA RDS
Pre-term, IDM
Complications of pneumonia
DIC
Shock
Hypoperfusion
Clinical Picture
Latent pd then acute onset of RDS
Apnea early on
Increasing need for O2
CXR: Similar to RDS
Patchy infiltrates
Pneumonia
Causative Organisms Pneumonia
Pneumococcus
Staph pneumonia
Group B strep
Cause of Hypoglycemia SGA
No stores (Symmetrical) or used all stores (asymmetrical) Decreased Supply of Enzymes
Cause of Hypoglycemia Preterm
Sm glycogen stores in the liver
Liver = immature
Caloric Needs SGA
130-150 cal/kg/24h
Normal or Larger
Position Bili Lights
The fluorescent “bili lights” should be positioned 18 to 20 inches from the infant
Accounts for 50% of all deaths in the 1st yr of life
CHD
Echo–>holes & narrowing
CHD
Hyperoxia test
cry test baseline Pulse Ox/abgs 100% O2/2MINS pULSE OX/ABGS respiratory problems stats increase
Loud Washing-Machine Murmur
VSD