HIGH RISK NEWBORN
Lecture 13
LEVELS OF NICU
Level I
 Basic neonatal care; minimum requirement for a
facility that provides inpatient maternity care.
 Able to perform neonatal resuscitation.
 Evaluate healthy newborns; provide standard care.
 Stabilize newborns til transfer to intensive care
Level II AKA Special Care Nurseries
 Basic care to moderately ill infants; ~ 32 – 42 wks.
 Step down from level III NICU; infants recover
Level III
 Newborns <32 wks, critical illness, needing surgical
intervention. RN’s - intensive training; ~ 6-8 mos.
National studies show:
 30% survival rate for 23 wk preemies.
 52 % for 24 wks.
 76 % for 25 wks.
 African American women: twice as likely to
deliver early, but babies more likely to survive.
High risk newborns in NICU:
 Use cardiac & apnea monitors; radiant warmers; O2 sat,
VS, BP monitoring.
 Assessed q 1-2 hrs. or continuously
 ^ risk of infections: GBS, septicemia, thrush
 Moms encouraged to visit NICU daily
 Skin care to prevent breakdown.
 Good hand washing - parents/staff.
RDS – Pre-Term
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Resp.distress syndrome: aka “hyaline membrane disease”
In preemie, insufficient surfactant in alveoli causing lungs to
collapse; not enough O2.
Most common disorder of preemies.
^ resistance causes fibrous tissue in bronchioles & alveoli
poor O2/CO2 exchange.
Self-limiting; ~ 72-96 hrs in most late preterm or full term.
VLBW (ELBW) - RDS can persist days/weeks. D/T immature
lungs, non-compliance, and low surfactant levels.
Causes of RDS - Term
In term infant:
– Sepsis [GBS]
– Persistent Pulmonary Hypertension of
Newborn (PPHN) – ductus arteriosus does
not close.
– Meconium aspiration r/t oligo,
uteroplacental insufficiency, & fetal distress
– Infants of diabetic moms.
– May need resuscitation @ birth.
In Pre-term infant: Immature lungs,
non-compliance, & low surfactant levels.
S/S of RDS (In PRETERM)
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Retractions - drawing back of chest muscles with breathing.
Infant works harder at lung expansion.
SOB and expiratory grunting –self-induced by infant - maintains ^
pressure in lungs by causing expiratory braking using vocal cords
(glottis partially closes increasing alveolar surface tension)
Nasal flaring; TTN [transient tachypnea = ^ 60 R/min.]
Management:
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ABG’s, O2 sats, CBC, bl.cx
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Skin/mouth care
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Suctioning (prn)
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Support for family
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Adequate fluids and electrolytes
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Replace surfactant [Curasurf man made; ET tube]
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O2 therapy [Oxyhood; CPAP; ventilator] [CPAP= cont.+ airway
pressure] helps keep small air sacs from collapsing; suction prn
Terms
AGA - Approp. for gestational age [5.7 – 9.1]
SGA - Small for gestational age. ~ < 5.7 lbs.
LGA - Large for gestational age. ~ > 9.1 lbs.
SGA: weight < 10th percentile compared to others of
same gestational age. [38 wk. weighs 5 lbs.]
 Aka IUGR aka Failure to thrive.
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Most common cause: placental anomaly; placenta not receiving
sufficient nutrition from uterine arteries or placenta.
Severe DM, pre-eclampsia, poor nutrition, smoking,
cocaine. Decreases blood flow to placenta.
Fundal height lower than expected for gest.age.
Bio Physical Profile: assesses placental function.
If infant not thriving in utero, will do C/S; weigh
pros/cons.
SGA infant: wasted look, dull hair, small liver [^^ bili’s],
poor skin turgor, low glucose, low temp.
Mature neuro responses, sole creases, + ear cartilage.
Lab findings: ^ HCT {low plasma levels} & ^ RBC
{polycythemia} Causes thicker blood making heart work
harder; ^ chance of thrombosis. Prolonged acrocyanosis.
Manage: ^ fluids & freq.feedings.
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LGA: aka macrosomic infant. > 90% percentile.
Appears healthy; may be gestationally immature
{immature neuro responses & respiratory effort}.
Assess: larger than average uterine size for gestational age
Do sono to estimate size. Check dates.
C/S for CPD or shoulder dystocia.
Causes: GDM, omphalocele, transposition great vessels.
Appearance: possible fx clavicles; facial/head
bruising, facial/neck palsy, caput, cephalohematoma.
Observe: hypoglycemia, polycythemia, irregular
HR, cyanosis [in transposition]
Preterm Infant
90% term births [full-term] & 11% preterm [< 37 wks]
Calculated by gestational age; not weight.
 Maturity determined by physical findings: sole creases,
skull firmness, ear cartilage, neurologic findings &
pregnancy dates.
 SGA & Pre-terms: 2 different causes w. diff. problems.
 Preterm: fetus has been doing well in utero but trigger
initiates labor & infant is born early.
 Problems: poor thermoregulation, hypoglycemia,
intracranial bleed, RDS, NEC, immature kidney function,
infection.
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80-90% of infant mortality in 1st yr. life esp. VLBW infants
Risk Factors of Preterm Delivery
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Women of middle/upper socioeconomic: ~ 4-8%
Lower socioeconomic levels: ~ 10-20%
Inadequate nutrition; lack of money & knowledge about
good nutrition; lack of support.
American Academy of Pediatrics: “live-born infant
weighing 2500 g. or less”.
World Health Organization (WHO) & American College of
Obstetricians and Gynecologists (ACOG) – both define it
as infant born prior to 37 wks.
Appearance of Preterm Infant
24-36 weeks
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Small, underdeveloped, head disproportionately large;
skin thin & ruddy [little subcut. fat]; veins noticeable;
prolonged acrocyanosis. vernix depends on gest.age.
< 24 wks.vernix not formed.
None/few sole creases.
Ear cartilage immature; no quick rebound of pinna.
Extensive lanugo.
Suck/swallow absent, weak cry < 33 wks. Ballard
Gestational scale to estimate age.
Infection – decreased maternal antibodies
Skin fragile; limit alcohol; rinse with water. Adhesives
cause skin tearing. Use skin barriers to protect skin.
Tegaderm tape. Handwashing a must !
**Former Extreme Premature Teen**
•13 year old female
•Ex-24 week preemie
•BPD, trach/vent
•15 mos in NICU
•G-tube 3 yrs
•Decannulated at age 4
•Intensive learning support
•Eating age-typical diet
•Mild articulation errors
Thermoregulation:
risk for hypothermia r/t large surface in relation to
body weight.
Limited stores of brown fat
Decreased or absent reflex control of skin capillaries
Immature temperature regulation in brain
Kangaroo care [skin to skin contact]
Assess Respiratory Effort
May need intubation to maintain respirations.
 < 32 wks: irregular respiratory pattern normal
Survanta in ET tube
Urinary/Elimination
Have high insensible water loss d/t
large body surface compared w/ total
body weight. Lower GFR d/t immature
kidneys. Fluid overload or dehydration.
 Strict I/O
 Immature kidneys secrete glucose
slowly > hyperglycemia can result.
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Insensible Water Loss
[Approx. water loss in body]
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Age group
Premature infant
Newborn infant
12-24 months
Adult
Water
90%
70-80%
64%
60%
Nutrition: promote normal growth & development
 Tries to maintain rapid rate of intrauterine growth.
 Lack of cough reflex: can aspirate formula.
 Have weak sucking, swallowing, gag reflexes
 Weak abdominal muscles; weak gag reflex
 ^ aspiration risk
 ^ BMR - High caloric needs but small stomach
capacity
 Limited store of nutrients
 Decreased ability to digest proteins and absorb
nutrients, and immature enzyme systems.
 TPN, PPN, Gavage, or IV feedings
Feeding
 Caloric requirement: PT: 95-130 kcal./kg/day.
 Term infant: 100-110.
 Smaller stomach capacity: sm.,freq. feedings [q 2-3
hrs].
 Formula: Calories for premie: 24 cal./oz. Term: 20
cal/oz.
 Breast milk good d/t immunologic properties.
 Gavage: nasogastric/orogastric. Gag reflex not
intact til infant 32 wks; avoid over filling stomach;
may cause respiratory distress. Use premie nipple.
Developmentally Supportive
Activities ** (new)
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Kangaroo Care/Skin to Skin Care
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Non Nutritive Sucking (Significantly
reduced length of hospital stay for
preterm infant)
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Non Nutritive at the Breast
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Parent Education & Support
(pacifer)
Non-Nutritive Sucking at
Breast **
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Improved milk production
Provides sucking experience
Prepares infant for breastfeeding
Long term effects:
– Increased length of exclusive breastfeeding
– Increased length of total breastfeeding
POTENTIAL COMPLICTATIONS of PT Infant
Anemia of Prematurity: red blood cell life is short. Low bone
marrow prod. until ~ 32 wks. Frequent blood testing.
Kernicterus: destruction of brain cells by invasion of
indirect bilirubin [bili ~20]. PT infants: low serum
albumin available to bind indirect bili & excrete it.
Persistent Patent Ductus Arteriosus: d/t hypoxia, lack of
surfactant, lack of musculature. Lungs are noncompliant.
^ blood stays in pulmonary artery > pulmonary artery HTN
>persistent PDA. Indocin stimulates PDA closure.
Bronchopulmonary Dysplasia. (Chronic Lung Disease)
Results from long term O2 & being vented (PPV).
Lungs immature; resp.infection, poor nutrition,
Pressure damages & stretches lung tissue; results in airway
edema & fibrotic buildup. Alveolar walls thicken; buildup of
secretions; pneumonia & atelectasis possible. Decreased
oxygenation results.
• S/S: tachypnea, tachycardia, hypoxia, grunting, retractions,
feeding & activity intolerance.
• TX: prevent further disease; promote oxygenation, promote
lung healing.
• O2, nutrition, steriods, bronchodilators, diuretics, antibiotic tx;
stop PPV; maintain venting @ lowest pressure.
• Nitric oxide; Vitamin A
Neonatal Sepsis
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Premies more susceptible; immature immune sys.
Transmission: viral, bacterial; transplacental
(syphilis, toxoplasmosis)
S/S: low temps, resp. distress, hypotension, ^HR,
^RR, lethargy, poor feeding, diarrhea, vomiting.
Mortality: 5-20%
CBC with diff (^bands, decreased neutrophils,
decreased platelets), blood cx,
TX: broad spectrum antibiotics; VS, nutrition, fluids,
O2. Parental support.
ROP: Retinopathy of Pre-maturity.
Caused by damage to immature blood vessels in
retina. Results in scarring. Caused by high O2 levels.
Blindness may result. 90% of cases no impairment.
Occurs in VLBW <1500 g.
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TX: reattachment of retina; Frequent eye evals.
Laser to reduce scarring.
Nursing Care: routine high risk premie care;
sepsis; VS; support groups & education
Intracranial Hemorrhage aka IVP
 germinal matrix – made up of fragile & vascular
capillaries. Grades 1-4 (3 & 4 worse)
 Bleeding into ventricles d/t hypoxia, ^ BP, ^ fluids.
 Dx with Cranial ultrasound
 Normal brain function assessed > bleed.
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IVH occurs in 20-25% of VLBW premies; suffer
more severe grades of IVH
IVH is an important predictor of adverse
neurodevelopmental outcome
½-3/4 of infants with Grade 3-4 IVH develop CP &
75% in some type of special education
NEC
NEC: necrotizing enterocolitis; common in PT baby;
can result in ulcers/tissue necrosis in intestinal wall.
Bacteria in bowel>infection>destroys bowel tissue>
sepsis.
Primary risk factor: prematurity & tube feedings;
RDS, congenital heart defects.
S/S abd. swelling, septic infant, emesis, blood in stool.
Tx: stop tube feedings, start IVF & TPN, AB [sepsis],
ventilator, platelet transfusion [control bleeding]
 Prevention: Delayed /Slow feedings: advance < 20
ml/kg/day; Enteral Antibiotics; Antenatal Steroids;
enteral IgG, IgA; Human Milk Feedings.
GDM
Infants [GDM moms] macrosomic if not well
controlled during pregnancy; lethargic d/t ^ glucose.
 Macrosomia: overstimulation of pituitary growth
hormone in fetus in preg. d/t ^ maternal insulin.
 Mom “insulin resistant”; glucose x placenta; more
insulin made by fetal pancreas.
 After delivery, glucose levels drop, but insulin
remain ^ for several hours.
Infant “jittery” on admission. Glucose checked for 1st
4 hrs; Hypoglycemia = < 40 mg/100 ml whole blood.
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GDM
Complications:
Immature lungs d/t ^ fetal insulin which interferes
with cortisol release; blocks formation of lecithin &
prevents lung maturity. ^ chance of birth injury
d/t ^ size; shoulder dystocia.
Hypoglycemia:
Check glucose on admission to NBN: 1, 1½, 2, 4
hrs. of life. If < 40; stat serum glucose & feed
formula [1/2 oz.] Repeat in ½ - 1 hr. as protocol.
Transient Tachypnea of Newborn: “TTN”
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Rapid, shallow RR 70-80/min. d/t slow absorption of
lung fluid.
Difficulty feeding; infant will not suck d/t rapid
breathing.
Chest x-ray shows fluid in lungs.
Infant must ^ resp.depth to aerate effectively.
Can signify obstruction. VS, O2 sat; give O2.
Send to NICU for close observation if not resolved
within 4-6 hrs.of life.
Occurs more w. term C/S & preterm infants.
Meconium Aspiration Syndrome:
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Present in fetal bowel as early as 10 wks. Infant
may aspirate meconium in utero or with 1st
breath.
Can cause severe respiratory distress,
inflammation or blockage of small bronchioles by
mechanical plugging
Ductus arteriosus may remain open; causes
blood to shunt from pulmonary artery to aorta
instead of passing thru lungs [^ pulmonary
resistance], causing ^ hypoxia.
Symptoms
Tachypnea [RR>60]
Retractions
SOB and expiratory grunting
Nasal flaring
Periods of apnea
Bluish color of skin and mucus membranes
Arms or legs puffy or swollen
Prevention
Oropharyngeal suctioning of infant > delivery
Laryngoscopic visualizaiton of vocal cords > intubation.
Additional suctioning of trachea.
Amnioinfusion: dilutes meconium. Thins out particulate
meconium. Do sepsis workup; CBC, bl.cx., chest x-ray. AB
therapy to prevent pneumonia.
SIDS: sudden infant death syndrome.
 Mainly in adolescent moms, closely spaced pregnancies,
underweight, PT infants. 2nd hand smoke.
 Appear well nourished. ^ African American males.
 Silent death; poss.laryngospasm.
 Use of sleep apnea monitor for first few wks.-mos. Peak
age: 2-4 mos. Cause unknown.
 Theories: HR abnormalities, decreased arousal [moro]
responses, prone position, low surfactant, brain stem
abnorm.
 In 2000 Amer. Academy of Pediatrics recommended
back or side position; not prone. Incidence declined 50%
since then. New data: use of pacifier for 2-4 mos.
Hyperbilirubinemia
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^ levels of unconjugated (indirect) bilirubin in blood.
Breakdown of RBC’s > Hgb > heme > Unconjugated bilirubin.
Bilirubin binds with plasma protein (albumin) = “bound” goes
to liver & converts to conjugated or H2O soluble where it ‘s
excreted via bile by feces.
Immature livers which cannot convert indirect to direct;
indirect bilirubin remains in bloodstream.
Unbound bilirubin = (indirect) jaundice.
If indirect level rises > 7, yellow color results.
Sclera, nail beds, then skin.
Cephalocaudal progression: head to toe.
Blanch skin
Depends on hours/days of life.
Younger infant (4-5 hrs.) high reading more significant; could
rise steadily .
Older infant (1-2 days), higher # less significant (more mature
liver).
Pathologic [within 24 hrs.]
 Bili rises quickly. By 5-7 mg/dl/day or more.
 Blood type incompatibilities ; sepsis; birth trauma.
Interventions: Early & frequent feedings to speed up
excretion in stool.
Phototherapy - bilirubin becomes water soluble to be
excreted.
 Cover genitalia & eyes. Prevent organ damage. Single,
double, triple phototherapy.
 Kernicterus: Indirect bilirubin of 20 > permanent brain
damage; bilirubin encephalophathy.
 Signs: hi-pitched cry, seizures, hypotonia
 Interventions: Immediate exchange transfusion;
followed by phototherapy & frequent bili levels.
Physiologic Jaundice: [> 24 hrs.] 2nd-3rd day.
 R/T low albumin (decreased binding sites for
bilirubin). ^ levels of RBC’s. Yellowing of skin
caused by breakdown of fetal red blood cells which
produces excessive amts. of bilirubin in blood
stream. Excess bilirubin in blood causes jaundice.
 Management: frequent feedings, frequent bili
levels. Bili declines within days.
 Teach parents to place near window to speed up
breakdown of bili. Sunlight will ^ breakdown.
Gastroschisis: weakness in abdominal wall
causing herniation of gut on umbilical cord
during early development; most commonly on
right side. Viscera lie outside abdominal cavity;
not covered with sac.
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1 in 4,000 live births
Mortality: 10%-15%
Assoc.w.prematurity; malrotation of
intestines; decreased abdominal capacity;
other anomalies rare.
TX: IV & NG tubes immediately; TPN; Silastic
(synthetic covering) over viscera; surgical
closure after contents returned to abd.cavity.
If necrotic bowel present, remove.
Nursing Care:
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thermoregulation (monitor temps, radiant warmer);
sterile technique (cover viscera - warm, sterile,
saline gauze & plastic); monitor VS, color, etc.)
strict I&O, daily weights, fontanels, pacifier,
electrolytes. Minimize movement of area.
encourage bonding asap; developmental
stimulation for long term hosp; support group for
parents; teach parents s/s bowel obstruction- ie.
vomiting, pain, firm abdomen, anorexia, irritability.
Omphalocele: large herniation of gut into
umbilical cord. Viscera outside of abd.cavity
& covered with peritoneal & amniotic
membranes
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1 in 5,000 to 10,000 live births
Assoc.w.malrotation of intestines; decreased
abdominal capacity. Stenosis common;
cardiac, genitourinary, or chromosomal
anomalies common (1/3 to ½ of cases)
Mortality: 20-30%; sepsis & intestinal
obstruction.
TX: same as for gastroschisis
Nursing Care: Same as for gastroschisis.
Bladder Exstrophy: extrusion of urinary
bladder to the outside of body through
developmental defect in lower abdominal
wall. Assoc.w.genital anomalies: wide
symphysis pubis.
Rare & congenital anomaly; bladder is “turned
inside out”
TX: protect exposed bladder tissue; cover with
saline gauze/plastic wrap til sugery. Prevent
UTI. Reconstruction of bladder & genitalia.
Provide support & education
EA (esophageal atresia) TEF (tracheoesophageal fistula)
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Cause unknown.
Congenital malformations – esophagus ends before
reaching stomach. (TEF) fistula may connect to
trachea.
1 in 2,000 - 4,500 live births. 30-50% have other
anomalies (cardiac, GI, nervous sys).
Premature or LBW common
EA without TEF : Inability to pass suction or NG
tube catheter @ delivery. Confirm with abd.x-ray;
Excessive oral secretions; vomiting; risk of
aspiration; Abdominal distention; Airless/sunken
abdomen.
Hx maternal polyhydramnios
TEF without EA: food enters trachea; choking;
cyanosis.
Statistics
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Esophageal atresia with distal TEF 87%
Isolated esophageal atresia without TEF 8%
Isolated TEF 4%
Esophageal atresia with proximal TEF 1%
Esophageal atresia with proximal and distal
TEF 1%
Management:
infant supine w. HOB to decrease
secretions. NG tube for frequent suctioning to
prevent aspiration of gastric secretions; IVF; assess
VS, resp.distress, measure abd.girth; provide
education & support to family.
Surgical repair: fistula ligation & end to end
anastomosis of atresia.
Provide post op care. IVF, G-tube & foley care; pain;
VS, I&O, skin care.