HIGH RISK

NEWBORNS
RESPIRATORY DISTRESS
SYNDROME
Description
A disease related to immaturity of lung tissue
May also be called Hyaline Membrane Disease
A complex disorder manifested by signs of
respiratory distress
Risk factors: prematurity, maternal DM, and
stress during delivery that produces acidosis in
the neonate
Is seen almost exclusively in preterm neonates
Is associated with a high risk of long-term
respiratory and neurologic complications

Prenatal diagnosis can evaluate lung
maturity while the fetus is in utero
- Evaluation of lecithin/sphingomyelin ratio
of the amniotic fluid is performed
- Lecithin and sphingomyelin are two
surfactant phospholipids
- Evaluation of fetal lung maturity gives
insight into how the fetus will face after
birth and may precipitate treatment to
delay labor or to mature the neonates
lungs before delivery
Pathophysiology
RDS is characterized by poor gas exchange
and ventilatory failure due to lack of surfactant
in the lungs
Surfactant is a phospholipid secreted by the alveolar
epithelium
It coats the alveoli, keeping them open so gas exchange
can occur
In preterm neonates, the lungs may not be fully
developed and therefore may not have sufficient
surfactant available
The result is the inability to maintain alveolar stability
The lack of surfactant leads to atelectasis, labored
breathing, respiratory acidosis, and hypoxemia
With worsening atelectasis, pulmonary vascular
resistance increases, which decreases blood flow
to the lungs
Right-to-left shunting of blood perpetuates fetal
circulation by keeping the foramen ovale and
dactus arteriosus patent
The alveoli can become necrotic and the
capillaries are damaged
Ischemia allows fluid to leak into the interstitial and
alveolar spaces and a hyaline membrane forms
The membrane greatly hinders respiratory function
by decreasing the compliance of the lungs
Assessment Findings

RDS can produce respiratory distress acutely
after birth or within a few hours of birth
Initial assessment may reveal various findings
Increase respiratory rate
Retractions
Satisfactory color
Good air movement on auscultation

As respiratory distress becomes obvious, other
findings may be noted
Further increased respiratory rate
Labored breathing
More pronounced substernal retractions
Fine crackles on auscultation
Cyanosis, pallor
Nasal flaring
Expiratory grunting
Seesaw breathing

S/Sx such as hypoxemia, hypercapnia, &
acidosis are non-specific to RDS
Specific laboratory tests must be carried out to evaluate
the neonate for complications
Tests include: blood, urine & CSF cultures and blood
glucose, serum calcium & arterial blood gas (ABG) levels
Radiographic evaluation reveals various
findings
Alveolar atelectasis shown by a diffuse granular pattern
that resembles ground glass over all lung fields
Dilated bronchoiles shown by dark streaks within granular
pattern

Treatment
Thermoregulation
Oxygen administration
Mechanical ventilation, if needed
Prevention of hypotension
Prevention of hypovolemia
Correction of respiratory acidosis by ventilatory support
Correction of metabolic acidosis by sodium bicarbonate
administration
Administration of surfactant and such other drugs like
antibiotic, sedative, and diuretic
Protection from infection
Administration of parenteral feedings
Glucocorticoid (Celestone) artificial surfactant given at
birth before the first breath or after diagnosis of RDS;
effective after the 72
nd
hour; hastens lung maturity.

Nursing Interventions:
Provide continuous monitoring and close observation
Obtain necessary specimens for laboratory testing
Continuously monitor pulse oximetry or transcutaneous
oxygen levels
. administer oxygen as ordered
. anticipate the need for ventilatory support, including
mechanical ventilation, continuous positive airway
pressure, or positive end-expiratory pressure

Suction the neonate as indicated
Institute measures to maintain thermoregulation
Provide parenteral nutrition and avoid gavage and oral
feedings during the acute stage of the disease because
these situations decrease respiratory rate and oxygen
consumption
Cluster nursing activities to provide the neonate with rest
periods; disturb the neonate with RDS as little as possible
to decrease oxygen consumption
Administer drugs as ordered
Provide meticulous skin and mouth care
Educate the parents about the disease, treatments, and
procedures as well as what to expect and provide
emotional support during the acute stage
Transient Tachypnea
of the Neonate (TTN)
Description
Also known as type II respiratory distress
syndrome or wet lung
A mild respiratory problem in neonates, typically
beginning after birth and generally lasting about
2 days
Results from delayed absorption of fetal lung
fluid after birth
TTN is commonly observed in neonates born by cesarean
delivery did not receive thoracic compression that helps
expel fluid during vaginal delivery.
7 42 ml of amniotic fluid are squeezed from the lungs
during vaginal delivery
Neonates who are small or preterm, or who were born
rapidly by vaginal delivery (may not have received
effective squeezing of the thorax to remove fetal lung
fluid)
Resolution of symptoms generally occurs within
48 hours
Once TTN goes away, the neonate usually recovers
completely & has no increased risk for further respiratory
problems
Pathophysiology
Before birth, the fetal lungs are filled with fluid
- All of the fetuss nutrients and oxygen come from the
mother through the placenta
- The fetus doesnt use his lungs to breathe
- During the birth process, some of the neonates lung fluid
is squeezed out as he passes through the birth canal
- After birth, the remaining fluid is pushed out of the lungs
as the lungs fill the air
- Any fluid that remains is later coughed out or reabsorbed
into the bloodstream
TTN results from aspiration of amniotic or
tracheal fluid compounded either by delayed
clearing of the airway or by excess fluid
entering the lungs
TTN spontaneously fades as lung fluid is
absorbed, usually 48 hours of life as respiratory
activity becomes effective


Assessment findings
Increased RR ( greater than 60 bpm)
Expiratory grunting
Nasal flaring
Slight cyanosis
Retractions
Tachypnea
ABG levels may reveal hypoxemia and decreased
carbon dioxide levels
Increased CO
2
levels may be a sign of fatigue and
impending respiratory failure
Chest x-ray the diagnostic standards for TTN, reveals
streaking (correlates with lymphatic engorgement of retained
fetal lung fluid)
Treatment
Oxygen administration
Ventilatory assistance (rarely needed)
Maintenance of acid-base balance
Thermoregulation
Adequate nutrition via gavage feedings or IVF
Difficulty with oral feedings because of increased RR and
increased work of breathing; coordination of neonatal
mechanisms of sucking, swallowing, and breathing
High risk of aspiration due to rapid RR
Transcutaneous oxygen monitoring
Protection from infection
Nursing Interventions
Closely monitor the neonates HR, RR, and
oxygenation status
Provide respiratory support, including
mechanical ventilation, if necessary
Institute measures to maintain a neutral thermal
environment
Minimize stimulation by decreasing lights and
noise levels
Provide nutritional support via gavage feedings
or parenteral nutrition
Educate the parents about the condition and its
usually quick resolution
Provide emotional support to the parents and
family
Bronchopulmonary Dysplasia
This chronic pulmonary condition affects
newborns who experienced respiratory
failure or have been oxygen-dependent for
more than 28 days.
X-ray findings are abnormal, indicating
areas of overinflation and atelectatsis.
Bronchopulmonary Dysplasia
Assessment
Tachypnea and tachycardia
Retractions
Nasal flaring
Labored breathing
Crackles and dec. air movement
Occasional expiratory wheezing



Bronchopulmonary Dysplasia
Interventions;
Monitor airway and cardiopulmonary
functions; provide oxygen therapy.
Fluid restrictions may be prescribed.
Medications include surfactant, diuretics,
cortisteroids , and bronchodilators

MECONIUM ASPIRATION
SYNDROME (MAS)
Involves aspiration of meconium into the lungs
- Meconium is the neonates first feces
- it may be seen in the amniotic fluid after 34 weeks
gestation and is thick, sticky, and greenish black
* MAS results when the neonate inhales the
meconium mixed with amniotic fluid; typically
occurs with the first breath or while the neonate
is in utero
Risk factors for MAS
- Maternal diabetes
- Maternal hypertension
- Difficult delivery
- Fetal distress
- Intrauterine hypoxia
- Advanced gestational age (greater than 40 weeks)
- Poor intrauterine growth

Pathophysiology
Asphyxia in utero leads to increased fetal
peristalsis, relaxation of the anal sphincter,
passage of meconium into the amniotic fluid,
and reflex gasping of amniotic fluid into the
lungs
- Neonates with MAS increased respiratory efforts to create
greater negative intrathoracic pressures and improve air
flow to the lungs
- Hyperinflation, hypoxemia, and acidemia cause increased
peripheral vascular resistance
- Right-to-left shunting commonly follows
Meconium creates a ball-valve effect, trapping
air in the alveolus and preventing adequate gas
exchange
Chemical pneumonitis results causing the
alveolar walls and interstitial tissues to thicken,
again preventing adequate gas exchange
Cardiac efficiency can be compromised from
pulmonary hypertension
Assessment findings
Fetal hypoxia as indicated by altered fetal activity and
heart rate
Dark greenish staining or streaking of the amniotic
fluid noted on rupture of membranes
Obvious presence of meconium in the amniotic fluid
Greenish staining of neonates skin (if the meconium was
passed long before delivery)
Signs of distress at delivery, such as neonate
appearing limp, Apgar scores below 6, pallor,
cyanosis, and respiratory distress
Coarse crackles when auscultating neonates lungs
Chest x-ray may show patches or streaks of
meconium in the lungs, air trapping, or hyperinflation
Treatment
Respiratory assistance via mechanical
ventilation
Maintenance of a neutral thermal environment
Administration of surfactant and an antibiotic
Extracorporeal membrane oxygenation in sever
cases

Nursing Interventions
During labor, continuously monitor the fetus for
S/Sx of distress
Immediately inspect any fluid passed with
rupture of membranes
Assist with immediate endotracheal suctioning
during delivery as indicated
Monitor lung status closely, including breath
sounds and RR and character
Frequently assess the neonates vital signs
Administer treatment modalities, such as
oxygen and respiratory support, as ordered
Institute measures to maintain a neutral thermal
environment
Teach the parents about the condition,
treatments, and procedures a well as what to
expect
Provide the parents and family with emotional
support and guidance
NECROTIZING ENTEROCOLITIS
NECROTIZING
ENTEROCOLITIS

An acute inflammatory disease of the
gastrointestinal tract.
Usually occurs 4 to 10 days after birth in a
term newborn.
Assessment
Increase abdominal girth
Decrease or absent bowel sound
Bowel loop distention
Vomiting
Bile stained emesis
Abdominal tenderness
Occult blood in stool
Intervention
Hold oral feedings
Insert oral gastric tube to decompress the
abdomen.
Intravenous antibiotics
IV fluids to correct fluid, electrolytes and
acid-base imbalances
Surgery if indicated.
SEPSIS
Description
Occurs when pathogenic microorganisms or
their toxins occur in the blood or tissues
Can occur before, during, or after delivery
Most common causative organisms are the
gram (-) Escherichia coli, Acrobacter, and
Klebsiella and the gram (+) beta-hemolytic
streptococci
Prolonged rupture of membranes increases the
neonates risk of sepsis
Assessment findings
Subtle, nonspecific behavioral changes, such
as lethargy and hypotonic
Temperature instability
Feeding pattern changes, such as poor sucking
and decreased intake
Apnea
Hyperbilirubinemia
Abdominal distention
Skin color changes, including mottling, pallor,
and cyanosis
Positive blood cultures
Lumbar puncture to rule out meningitis
Urine, skin, blood, and nasopharyngeal cultures
Gastric aspiration
Antibiotic administration

Nursing interventions
Collect specimens to identity the causative
organism
Assess the neonates V/S at least once per
hour or more frequently as indicated
Expect to administer a broad spectrum
antibiotic before culture results are received &
to switch to specific antibiotic therapy after
results are received
Provide supportive care, including maintenance
of a neutral thermal environment
Administer nutritional support
Assist with respiratory support measures,
including oxygen therapy as ordered
Monitor F/E balance; administer IVF therapy as
ordered
Institute measures to provide cardiovascular
support
HYPERBILIRUBINEMIA
Also called pathologic jaundice
Characterized by a bilirubin level that exceeds 6
mg/dl within the first 24 hours after delivery and
remains elevated beyond 7 days in a full-term
neonate and beyond 10 days in a pre-term
neonate
- A bilirubin level that rises by more than 5 mg/day
- A level thats greater than 12 mg/dl in premature or term
neonates
- Conjugated (direct) bilirubin level that exceeds 1.5 to 2 mg/dl
The prognosis for hyperbilirubinemia varies
depending on the cause
Pathophysiology
Hyperbilirubinemia can develop several ways
- Certain drugs (such as aspirin, tranquilizers, and
sulfonamides) and conditions (such as hypothermia,
anoxia, hypoglycemia, and hypoalbuminemia) can disrupt
conjugation and usurp albumin-binding sites
- Decreased hepatic function can result in reduced bilirubin
conjugation
- Increased erythrocyte production or breakdown can
accompany a hemolytic disorder or Rh or ABO
incompability
- Biliary obstruction or hepatitis may block normal bile flow
- Maternal enzymes present in breast milk can inhibit the
neonates glucuronosyltransferase-conjugating activity
As erythrocytes breakdown at the end of their
neonatal life cycle, hemoglobin separates into
globin (protein) and heme (iron) fragments
Heme fragments form unconjugated (indirect)
bilirubin, which binds with albumin for trasport
to liver cells to conjugate with glucuronide,
forming direct bilirubin
Unconjugated bilirubin is fat-soluble and cant
be excreted in the urine or bile; it may escape
to extravascular tissue, especially fatty tissue
and the brain, resulting in hyperbilirubinemia
Unconjugated bilirubin can infiltrate the nuclei of
the cerebral cortex and thalamus, leading to
kernicterus (an encehalopathy)
- Although exact level is unknown, kernicterus may occur
with serum bilirubin levels at or above 20 mg/dl (full-term)
and at lower levels (about 14 mg/dl) in preterm neonates
- S/Sx of kernicterus: lethargy, decreased reflexes,
seizures, opisthotonos, & high-pitched cry
Possible causes include include hemolytic
disease of the neonate, sepsis, imparied
hepatic functioning, polycythemia, enclosed
hemorrhage, hypothermia, hypoglycemia, and
asphyxia neonatorum
Glucose-6-phosphate deficiency (G6PD)
increases the incidence of jaundice.
Assessment findings

Jaundice appearing anytime after the first day
of life and persisting beyond 7 days
Elevated serum bilirubin levels levels greater
than 12 mg/100 ml in a term neonate, levels
greater than 15 mg/100 ml in a preterm
neonate, or levels that increase more than 5
mg/100 ml in 24 hours
hepatoaplenimegaly
Exchange transfusion to replace the neonates
blood with fresh blood (less than 48 hours old),
removing some of the unconjugated bilirubin in
serum
Phototherapy
- Considered the treatment of choice for hyperbilirubinemia
due to hemolytic disease of the neonate (after the initial
exchange transfusion)
- uses fluorescent light to decompose bilirubin in the skin by
oxidation
- Usually discontinued after bilirubin levels fall below 10
mg/100 ml and continue to decrease for 24 hours
Albumin administration (1g/kg of 25% salt-poor
albumin) to provide additional albumin for
binding unconjugated bilirubin; done 1 to 2
hours before exchange or as a substitute for a
portion of the plasma in the transfused blood
Treatment of anemia caused by hemolytic
disease
To prevent hyperbilirubinemia encourage the
mother to breastfeed at least 8 to 12 times per
day. Dont skip feedings because fasting
stimulates the conversion of heme to bilirubin.
Also, dont supplement non-dehydrated
breastfed infants with water or water and
dextrose
Assess and record the neonates jaundice in
the first 24 hours after birth, and note the time it
began; immediately report the jaundice and
serum or transcutaneous bilirubin levels
Obtain lab values as ordered, which may
include blood type, Coombs test, CBC,
reticulocyte count, G6PD, U/A & total and direct
bilirubin
Institute phototherapy as ordered
- Clean the neonates eyes periodically to remove drainage
- Offer extra water to promote bilirubin excretion
- Explain that the neonates stool contains some bile and
may be breenish
Assist with an exchange transfusion if indicated
Administer Rh
o
(D) immune globulin (human),
as ordered, to an Rh (-) mother after
amniocentesis or to an Rh (-) mother during the
third trimester (for the purpose of preventing
hemolytic disease once the neonate is born),
after the birth of an Rh (+) neonate, or after
spontaneous or elective abortion
Reassure parents that most neonates
experience some degree of jaundice
Explain hyperbilirubinemia, its causes,
diagnostic tests, and treatment; provide written
information
Assess all neonates for risk of
hyperbilirubinemia before discharge
Explain the importance of follow-up visit to
assess for hyperbilirubinemia
Performing Phototherapy
Set up the phototherapy unit about 18 inches (45.7 cm)
above the neonates bassinet & verify placement of the
lightbulb shield
If the neonate is in an incubator, place the phototherpay
unit at least 3 (7.6 cm) above the incubator, and turn on
the lights
Place a photometer probe in the middle of the bassinet to
measure the energy emitted by the lights. The average
range is 6 to 8 w/cm
2
/nanometer
Explain the procedure to the parents
Record the newborns initial bilirubin level and his
axillary temp.
Place the opaque eye mask over the neonates closed
eyes, & fasten securely
Undress the neonate, & place a diaper under him.
Cover male genitalia with a surgical mask or small
diaper to catch urine & prevent possible damage from
the heat & light waves
Take the neonates axillary temp every 2 hours &
provide additional warmth by adjusting the warming
units thermostat
Monitor elimination, & weigh the neonate twice daily.
Watch for signs of DHN (dry skin, poor turgor,
depressed fontanels), & check urine specific gravity
with a urinometer to gauge hydration status
Take the neonate out of the bassinet, turn off the
phototherapy lights, & unmask his eyes at least
every 3 to 4 hours (with feedings). Assess his eyes
for inflammation or injury
Reposition the neonate every 2 hours to expose all
body surfaces to the light and to prevent head
molding and skin breakdown from pressure
Check the bilirubin level at least once every 24
hours more often if levels rise significantly. Turn
off the phototherapy unit before drawing venous
blood for testing because the lights may degrade
bilirubin in the blood. Notify the health care
provider if the bilirubin level nears 20 mg/dl
fullterm or 15 mg/dl if premature.
HEMOLYTIC DISEASE
Description
Formerly called Erythroblastosis fetalis
Involves a breakdown of RBCs
The majority of neonates affected are female
Pathophysiology
During pregnancy, maternal antibodies are passed
via the placenta to the fetus, causing RBC
breakdown
The disorder is usually caused by ABO
incompatibility but may also be caused by Rh
incompatibility
ABO incompatibility can occur when fetal
blood type differs from maternal blood type
- The most common incompatibility occurs when a type O
mother carries a type A or type B fetus; type O blood
contains anti-A and anti-B antibodies that travel
transplacentally to the fetus, causing jaundice &
hepatosplenomegaly
- ABO incompatibility can occur with the first pregnancy and
is usually milder and of shorter duration than Rh
incompatibility
Rh incompatibility occurs when the Rh (-)
mother carries an Rh (+) fetus
- Leakage of fetal Rh antigens commonly occurs during
delivery, at the time of placental separation
- Maternal antibodies are produced in response in a
subsequent pregnancy with an Rh (+) fetus, maternal
antibodies enter the fetal circulation transplacentally,
causing erythroblastosis
Assessment findings
Hemolytic anemia
Hyperbilirubinemia w/in 24 H after birth
Jaundice
Hepatosplenolegaly
Treatment
Drug therapy such as erythropoietin to stimulate
RBC formation
Initiation of early feeding (breast- or bottle-
feeding)
Family support
Phototherapy
Exchange transfusion
Monitoring of bilirubin levels


Nursing interventions
During pregnancy, institute preventive
measures
- Prevention involves administration of Rh immune globulin
(RhoGAM) within 72 H of delivery to prevent antibody
formation
- RhoGAM is ineffective when the patient is already
sensitized
- RhoGAM should be administered to an Rh (-), D
u
(-)
patient who has had an abortion or whose neonate is Rh
(+) or D
u
(+)
- RhoGAM can be administered at 28 weeks gestation to
decrease the incidence of maternal isoimmunization

Keep in mind that Rh sensitization can occur
during pregnancy if the cellular layer separating
maternal & fetal circulation is disrupted
Encourage the patient to feed the neonate, if
appropriate
Prepare the neonate and parents for treatment
procedures, such as phototherapy or exchange
transfusion
TRACHEOESOPHAGEAL
FISTULA
Description
Refers to a congenital anomaly resulting from
exposure to some teratogen that doesnt allow
the esophagus and trachea to separate
normally
Theres an abnormal connection between the
trachea and esophagus
TRACHEOESOPHAGEAL
FISTULA
Pathophysiology
Abnormal development of the trachea and esophagus
occurs during the embryonic period
Typically, the esophagus ends in blind pouch with
trachea communicating by a fistula with lower
esophagus and stomach
Assessment findings
Signs of respiratory distress
Excessive frothy oral mucus outstanding symptom
Difficulty inserting a NGT
Difficulty feeding (results in choking or aspiration)
Triad C: Choking, Coughing and Cyanosis
Treatment
Maintenance of patent airway
Withholding of food and fluids (NPO) until repaired
Surgical correction esophageal anastomosis & division of
fistula
Positioning of neonate in high Fowlers position to
prevent aspiration of gastric contents
- with fistula head is extended 30
o
- Without fistula Trendelenberg position to drain secretions
Laryngoscope and endotracheal tube at bedside in
case of extreme edema causing obstruction
Frequent shallow suctioning
Pacifier to meet sucking needs
Possible gastrostomy tube feedings postoperatively
Nursing intervention
Keep the neonate on NPO status
Administer IVF to maintain hydration & provide
nutrition; offer a pacifier to meet the neonates
sucking needs
Assess airway for patency
Frequently monitor V/S and respiratory status;
watch for S/Sx of aspiration
Position the neonate upright or on his right side
to minimize the risk of gastric secretions
entering the lungs
Maintain a neutral thermal environment
Provide comfort measures & institute measures
to reduce the risk of neonates crying; the risk
for vomiting & aspiration increases without
crying because air entering the stomach from
the fistula leads to distention
Prepare the parents and neonate for surgical
correction
Provide post-op care as appropriate
- Change position frequently & stimulate baby to cry BUT
avoid hyperextension of the neck to prevent tension on
the suture line
Offer emotional support to the parents and
family
DEVELOPMENTAL
DYSPLASIA OF THE HIP
Description
Refers to the improper formation & function of the hip
socket
Commonly called congenital hip dysplasia
Causes the femur head to ride out of or dislocate from
the acetabulum
Pathophysiology
Exact cause is unknown
The acetabulum is flattened or too shallow
As a result the head of the femur dislocates upward &
backward
Assessment findings
Positive Ortholanis sign
Positive Barlows sign
Shortened femur on affected side Galeazzis sign
Asymmetrical gluteal folds
Waddling gait
Treatment
Positioning & maintaining the head of the femur in the
acetabulum with triple diapers, a Frejka pillow splint,
or Pavlik harness
Hip-spica cast & braces if other means prove
ineffective
Possiblr surgical correction
Parent education about use of device for maintaining
position
Nursing interventions
Maintain the affected hip in a flexed, abducted position
Instruct the parents in measures to position & maintain
the head of the femur
- Teach the parents how to apply triple diaper, a splint or a harness
- Show parents how to properly care for the skin, especially areas
under the device
Offer emotional support & guidance to parents
Encourage parents to interact w/ the neonate & hold
the neonate even with a device in place
Inform parents about the possibility of the need for
surgical correction later on when the neonate is older.
Maintain skin integrity
CONGENITAL SYPHILIS
Description
Results fro infection by the spirochete of
Treponema pallidum
Occurs when the spirochete crosses the
placenta froma pregnant infected patient to her
fetus
Diagnosed with serologic tests at 3 to 6 months
The development of antibodies is necessary to
make a diagnosis
CONGENITAL SYPHILIS
Assessment findings
Vesicular lesions on the soles and palms
Irritability
Anemia, jaundice
Hepatosplenomegaly
Ascites,
Red rash around mouth and anus
Copper rash on face, soles, and palm
Treatment
Penicillin therapy
Infection-control precautions
Covering of neonatal hands to minimize skin
trauma from scratching
Nursing interventions;
Monitor for signs of syphilis,(palmar rash,snuffles etc.)
Make sure all pregnant patients are screened for
syphilis at the first prenatal visit
Assist with laboratory testing
(VDRL or rapid plasma reagent) on neonatal cord
blood to check for intrauterine exposure
Administer drugs as ordered
Used standard precautions and drainage and
secretions (contact) precautions with suspected
syphilis.
Wear gloves handling the newborn until antibiotic
therapy has been administered for 24 hrs.

OPHTHALMIA NEONATORUM
Description
A severe eye infection that occurs in neonates
at birth or during the first few months
Results from exposure to the causative
organism during vaginal delivery
Most commonly cause by Neiserria gonorrhea
or Chlamydia trachomatis
Prophylactic administration of antibiotic
ointment at birth to all neonates is a primary
preventive strategy
OPHTHALMIA
NEONATORUM
Assessment findings
Fiery red conjunctivae
Thick purulent discharge from the eye
Eyelid edema
Corneal ulceration and destruction, if untreated
Culture of exudate reveals causative organism
Treatment
I.V. antibiotic therapy
Standard & contact infection control
precautions
Sterile saline solution eye irrigation
Treatment of mother for infection
Nursing Interventions
Administer prophylactic antibiotic eye ointment
to all neonates after delivery
Monitor the appearance of the eyes for redness
and drainage
Institute standard and contact precautions
Perform eye irrigation as ordered; wear goggles
is splashing is likely
Advised the mother to receive treatment for her
infection; also suggest treatment for the
mothers sexual partners
HYDROCEPHALUS
An excessive accumulation of CSF within the
ventricular spaces of the brain
This accumulation leads to dilation of ventricles, which
causes potentially harmful pressure on the brain tissue
Compression of brain tissue and cerebral blood
vessels may lead to ischemia and, eventually, cell
death
May be communicating or non-communicating:
- Communicating hydrocephalus results from faulty absorption of
CSF
- Non-communicating hydrocephalus occurs as a result of obstruction
of CSF flow
HYDROCEPHALUS
Causes of hydrocephalus arent well
understood; possible causes include:
- Genetic inheritance
- Neural tube defects, such as spina bifida and
enancephalocele
- Complications of preterm birth such as intraventricular
hemorrhage
- Meningitis
- Tumors
- Traumatic head injury
- Subarachnoid hemorrhage
- Prenatal maternal infection
Pathophysiology
With hydrocephalus, CSF production is
increased, flow is obstructed, or reabsorption is
altered.
As a result, intracranial pressure increases
causing brain displacement or motor and
mental damage
Assessment findings
Increased head circumference
Bulging fontanels
Sunset eyes
Widened sutures
Forehead prominence
Thin, shiny fragile-looking scalp skin
Irritability
Weakness
Seizures
Sluggish pupils with unequal response to light
High-pitched, shrill cry
Projectile vomiting
Feeding problems
Treatment;

Skin care to prevent breakdown and infection
Careful head support during handling
Measurement of head circumference
Emotional support and education for the parents
Assessment of neurologic status and progression
of symptoms
Shunt insertion to eliminate excess CSF
Management of shunt and prevention of infection
at the surgical site.
Monitor S/Sx of increasing ICP
Nursing Intervention
Assess closely for S/Sx of increasing ICP
Frequently measure HC, reporting any changes
Maintain adequate nutrition
-Provide a flexible feeding schedule to accommodate
schedule
-Offer small, frequent feedings, allowing extra time for
feedings as necessary
Provide meticulous skin care, repositioning the
neonates head often to reduce the risk of skin
breakdown
Teach the parents about the condition,
treatments and procedures
Provide the parents and family with emotional
support
Prepare the neonate for shunt insertion as
indicated; complete all preoperative procedures
and teaching
Perform postoperative care, including
positioning the neonate on the unaffected side,
monitoring the surgical site closely, and
obtaining head circumference
TORCH SYNDROME
Refers to a group of maternal infectious diseases
(Toxoplasmosis, Other infections, Rubella,
Cytomegalovirus, Herpes simplex virus type III)
Can lead to serious complications in the embryo,
fetus, or neonate
Pathophysiology:
-Infection results when the organisms cross the
placenta or travel up through the birth canal
-Once present, the organisms can cause severe
problems with fetal growth and development
TOXOPLASMOSIS
Is transmitted to the fetus primarily via the
mothers contact with contaminated cat box filler
A therapeutic abortion is recommended if the
diagnosis is made before the 20
th
week of
gestation
Effects include increased frequency of stillbirths,
neonatal deaths, severe congenital anomalies,
deafness, retinochoroiditis, seizures, and coma
Maternal treatment involves anti-infective
therapy with a sulfa or clindamycin
RUBELLA
Is a chronic viral infection
The greatest risk occurs within the first trimester
Effects include congenital heart disease,
intrauterine growth retardation, cataracts,
mental retardation, and hearing impairment
Management includes therapeutic abortion if the
disease occurs during the first trimester, and
emotional support to for parents
Women of childbearing age should be tested for
immunity and vaccinated if necessary
The neonate may persistently shed the virus for
up to 1 year
CYTOMEGALOVIRUS (CMV)
CMV is a herpesvirus that can be transmitted
from an asymptomatic mother transplacentally
to the fetus or via the cervix to the neonate at
delivery
Its the most common cause of viral infections in
fetuses
CMV is a common cause of mental retardation
Principal sites of damage are the brain, liver and
blood
Other effects include auditory difficulties and a
birth weight thats small for gestational age
The neonate may also demonstrate a
characteristic pattern of petechiae called
BLUEBERRY MUFFIN SYNDROME
antiviral drugs cant prevent CMV or treat
the neonate

HERPESVIRUS TYPE II
The fetus can be exposed to the herpesvirus
through indirect contact with infected genitals or
via direct contact with those tissues during
delivery
Affected neonates may be asymptomatic for 2 to
12 days but then may develop jaundice, seizures,
increased temperament, and characteristic
vesicular lesions
a cesarean delivery can protect the fetus from
infection
Pharmacologic treatment may include acyclovir
and vidarabine I.V. after exposure
HERPESVIRUS TYPE II
RETINOPATHY OF PRETERM BIRTH
Refers to an alteration in vision leading to partial or
total blindness
Typically results from prolonged exposure to high
concentrations of oxygen or fluctuations in oxygen
administration levels
Pathophysiology:
High concentrations lead to vasoconstriction of
immature retinal blood vessels
Fluctuating oxygen administration levels lead to
rapid vasodilation and vasoconstriction of immature,
fragile retinal blood vessels
Subsequent rupture of vessels occur with partial or
complete retinal detachment
RETINOPATHY OF PREMATURITY
This illustration highlights the differences between normal retinal blood-vessel
development (at left) and the pathological vessel growth (at right) in the eye of a
child with retinopathy of prematurity. Red blobs represent abnormal vessel
development in the diseased eye
RETINOPATHY OF
PREMATURITY

Vascular disorder
involving gradual
replacement of retina
by fibrous tissue and
blood vessels.
Primarily caused by
prematurity and use of
supplemental oxygen
(30%)
RETINOPATHY OF
PREMATURITY

Intervention:

Laser photocoagulation therapy
-a laser is used to
finely cauterize ocular
blood vessels
A premature
infant with
retinopathy of
prematurity is
examined by a
pediatric
opthamologist
USING A
RETINAL
SCANNER
http://www.ssc.education.ed.ac.uk/courses/vi&multi/vmar06iv.html
CRYOTHERAPY / CRYOSURGERY
LASER THERAPY / TREATMENT
http://www.retina-associates.net/ROP_seven.htm
Assessment Findings
Include retinal changes, which are evident upon
ophthalmologic examination
Treatment
-Monitoring of oxygen concentration
-Monitoring ABG levels
-Monitoring of transcutaneous oxygen levels and pulse
oximetry
-Ophthalmologic examinations at regular intervals during
and after hospitalization
-Administration of vit. E (reduces the incidence of
retinopathy or prematurity by modifying tissues
response to effects of oxygen)
-Cryosurgery or laser surgery
Nursing Interventions
Closely monitor oxygen concentration levels
being administered; obtain transcutaneous
oxygen and ABG levels and pulse oximetry
readings as ordered
Administer oxygen carefully, ensuring that the
lowest concentration necessary is being used
Explain the condition and its treatments to the
parents
Instruct the parents in the need for follow-up eye
examination
Provide preoperative and postoperative care as
indicated
FETAL ALCOHOL SYNDROME
(FAS)
Is caused by maternal
alcohol use during
pregnancy.
Causes mental and physical
retardation.
FETAL ALCOHOL SYNDROME (FAS)
A cluster of birth defects (growth retardation,
CNS abnormalities, and facial malformations)
resulting from in utero exposure to alcohol.
Commonly found in neonates of patients who
ingested varying amounts of alcohol during
pregnancy
Birth defects associated with prenatal alcohol
exposure can develop in the first 3 to 8 weeks of
pregnancy before a woman even knows shes
pregnant.
The risk of teratogenic effects increases
proportionally with increased daily alcohol intake
No safe level of alcohol intake during pregnancy
has been established
FAS has been detected in neonates of moderate
drinkers (7 to 2 oz or 30 to 59 ml alcohol daily.)
PATHOPHYSIOLOGY
Alcohol is teratogenic substance thats
particularly dangerous during critical periods of
organogenesis
alcohol interferes with the passage of amino
acids across the placenta barrier
When a pregnant woman ingests alcohol, so
does her unborn child
Alcohol crosses through the placenta and enters
the blood supply of the fetus
Alcohol interferes with healthy development of
the fetus
Variables that affect the extent of damage
caused to the fetus by alcohol include the
amount of alcohol consumed, timing of
consumption, and pattern of alcohol use

ASSESSMENT FINDINGS
Prenatal and postnatal growth retardation
Characteristic findings within the first 24 hours of life
-Difficulty establishing respirations
-Irritability
-Lethargy
-Seizure activity
-Tremulousness
-Opisthotonos
-Poor sucking reflex
-Flat midface
-Short upturned nose
-Respiratory distress (apnea, cyanosis)
-Congenital heart disorder
Facial anomalies, such as microcephaly,
micro-ophthalmia, maxillary hypoplasia, and
+Eyes - short palpebral fissures, strabismus,
ptosis, myopia
+Nose short, upturned, flat or absent groove
above upper lip
+Mouth thin upper lip, receding jaw
CNS dysfunction, including decreased IQ,
developmental delays, learning disabilities,
neurologic abnormalities such as decreased
muscle tone, poor coordination, and small brain

TREATMENT
-Prevention through public
education
-Careful prenatal history and
education
-Identification of women at
risk, with referral to alcohol
treatment centers if
necessary
-Prompt identification of
neonates with FAS to ensure
early intervention and
appropriate referrals

NURSING INTERVENTIONS
Institute measures for prevention
Increase public awareness about the dangers of
alcohol consumption during pregnancy
Ensure increased access to prenatal care
Provide educational programs
Assist with screening women of reproductive age
for alcohol problems
Use appropriate resources and strategies for
decreasing alcohol use
Closely assess any neonate born to a mother who
has used alcohol
Intervention;
Monitor for respiratory distress.
Position the newborn on the side to facilitate
drainage of secretions.
Keep resuscitation equipment at the bedside.
Monitor for hypoglycemia.
Assess for suck and swallow reflex.
Administer small feedings and burp well.
Suction as necessary.
Monitor I & O, weight and head circumference.
Dec. environmental stimuli.

Prevent and treat respiratory distress, including
assessing breath sounds frequently, being alert for
signs of distress, and suctioning as needed
Encourage successful feeding; assist with developing
measures to enhance neonates intake
Monitor weight and measure intake and output
Promote parent-neonate attachment
-Encourage frequent visiting and rooming in if
possible
-Encourage physical contact between the parents
and the neonate
-Educate parents about neonates complications
Provide emotional support
ADDICTED NEWBORN
A newborn can
become passively
addicted to drugs that
have passed through
the placenta.
Assessment findings
and withdrawal times
may vary depending
on the specific
addicting drugs

ADDICTED NEWBORN
Assessment:
Irritability
Tremors
Hyperactiviy & Hypertonicity
Vomiting
High-pitched cry
Sneezing
Fever
Excessive sweating
Extreme sucking of fists


Intervention
Monitor respiratory and cardiac status
frequently, also VS and I & O.
Hold newborn firmly and close to the body
during feeding & when giving care.
Swaddle the newborn
Provide quiet room and reduce stimulation.
Provide small frequent feeding and allow
longer feeding period.
Allow the mother to express feelings of guilt
and anxiety, then Refer her for tx. of the
abuse problem.



New born of a HIV Mother
The fetus of a client who is positive for HIV
antibody should be monitored closely throughout
the pregnancy.
Serial Ultrasound screenings should be done
during pregnancy to identify intrauterine growth
restriction.
Weekly restriction.
Weekly nonstress testing after 32 weeks of
gestation and biophysical profiles may be
necessary during pregnancy.
New born of a HIV Mother
Newborns born to HIV mother may test positive
because the mothers antibodies may persist in
the newborn for 18 mos. After birth.
The use of antiviral drug, the reduction of
exposure to maternal blood and body fluids, and
the early identification of HIV in pregnancy
reduce the risk of transmission to the newborn.
All newborns born to HIV positive mother
acquire maternal antibody to HIV infection, but
not all acquire the infection.
The newborn maybe asymptomatic for the first
several months to years of life.


New born of a HIV Mother
Transmission;
1. Across placental barrier
2. During labor and delivery
3. breastmilk
New born of a HIV Mother
Assessment;
1.Possibly no outward signs at birth
2. Signs of immunodefiency
3. Lymphadenopathy
4. Hepatomegaly
5. Splenomegaly
6. Impairment in growth and development.

New born of a HIV Mother
Intervention;
1. Clean the newborns skin carefully before any
invasive procedure, such as administration of
Vit. K, heel stick, or venipunctures.
2. Circumcisions are not done on newborns with
HIV positive mothers until the newborns status
is determined.
3. Newborn can room with mother.
4. All HIV exposed newborns should be treated
with medication to prevent infection by
Pneumocystis jiroveci.
New born of a HIV Mother
5. Antiviral medications may be administered as
prescribed for the first 6 weeks of life.
6. Monitor for early signs of immunodeficiency, such
as enlarged spleen or liver, lymphadenopathy and
impairment in growth & development.
7. Newborns at risk for HIV infection should be seen
by the physician at birth and at 1 week, 2 weeks,
1 mo. and 2 mos. of age.
8. Inform the client that HIV culture is recommended
at 1 mo. and 4 mos. Of age.

New born of a HIV Mother
Immunization
MMR and varicella vaccines are not given
until newborns infant or child status is not
confirmed.
If infected, live vaccines will not be given.

APNEA

PRETERM BIRTH
An infant born before the 37
th
week
gestation.
Primary concern relates to immaturity of all
body systems.

CHARACTERISTICS:
-Weight is less than 2500 gm (2350 gm for
Filipinos) and the length is less than 47 cm at
birth
-The cry is more feeble, sucking is weaker, and
there is general weakness with sluggish
movements; they often assume frog-like position
-Scarf sign elbow passes the midline of the body
-Square window wrist wrist at a 90
o
angle
-There is abundance of lanugo; nails are soft;
physiologic weight loss is exaggerated
-Skin is thin and wrinkled; minimal amount/
underdeveloped of subcutaneous tissue to act
insulation. NEED: to place inside the incubator
with temperature regulated to 33.3 34.4
o
C,
humidity of 55-56%; and frequent positioning on
the right side to promote closure of the foramen
ovale.
-The head appears relatively large, but the
circumference is less than 33 cm with a
characteristic wizened face
-Are poikilothermic (easily take on the
temperature of the environment)
-Labia are narrow in girls.
-Testes are descended in boys
-Respirations are irregular
-Body temperature is below normal
-The newborn has poor suck and swallow
reflex
-Bowel sounds are diminished.
-Urinary output is inc. or decreased.
-Extremities are thin, with minimal creasing
on soles and palms.

Lanugo on the skin and in the hair on the
newborns head, is present in woolly
patches.
Skin is thin, with visible blood vessels and
minimal subcutaneous fat pads.


Intervention
Monitor vital signs every 2 to 4 hours.
Maintain airway and cardiopulmonary functions.
Administer oxygen and humudification as
prescribed.
Monitor I & O, weight, and electrolyte imbalance.
Reposition newborn every 2 hours and handle it
carefully.
Avoid exposure to infections
Provide appropriate stimulation, such as touch
and cuddling.


Oxygen administration
SMALL FOR GESTATIONAL AGE
Birth weight is less than expected for the
specific gestational age; e.g. babies born on
the 38
th
week of gestation who weighs 5
lbs.
Newborn who is plotted at or below the 10
th

percentile on the intrauterine growth curve.



LARGE FOR GESTATIONAL AGE
Birth weight is more than expected for the
specific gestational age; e.g., baby born on
the 36
th
week of gestation who weighs 8
lbs.

POSTMATURITY

HUMAN IMMUNODEFICIENCY
VIRUS INFECTION

GENETIC DISORDERS
GENETICS is the study of heredity, the
passing of traits from parents to their
children.
Physical traits such as eye color are
inherited as well as biochemical and
physiological traits, including the tendency
to develop certain diseases.

INHERITANCE
Inherited traits are transmitted from parents of
offspring through genes in germ cells, or gametes.
Human gametes are eggs, or ova, and sperm.
A persons genetic make-up is determined at
fertilization.
In the nucleus of each germ cell are structures called
chromosomes.
Each chromosome contains a strand of genetic
material called DNA.
DNA is a long molecule that is made up of thousands
of segments called genes. Each of the traits a person
inherits from blood type to toe shape and a myriad of
others in between is coded in their genes.
HUMAN CHROMOSOMES
A human ovum and a sperm contains 23
chromosomes.
When ovum and sperm unites, the corresponding
chromosomes pair up. The result is a fertilized cell
with 46 chromosomes in the nucleus.
The fertilized cell soon undergoes cell division
(mitosis).
In mitosis, each 46 chromosome produces an exact
duplicate of itself. The cell then divides and each new
cell receives one set of 46 chromosomes.
Each cell in a persons body (except the ova and
sperm) contains 46 identical chromosomes.
The ova and sperm are formed by a different cell
division process called meiosis.
The location of a gene on a chromosome
is called LOCUS.
The locus of each gene is specific and
does not vary from person to person. This
allows each of the thousands of genes in
an ovum to join the corresponding gene
from a sperm when the chromosomes pair
up at fertilization.
GENETIC MUTATION
A mutation is a permanent change in genetic
material.
When a gene mutates, it may produce a trait
that is different from its original trait.
Gene mutations in a gamete may be
transmitted during reproduction. Some
mutations cause serious or deadly disorders
that occur in three different forms: SINGLE-
GENE DISORDERS, CHROMOSOMAL
DISORDERS, AND MULTIFACTORIAL
GENETIC DISORDERS.
SINGLE-GENE DISORDERS
are inherited in clearly identifiable patterns. Two
important inheritance patterns are called autosomal
dominant and autosomal recessive. Because there are
22 pairs of autosomes and only 1 pair of sex
chromosomes, most heredity disorders are caused by
autosomal defects.
In a third inheritance pattern, sex-linked inheritance,
single-gene disorders are passed through the X
chromosome.
Dominant genes produce abnormal traits in offspring
even if only one parent has the gene; recessive genes
do not produce abnormal traits unless both parents
have the gene pass them to their offspring.
Autosomal Dominant Inheritance
Male and female offspring are affected
equally;
one of the parents is also usually affected;
and if one parent is affected, the children
have a 50% chance of being affected, and
if both parents are affected, all of the
children will be affected.
e.g. Marfan syndrome
Autosomal Recessive Inheritance
Male and female offspring are affected equally;
If both parents are unaffected but heterozygous for the trait
(carriers), each of their offspring has a one in four chance of
being affected; and
If both parents are affected, all of their offspring will be affected.
If one parent is affected and the other is not a carrier, all of the
offspring will be unaffected but will carry the altered gene.
If one parent is affected and the other is a carrier, each of the
offspring have a one in two chance of being affected and if
certain autosomal recessive conditions are more common in
specific ethnic groups; e.g., cystic fibrosis in Whites & sickle cell
anemia in Blacks.
In many cases, no evidence of the trait appears in past
generation, may be indicative that client has a negative family
history
Sex-Linked Inheritance
Because Y chromosome is not known to carry disease-
causing genes, the terms X-linked and sex-linked are
interchangeable.
Because female receive two X chromosomes (one from
each parent), they can be homozygous for a disease
allele, or heterozygous.
Because males have only one X-chromosome, a single
X-linked recessive gene can cause disease in a male. In
comparison, a female needs two copies of diseased
gene. Therefore, males are more commonly affected by
X-linked recessive diseases than female.
X-linked Dominant Inheritance
A person with the abnormal trait typically will have one
affected parent; if the father has a X-linked dominant
disorder, all of his daughters and none of his sons will be
affected;
If a mother has a X-linked dominant disorder, theres a
50% chance that each of her children will be affected.
Evidence of the inherited trait most commonly appears in
the family history, and in X-linked dominant disorders are
commonly lethal in males (prenatal or neonatal deaths).
The family history may show miscarriages and the
predominance of female offspring.
X-linked Recessive Inheritance
In most cases, affected people are males with
unaffected parents.
In rare cases, the father is affected and the
mother is a carrier.
All of the daughters of an affected male will be
carriers.
Sons of an affected male are unaffected.
Unaffected sons cant transmit the disorder and
the unaffected male children of a female carrier
dont transmit the disorder.
e.g., Hemophilia
CHROMOSOMAL DISORDERS
May also be caused by chromosomal
aberrations deviations in either the
structure or the number of chromosomes.
Deviations involve the loss, addition,
rearrangement, or exchange of genes.
If the remaining genetic material is
sufficient to maintain life, an endless
variety of clinical manifestations may
occur.
Nondisjunction
During cell division, chromosomes normally separate
in a process called disjunction. Failure to do so is
called disjunction causes an equal distribution of
chromosomes between the two resulting cells.
Gain or loss of the chromosomes is usually due to
nondisjunction of autosomes or sex chromosomes
during meiosis
May occur during very early cell divisions after
fertilization and may or may not involve all the
resulting cells. A mixture of cells, some with a specific
chromosome aberration and some with normal cells,
result in mosaicism. The effect on the offspring
depends on the percentage of normal cells.
The incidence of nondisjunction increases with
parental age. Miscarriages cal also result from
chromosomal aberrations. Fertilization of an ovum
with a chromosome aberration by a sperm with a
chromosome aberration usually does not occur.
When chromosomes are gained or lost, the name of
the affected cell contains the suffix somy.
A cell that contains one fewer than the normal number
of chromosomes is called MONOSOMY.
If the monosomy involves an autosome, the cell will be
nonvisible. However, monosomy X can be viable and
result in a female who has Turners syndrome.
A cell that contains one extra chromosome is called
TRISOMY.
Translocation
Is the shifting or moving of a chromosome. It occurs
when chromosomes break and rejoin in an abnormal
arrangement. When the rearrangements preserve
the normal amount of genetic material (balanced
translocation), there are usually no visible
abnormalities.
When the rearrangements alter the amount of
genetic material, typically, there are visible or
measurable abnormalities. The children of parents
with balanced translocations may have serious
chromosomal aberrations, such as partial
monosomie or partial trisomies. Parental age doesnt
seem to be a factor.
MULTIFACTORIAL DISORDERS
Disorders caused by both genetic and environmental
factors.
Examples are cleft lip, cleft palate, and
myelomeningocele.
Environmental factors that contribute include:
maternal age, use of chemicals by father and
mother, maternal infections during pregnancy or
existing diseases in the mother, maternal or parental
exposure to radiation, maternal nutrition or parental
health, high altitude, maternal-fetal blood
incompatibility, maternal smoking, and poor-quality
prenatal care.
ACHONDROPLASIA
Is a genetic condition that results in abnormally
short stature with disproportionately short limb.
The average height of an adult is 131 cm (52
inches, or 44) in males and 124 cm (49 inches
or 41) in females.
CLEFT LIP

CLEFT PALATE

CYSTIC FIBROSIS

CYSTINURIA

EHLERS-DANLOS SYNDROME

HEMOPHILIA

HUNTINGTONS DISEASE

JACOBS SYNDROME

KLINEFELTERS SYNDROME

LESCH-NYHAN SYNDROME

MARFAN SYNDROME

MUCOOPOLYSACCHARIDOSES

MUSCULAR DYSTROPHY

NEUROFIBROMATOSIS

OSTEOGENESIS IMPERFECTA

POLYCYSTIC KIDNEY DISEASE

SICKLE CELL ANEMIA

TAY SACHS DISEASE

TRISOMY 21 (DOWNS SYNDROME)

TRISOMY 13 (PATAU SYNDROME)

TRISOMY 18 (EDWARDS SYNDROME)

TURNER SYNDROME

XXX (TRIPLE X) SYNDROME