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‡ 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 neonate·s lungs before delivery
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‡ RDS is characterized by poor gas exchange and

ventilatory failure due to lack of surfactant in the lungs
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‡ 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
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‡ RDS can produce respiratory distress acutely

after birth or within a few hours of birth
‡ Initial assessment may reveal various findings
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‡ ulso known as j

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‡ u 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
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‡ Before birth, the fetal lungs are filled with fluid

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‡ 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
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‡ Increased RR ( greater than 60 bpm)
‡ Expiratory grunting
‡ Nasal flaring
‡ Slight cyanosis
‡ Retractions
‡ Tachypnea
‡ uBG levels may reveal hypoxemia and decreased
carbon dioxide levels
‡ Increased CO2 levels may be a sign of fatigue and
impending respiratory failure
‡ Chest x-ray the diagnostic standards for TTN, reveals
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‡ Oxygen administration
‡ Ventilatory assistance (rarely needed)
‡ Maintenance of acid-base balance
‡ Thermoregulation
‡ udequate nutrition via gavage feedings or IVF
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‡ Transcutaneous oxygen monitoring
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‡ Closely monitor the neonate·s 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
  

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‡ Involves aspiration of meconium into the lungs
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meconium mixed with amniotic fluid; typically
occurs with the first breath or while the neonate
is in utero
‡ Risk factors for MuS
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‡ usphyxia 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
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‡ 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
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‡ 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 neonate·s skin ( ' 

  
 
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‡ Signs of distress at delivery, such as neonate
appearing limp, upgar scores below 6, pallor, cyanosis,
and respiratory distress
‡ Coarse crackles when auscultating neonate·s lungs
‡ Chest x-ray may show patches or streaks of meconium
in the lungs, air trapping, or hyperinflation
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‡ Respiratory assistance via mechanical
ventilation
‡ Maintenance of a neutral thermal environment
‡ udministration of surfactant and an antibiotic
‡ Extracorporeal membrane oxygenation in sever
cases
› 
  

‡ During labor, continuously monitor the fetus for
S/Sx of distress
‡ Immediately inspect any fluid passed with
rupture of membranes
‡ ussist with immediate endotracheal suctioning
during delivery as indicated
‡ Monitor lung status closely, including breath
sounds and RR and character
‡ Frequently assess the neonate·s vital signs
‡ udminister 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




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‡ 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 (-) à  ,  j, and
 and the gram (+) beta-hemolytic
streptococci
‡ Prolonged rupture of membranes increases the
neonate·s risk of sepsis
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‡ Subtle, nonspecific behavioral changes, such as
lethargy and hypotonic
‡ Temperature instability
‡ Feeding pattern changes, such as poor sucking
and decreased intake
‡ upnea
‡ Hyperbilirubinemia
‡ ubdominal 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
‡ untibiotic administration

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‡ Collect specimens to identity the causative
organism
‡ ussess the neonate·s 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
‡ udminister nutritional support
‡ ussist with respiratory support measures,
including oxygen therapy as ordered
‡ Monitor F/E balance; administer IVF therapy as
ordered
‡ Institute measures to provide cardiovascular
support
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‡ ulso called
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‡ 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
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depending on the cause
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‡ Hyperbilirubinemia can develop several ways

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‡ us 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)
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‡ 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.
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‡ Jaundice appearing anytime after the first day

of life and persisting beyond 7 days
‡ Elevated serum bilirubin levels ² 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 neonate·s
blood with fresh blood (less than 48 hours old),
removing some of the unconjugated bilirubin in
serum
‡ Phototherapy
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‡ ulbumin 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. Don·t skip feedings because fasting
stimulates the conversion of heme to bilirubin.
ulso, don·t supplement non-dehydrated
breastfed infants with water or water and
dextrose
‡ ussess and record the neonate·s 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, Coomb·s test, CBC, reticulocyte
count, G6PD, U/u & total and direct bilirubin
‡ Institute phototherapy as ordered
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‡ ussist with an exchange transfusion if indicated
‡ udminister Rho (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
‡ ussess all neonates for risk of
hyperbilirubinemia before discharge
‡ Explain the importance of follow-up visit to
assess for hyperbilirubinemia
 Performing Phototherapy
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‡ Formerly called Erythroblastosis fetalis
‡ Involves a breakdown of RBCs
‡ The majority of neonates affected are female

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‡ 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
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can occur when fetal
blood type differs from maternal blood type
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 occurs when the Rh (-)
mother carries an Rh (+) fetus
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‡ Hemolytic anemia
‡ Hyperbilirubinemia w/in 24 H after birth
‡ Jaundice
‡ Hepatosplenolegaly
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‡ 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
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‡ During pregnancy, institute preventive measures
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‡ 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
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‡ Refers to a congenital anomaly resulting from exposure
to some teratogen that doesn·t allow the esophagus and
trachea to separate normally
‡ There·s an abnormal connection between the trachea
and esophagus
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‡ 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
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‡ Signs of respiratory distress
‡ Excessive frothy oral mucus ²    

‡ Difficulty inserting a NGT
‡ Difficulty feeding (results in choking or aspiration)
‡ Triad ´Cµ: Choking, Coughing and Cyanosis
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‡ Maintenance of patent airway
‡ Withholding of food and fluids (NPO) until repaired
‡ Surgical correction ²  
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‡ Positioning of neonate in high Fowler·s position to prevent
aspiration of gastric contents
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‡ 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
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‡ Keep the neonate on NPO status
‡ Administer IVF to maintain hydration & provide
nutrition; offer a pacifier to meet the neonate·s 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 neonate·s 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
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‡ Offer emotional support to the parents and family
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‡ 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
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‡ Exact cause is unknown

‡ The acetabulum is flattened or too shallow
‡ As a result the head of the femur dislocates upward & backward
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‡ Positive Ortholani·s sign
‡ Positive Barlow·s sign
‡ Shortened femur on affected side ² Galeazzi·s sign
‡ Asymmetrical gluteal folds
‡ Waddling gait
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‡ 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
› 
  

‡ Maintain the affected hip in a flexed, abducted position
‡ Instruct the parents in measures to position & maintain the
head of the femur
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‡ 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
 


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‡ 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
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‡ Vesicular lesions on the soles and palms
‡ Irritability
‡ Small for gestational age
‡ Failure to thrive
‡ Rhinitis
‡ Red rash around mouth and anus
‡ Copper rash on face, soles, and palm
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‡ Penicillin therapy
‡ Infection-control precautions
‡ Covering of neonatal hands to minimize skin trauma
from scratching
› 
  

‡ Make sure all pregnant patients are screened for
syphilis at the first prenatal visit
‡ Assist with laboratory testing (VDRL or rapid plasma
reagin) on neonatal cord blood ro check for intrauterine
exposure
‡ Administer drugs as ordered
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‡ 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
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‡ Fiery red conjunctivae
‡ Thick purulent discharge from the eye
‡ Eyelid edema
‡ Corneal ulceration and destruction, if untreated
‡ Culture of exudate reveals causative organism
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‡ I.V. antibiotic therapy
‡ Standard & contact infection ² control precautions
‡ Sterile saline solution eye irrigation
‡ Treatment of mother for infection
› 
  

‡ 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 mother·s
sexual partners
 | V |

‡ 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:
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‡ Causes of hydrocephalus aren·t well understood;
possible causes include:
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‡ With hydrocephalus, CSF production is
increased, flow is obstructed, or reabsorption is
altered.
‡ us a result, intracranial pressure increases
causing brain displacement or motor and
mental damage
 


‡ Increased head circumference
‡ Bulging fontanels
‡ ´Sunset eyesµ
‡ 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
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‡ Skin care to prevent breakdown and infection
‡ Careful head support during handling
‡ Measurement of head circumference
‡ Emotional support and education for the
parents
‡ ussessment 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
  




‡ ussess closely for S/Sx of increasing ICP
‡ Frequently measure HC, reporting any changes
‡ Maintain adequate nutrition
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‡ Provide meticulous skin care, repositioning the
neonate·s 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
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