Respiratory
Distress
Syndrome
Prepared by:
Lina Lontoc De Ramos
Infant Respiratory
Distress Syndrome
Infant respiratory distress
syndrome (IRDS)
• neonatal respiratory distress
syndrome
• respiratory distress syndrome of
newborn
• previously called hyaline membrane
disease
It is a syndrome
in premature infants
Developmental caused by
insufficiency of surfactant production
and structural immaturity in
the lungs
• result from a genetic problem with
the production of surfactant
associated proteins.
• is the leading cause of death
in preterm infants
frequent in infants of diabetic
mothers and in the second born of
premature twins
Decreased blood perfusion of the
lungs
Meconium aspirations
Risk factors:
– Low gestational age
– Male
– Born to diabetic mothers
– Born after an asphyxial insult before
birth
– Born after maternal-fetal hemorrhage
– Multiple gestation
Pathologic features of RDS
• Hyaline like (fibrous) membrane
formed from an exudate of an
infant’s blood that begins to line the
terminal bronchioles, alveolar ducts
and alveoli
Pathologic…
• This membrane prevents exchange
of O2 and CO2 at the alveolar-
capillary membrane
Causes:
1. Low level or absence of surfactant
2. Phospholipid that normally lines the
alveoli
3. Reduce surface tension to keep the
alveoli fromcollapsing on expiration
Pathophysiology
• The lungs of infants with
respiratory distress syndrome are
developmentally deficient in a
material called surfactant,
Patho…
• which helps prevent collapse of
the terminal air-spaces
throughout the normal cycle of
inhalation and exhalation.
Patho…
• High pressure is required to fill
the lungs with air for the first
time and overcome the pressure
of the lung fluid
Patho…
• Alveoli collapse with each
expiration- as happens when
surfactant is deficient
• With the deficient surfactant, areas
of hypoinflation begin to occur
Patho…
• Pulmonary resistance increases
• Lungs are poorly perfused, affecting
gas exchange
• As a result of decrease production
of surfactant
Patho…
• Poor oxygen exchange that results to
tissue hypoxia
• Tissue hypoxia- causes the release of
lactic acid
• Lactic acid combined with increasing
CO2 resulting formation of hyaline
membrane
Patho…
• formation of hyaline membrane leads
to severe acidosis
• Acidosis causes:
[Link]
[Link] tissue perfusion
• Resulting limit surfactant production
Macrosomia
• Birth Weight > 4000 g or > 90th %-ile
• Incidence 15 to 45% among IODM
• Increased rate of C-section
• Birth Trauma
shoulder and body dystocia
brachial plexus injury
facial nerve injury
asphyxia
abdominal trauma
Intrauterine Growth Restriction
• Incidence reported as high as 20 %
• Contributing factors:
– Maternal vascular disease
– Hypertension
– Intrauterine infection
– Chromosomal abnormalities
Intrauterine Growth Restriction
• Oligohydramnios
• Hypoxia
• Fetal distress
• Asphyxia
• Intrauterine and neonatal death
Normal Arterial Blood Gas Values
for the Newborn
• pH : 7.31 - 7.45
• Arterial oxygen pressure (Pao2) :
50–70 mm Hg
• Carbon dioxide pressure (Paco2) :
33-48 mm Hg
• Bicarbonate : 16-24 mEq/L
• Oxygen saturation : > 90%
Signs and Symptoms
tachypnea
Tachycardia
chest wall retractions
(sternal and subcostal)
expiratory grunting
nasal flaring
Cyanosis
S/S
As the disease progresses, the
baby may develop
ventilatory failure (rising carbon
dioxide concentrations in the
blood)
Apnea
S/S
• Seesaw respirations (on
inspiration, the anterior chest wall
retracts and the abdomen
protrudes; on expiration, the
sternum rises)
• Heart failure
S/S
• Pale grey skin
• Bradycardia
• Pneumothorax
Treatment
Therapeutic Management
Oxygen
intravenous fluids are
administered to stabilize the
blood sugar, blood salts, and
blood pressure
Therapeutic
If the baby's condition worsens
endotracheal tube
continuous positive airway pressure
(CPAP) that delivers slightly
pressurized air through the nose can
help keep the airways open
Therapeutic
Extracorporeal membrane
oxygenation (ECMO)
to directly put oxygen in the blood if
a breathing machine can't be used
Therapeutic
• ECMO - providing oxygenation
through an apparatus that
imitates the gas
exchange process of the lungs.
Therapeutic
• Administration of surfactant
• Surfactant replacement-
[Link]
replacement- as a
preventive measure
2. extracted from animal lungs
Medical management
• Oxygenation: oxyhood, Nasal cannula
• Ventilatory support: ventilator, ECMO,
nitrous oxide
• Transcutaneous O2 and CO2
monitoring, pulse oximetry
Therapeutic
• Blood gas monitoring
• Correction of acid-base imbalance
• Environmental temperature regulation
• Adequate nutrition: oral, gavage, and TPN
• Protection from infection
Nursing Assessment and
Diagnosis
Assessment
• Increasing cyanosis
• Tachypnea (60 or > breaths per minute)
• Grunting respirations
• Nasal flaring
• Significant retractions, labored
respirations
• Apnea (episode of nonbreathing for
more than 20 seconds)
• Flaccid, hypotonic, unresponsive to
stimuli
• Seizures (indicative of deterioration
and possible CNS damage.
Diagnosis
• Impaired Gas exchange
• Altered Nutrition: Less than Body
Requirements
• Risk for infection
Nursing care plan
• Admit directly to the special care
nursery
• Lab as ordered: blood type, Rh,
Coombs, CBC
• Administer antibiotics as ordered.
• IV access for meds, hydration and
nutritional support.
• Assist MD/NP with placement of arterial
catheter lines.
• Attach servo probe to infant’s skin,
radiant warmer on servo control.
• Attach 3 lead EKG for continuous
cardiac and respiratory monitoring.
• Attach pulse ox to infant extremity.
• Monitor oxygen administration
Complications
• Air or gas may build up in:
• The space surrounding the lungs
(pneumothorax)
• The space in the chest between two
lungs (pneumomediastinum)
Complication
• The area between the heart and
the thin sac that surrounds the
heart (pneumopericardium)
Complication
• Bleeding into the brain
(intraventricular hemorrhage)
• Bleeding into the lung
• Blood clots due to an umbilical
arterial cathete
Complication
• Bronchopulmonary dysplasia
• Delayed mental development and
mental retardation associated with
brain damage or bleeding
• Retinopathy of prematurity and
blindness
Evaluation
• Prompt identification and early intervention
occurred.
• Newborn is free of respiratory distress and
metabolic alterations.
• Parents verbalize concerns, survival
factors and understanding of treatment
rationales.
Meconium Aspiration
Syndrome
Meconium aspiration syndrome
• is a serious condition in which a
newborn breathes a mixture of
meconium and amniotic fluid into
the lungs around the time of
delivery.
Meconium
present in the fetal bowel as early
as 10 weeks’ gestation
first intestinal discharge from
newborns
a viscous, dark green substance
composed of intestinal epithelial
cells
babies born breech
the appearance of the fluid at
birth is green to greenish black
from the staining
Meconium Aspiration Syndrome
an infant may aspirate
meconium either in utero or with
the first breath after birth.
Once the meconium has passed
into the surrounding amniotic
fluid, the baby may breathe
meconium into the lungs
meconium can block the infant's
airways right after birth
cause breathing difficulties due
to swelling (inflammation) in the
baby's lungs after birth.
CRITERIA
• Mild: requires <40%O2 for <48hrs
• Moderate: >40%O2 for >48hrs, no air
leak.
• Severe: assisted ventilation for >48hrs
Effect of meconiumaspiration
• causes inflammation of the
bronchioles
• can block small bronchioles by
mechanical plugging
• can cause a decrease in surfactant
production
Etiology
Placental insufficiency
Maternal HPN
Preeclampsia
oligohydramnios
maternal drug abuse, especially of
tobacco and cocaine.
Diabetes in the pregnant mother
CLINICAL FEATURES
Physical examination
• Evidence of postmaturity:
[Link] skin
[Link] fingernails
[Link] vernix
.
• The vernix, umbilical cord, and
nails may be meconium-stained,
depending upon how long the
infant has been exposed in utero.
• nails will become stained after 6 hours
• vernix after 12 to 14 hours of exposure
Manifestations
• respiratory distress with marked
tachypnea and cyanosis.
• Reduced pulmonary compliance
• use of accessory muscles of respiration
are evidenced by:
[Link] and subcostal retractions
[Link] (paradoxical) breathing
[Link]
4. nasal flaring.
• chest typically appears barrel-
shaped, with an increased anterior-
posterior diameter caused by
overinflation.
• Auscultation reveals rales and rhonchi
-immediately after birth.
• Some patients are asymptomatic at
birth
• develop worsening signs of respiratory
distress as the meconium moves from
the large airways into the lower
tracheobronchial tree.
S/S
- enlargement of the
anteroposterior diameter of the
chest( barrel chest)
-
S/S
• bilateral coarse infiltrates in the
lungs with spaces of hyper
aeration as shown in the x-ray
S/S
• Hypoxemia
• carbon dioxide retention
• an intrapulmonary and extra
pulmonary shunting
• secondary infection
Diagnosis
MAS must be considered in any
infant born through MSAF who
develops symptoms of RD.
• chest radiograph.
• The initial CXR may show streaky,
linear densities similar in appearance
to transient tachypnea of the newborn
(TTN).
• As the disease progresses, the lungs
typically appear hyperinflated with
flattening of the diaphragms.
• Diffuse patchy densities may alternate
with areas of expansion.
Coarse focal consolidation with
emphysema.
Hyperinflation and patchy asymmetric
airspace disease that is typical of MAS.
Coarse interstitial infiltrates +L side
pneumothorax
Nursing Diagnosis
• Ineffective Gas Exchange
• Altered Nutrition: Less than Body
Requirements
• Ineffective Family Coping:
Compromised
Nursing Care Plan
• Prevention of meconium aspiration
• Maintaining adequate oxygenation and
ventilation
• Regulating temperature
• Observing intravenous fluids
• Providing caloric requirements
• Monitoring antibiotic treatment
nt
Amniotransfusion- used to
dilute the amount of amniotic
fluid and reduce risk of
aspiration
oxygen administration and
assisted ventilation after birth
tracheal suction
Antibiotic therapy
• Radiant warmer -neutral
environment
• observed closely for signs of
trapping air in the alveoli
• chest physiotherapy with
clapping and vibration
Complications
• Aspiration pneumonia
• Brain damage
• Breathing difficulty
• Collapsed lung (pneumothorax)
• Persistent pulmonary hypertension
Prevention
Risk factors should be identified
as early as possible
Assess rupture of BOW
fluid was clear
stained with a greenish or brown
substance.
Evaluation
• The newborn is free of respiratory
distress and metabolic complications
• Parents can verbalize concern,
understanding of treatment.
Neonatal
Sepsis
What is Neonatal Sepsis?
- a term used for a severe infection in
newly born infants.
Neonatal Sepsis affects approximately
2 infants per 1000 births with a
higher incidence in premature & low
birth weight infants.
Early Onset
Late Onset
Neonatal sepsis
• Clinical syndrome of systemic illness
accompanied by bacteremia occurring
in the first month of life
Early Onset
• First 5-7 days of life
• Usually multisystem fulminant illness
with prominent respiratory symptoms
(probably due to aspiration of infected
amniotic fluid)
• High mortality rate
– 5-20%
• acquired during intrapartum period
from maternal genital tract
– Associated with maternal
chorioamnionitis
Late Onset
• May occur as early as 5 days but is
most common after the first week of life
• Less association with obstetric
complications
• Usually have an identifiable focus
– Most often meningitis or sepsis
• Acquired from maternal genital tract or
human contact
Nosocomial sepsis
• Occurs in high-risk newborns
Pathogenesis is related to
– the underlying illness of the infant
– the flora in the NICU environment
– invasive monitoring
• Breaks in the barrier function of the
skin and intestine allow for
opportunistic infection
Causative organisms
• Primary sepsis
– Group B streptococcus
– Gram-negative enterics (esp. E. coli)
– Listeria monocytogenes,
Staphylococcus, other streptococci
(entercocci), anaerobes, H. flu
• Nosocomial sepsis
– Varies by nursery
– Staphylococcus epidermidis,
Pseudomonas, Klebsiella, Serratia,
Proteus, and yeast are most common
Causes:
The primary causes of sepsis -
pathogens, such
As:
• Staphylococcus
• Group Beta Streptoccocus
These pathogens can enter a
neonate’s
body during the:
[Link]
[Link]
[Link] period
Major Risk Factors
• Ruptured membranes > 24 hrs.
• Maternal Fever (100.4 o F(38 o C)
• Chorionamnionitis
• Sustained fetal heart rate
>160/min
Minor Risk Factors
• Ruptured membranes > 12 hrs.
• Foul smelling amniotic fluid
• Maternal Fever > 99.5 o F (37.5 o
C)
• Low APGAR < 5 at 1 min, < 7 at 5
min
• Prematurity
• Multiple gestation
• Presence of 1 major or 2 minor
risk factors -> High Risk of
Sepsis
Factors:
• immaturity of the neonate’s
immune system
• genetic predisposition that is
caused by polymorphisms
Risk factors
• Maternal peripartum fever
• Amniotic fluid problems (i.e. mec,
chorio)
• Resuscitation at birth, fetal distress
• Multiple gestation
• Invasive procedures
• Galactosemia
• Other factors: sex, race, variations in
immune function, hand washing in the
NICU
Clinical signs and
symptoms
– RDS
– Metabolic disease
– Hematologic disease
– CNS disease
– Cardiac disease
– Other infectious processes (i.e.
TORCH)
Clinical presentation
• Temperature irregularity (high or low)
• Change in behavior
• Lethargy, irritability, changes in
tone
• Skin changes
• Poor perfusion, mottling, cyanosis,
pallor, petechiae, rashes, jaundice
• Feeding problems
• Intolerance, vomiting, diarrhea,
abdominal distension
Diagnosis
• Cultures
– Blood
• Confirms sepsis
• 94% grow by 48 hours of age
– Urine
• Don’t need in infants <24 hours old
because UTIs are exceedingly rare in
this age group
– CSF
• Controversial
• May be useful in clinically ill newborns
or those with positive blood cultures
Radiology
• CXR
– Obtain in infants with respiratory
symptoms
– Difficult to distinguish GBS or
Listeria pneumonia from
uncomplicated RDS
• Renal ultrasound and/or VCUG in
infants with accompanying UTI
Maternal studies
• Examination of the placenta and fetal
membranes for evidence of
chorioamnionitis
Management
• Antibiotics
– Primary sepsis: ampicillin and
gentamicin
– Nosocomial sepsis: vancomycin and
gentamicin or cefotaxime
– Change based on culture sensitivities
– Don’t forget to check levels
Supportive therapy
• Respiratory
• Oxygen and ventilation as
necessary
• Cardiovascular
• Support blood pressure with
volume expanders and/or pressors
• Hematologic
• Treat DIC with FFP and/or cryo
• CNS
• Treat seizures with phenobarbital
• Watch for signs of SIADH (decreased
UOP, hyponatremia) and treat with
fluid restriction
• Metabolic
• Treat hypoglycemia/hyperglycemia
and metabolic acidosis
Prevention is better than
cure
Thank you
God bless!
THANK YOU
&
GOD BLESS!