Perinatal and Pediatric
Respiratory Care
Ch. 1
Fetal Lung Development
•https://www.youtube.com/watch?v=RS1ti23SUSw
Introduction
• The bronchial tree develops by week 16 of
intrauterine life
• Birth does not signal the end of lung
development
• After birth the alveoli develop in increasing
numbers until the age of 8 years, and increase
in size until growth of the chest wall is finished
• Preacinar arteries and veins develop after the
alveoli are generated
Introduction
• Term infants have approximately 50 million
alveoli which undergo increases in surface
area and number, increasing to 250 million at
maturity
• There are more than 40 cell types in the lung
• There are 5 well recognized stages of lung
development: Embryonal, pseudoglandular,
canalicular, saccular and alveolar
Stages of Fetal Development
Embryonal Phase (Day 26 to Day 52)
Embryonal Stage (Day 26 to Day 52)
• Covers first two months of gestation
• The lung emerges as a bud from the pharynx 26 days
after conception
• This bud elongates and forms two bronchial buds and
the trachea which then separates from the esophagus
through the development of the transeoesophageal
septum
• Growth factors such as fibroblasts mediate
morphogenesis of the tubular epithelium which result
in airway branching (10 on the right and 9 on the left)
•
•
http://commons.wikimedia.org/wiki/File:Shape-Self-Regulation-in-Early-LungMorphogenesis-pone.0036925.s007.ogv
http://www.youtube.com/watch?v=_y4-bfWB5C4
Transesophageal fistula (TEF)
• Malformation of septum during embryonal
development
• Causes a congenital defect which can lead to
stomach content aspiration
• Treatment involves surgical repair
• https://www.youtube.com/watch?v=AWlveIxOKM
Embryonal Stage (Day 26 to Day 52)
• The left and right pulmonary arteries form plexuses (A
plexus is a branching network of axons outside of the
central nervous system)
• Left and right pulmonary veins start to develop about 5
weeks from the SA node area of the heart
• Respiratory epithelium develops from the foregut bud;
The foregut is the anterior part of the alimentary canal,
from the mouth to the duodenum at the entrance of
the bile duct. At this point it is continuous with the
midgut. Pain in the foregut is typically referred to the
epigastric region, just below the intersection of the
ribs.
Embryonal Stage (Day 26 to Day 52)
• Respiratory epithelium is a type of epithelium found lining
the respiratory tract, where it serves to moisten and
protect the airways. It also functions as a barrier to
potential pathogens and foreign particles, preventing
infection and tissue injury by action of the mucociliary
escalator
• Respiratory epithelium also lines the nasal cavities and the
paranasal sinuses in continuity with the mucosa of the
nasal cavity.
• Respiratory epithelium is pseudostratified, which means
that on histological section, resembles layers upon a
basement membrane. In reality, each cell is in contact with
the basement membrane.
Embryonal Stage (Day 26 to Day 52)
• Three primary germ layers
– Endoderm
– Mesoderm
– Ectoderm
– http://www.youtube.com/watch?v=UTNBq5IUtwo
Respiratory epithelium derives from the
endodermal layer construct of the foregut and
interacts with the bronchial mesoderm
Embryonal Stage (Day 26 to Day 52)
• The Mesenchyme is a network of embroyic connective
tissue in the mesoderm which causes development of
the pulmonary interstitium, smooth muscle, blood
vessels, and cartilage
• Mesenchyme is a type of undifferentiated loose
connective tissue that is derived mostly from
mesoderm, although some is derived from other germ
layers
• The term mesenchyme essentially refers to the
morphology of embryonic cells, however, they do
persist as stem cells into adulthood. Mesenchymal cells
are able to develop into the tissues of the lymphatic
and circulatory systems, as well as connective tissues
throughout the body, such as bone and cartilage. A
sarcoma is a cancer of mesenchymal cells.
Embryonal Stage (Day 26 to Day 52)
• Mesenchyme is characterized morphologically
by a prominent ground substance matrix
containing a loose aggregate of reticular fibrils
and unspecialized cells
• Mesenchymal cells can migrate easily, in
contrast to epithelial cells, which lack mobility
and are organized into closely adherent
sheets, are polygonal in shape, and are
polarized in an apical-basal orientation.
Embryonal Phase (Day 26 to Day 52)
• Review:
– Lung and esophagus emerge and develop
– Pulmonary arteries and veins develop
– Pulmonary interstitium, smooth muscle, blood
vessels, and cartilage develop
Stages of Fetal Development
Pseudoglandular Phases (Day 52 to Week 16)
• Lungs have gland like appearance
• Histologic structures are separated by
mescenchyme.
• Second month to sixteenth week
• Subdividing of conducting airways
• Acinus may appear
• Cilia are seen on the epithelium
• Development of goblet, submucosal
glands, and airway cartilage
1 Lung
2 mesenchyma
3 Type II
pneumocytes
Capillaries
Pseudoglandular Phases (Day 52 to
Week 16)
• Extensive subdivsion of conducting airway system
(as a person grows, the size of these conducting
airways increases but the number does not)
• The entire air-conducting bronchial tree up to
the terminal bronchioli are set down in this
phase (16 generations). Recent morphometric
studies have shown that with the end of the
pseudoglandular phase 20 generations are
partially present in the lungs, which means that
at this point in time the respiratory ducts have
already been formed.
Pseudoglandular Phases (Day 52 to
Week 16)
• Terminal bronchioles differentiate into the
respiratory bronchioles and alveolar ducts
• Gas exchanging pulmonary acini/terminal
respiratory units are also laid down
• Growth factors and chemical mediators develop
tracheal epithelium into respiratory type II cells
• Also Ciliated epithelium and of the secretory
cells develop, the first ciliated epithelial cells can
be found in the 13th week of pregnancy
Primary ciliary dyskinesia (PCD),
• also known as immotile ciliary syndrome, is a
rare, ciliopathic, autosomal recessive genetic
disorder that causes a defect in the action of the
cilia lining the respiratory tract (lower and upper,
sinuses, Eustachian tube, middle ear) and
fallopian tube, and also of the flagella of sperm in
males.
• Malformation occurs in the Pseudoglandular
Phases
http://www.youtube.com/watch?v=RakqKYHenx
U
Pseudoglandular Phases (Day 52 to
Week 16)
• Goblet cells develop and appear in the
bronchial epithelium at 13-14 weeks and
submucosal glands arise as solid buds from
basal layers of the surface epithelium at 15-16
weeks
• Smooth muscle cells derive from the primitive
mesenchyme at the end of week 7 and by
week 12 form the posterior wall of the large
bronchi
Pseudoglandular Phases (Day 52 to
Week 16)
• The development of cartilage is present at 24 weeks,
but may develop earlier in a immature form
• Lymphatics appear in the hilar region of the lung
during week 8
• The cells developed during this stage contain glycogen
(Glycogen is a multibranched polysaccharide that
serves as a form of energy storage in humans, glycogen
is made and stored primarily in the cells of the liver
and the muscles, and functions as the secondary longterm energy storage (with the primary energy stores
being fats held in adipose tissue).
Pseudoglandular Phases (Day 52 to
Week 16)
• By the end of this stage, the airways, arteries,
and veins have developed in the pattern
corresponding to that found in an adult
• By 14 weeks the immune system develops,
including T lymphocytes
• Fetal immune responses to allergens develop
early and can be detected in cord blood (fetus
is exposed through the placenta or fetal gut by
swallowing amniotic fluid)
Pseudoglandular Phases (Day 52 to
Week 16)
• Review
– Conducting airways further develop
– Respiratory airways develop
– Cilia, cartilage, goblet cells and submucosal glands
develop
– Immune system develops, lymphatic system
appears
Stages of Fetal Development
Canalicular Phase (Week 17 to week 26)
• Growth of vascular bed
– Air exchange
• Capillaries have sufficient surface area
• Proximity to alveoli
• Lobules containing 3-5 terminal bronchioles,
25,000 terminal bronchioles by 28 weeks
• Extrauterine viability
– 22 to 24 weeks
– Vascularity development
– Surfactant production creating a air-blood
barrier
Stages of Fetal Development
Canalicular Phase (Week 17 to week 26)
• Appearance of vascular channels/capillaries at
20 weeks, forming a capillary network around
air passages, surfactant also develops
(capillaries and surfactant = this is what makes
them viable for life at around 22-24 weeks)
• Blood vessels grow alongside conducting
airways and undergo muscularization
• Bronchial artery system develops
1 Type I
2 pneumocytes
3 Type II
pneumocytes
Capillaries
Stages of Fetal Development
Canalicular Phase (Week 17 to week 26)
• Along the acinus, which develops from the
terminal bronchiolus, an invasion of
capillaries into the mesenchyma occurs. The
capillaries surround the acini and thus form
the foundation for the later exchange of gases.
The lumen of the tubules becomes wider and
a part of the epithelial cells get to be flatter.
From the cubic type II pneumocytes develop
the flattened type I pneumocytes
Stages of Fetal Development
Canalicular Phase (Week 17 to week 26)
• A sufficient differentiation of the type II pneumocytes
into the type I pneumocytes and the proliferation of
the capillaries into the mesenchyma marks an
important step towards the fetus being able to
survive outside the uterus after roughly the 24th week
of pregnancy.
• The first breathing movement can be registered
• They are controlled by a breathing center in the brain
stem. Nevertheless, these breathing movements are
paradoxical in that when the diaphragm contracts, the
thorax moves inwardly and vice versa.
Stages of Fetal Development
Saccular Stage (Week 26 to week 36)
• The major changes that occur during the
saccular stage are further compression of the
intervening interstitium, thinning of the
epithelium, and the beginning of alveolar
septation, with the formation of small
mesenchymal ridges
Stages of Fetal Development
Saccular Stage (Week 26 to week 36)
• There is lengthening and widening of saccules distal to
the terminal bronchioles and the addition of the last
generations of future alveolar spaces.
• Continual differentiation of type I and II alveolar cells
occurs during this period, so that the alveolar epithelial
cells become the most abundant epithelial cells in the
lung. The flattened type I alveolar cells make up the
majority of these cells.
• Type II cells, ultrastructurally distinguished by their
production of lamellar bodies, expand in size and
number, with increased storage of surfactant lipids and
less cytoplasmic glycogen
Stages of Fetal Development
Alveolar Stage (Week 36 to term)
• Not easily
distinguishable
from Saccular
phases
• About 36 weeks
to 18 months
postnatal
Stages of Fetal Development
Alveolar Stage (Week 36 to term)
• Several million alveoli form before birth although this
final stage of lung development primarily occurs during
postnatal life
• The beginning of this stage is not sharply defined
• Alveolar formation is closely linked to the deposition of
• elastin in the saccular lung.
• Terminal saccules become invaginated by protrusions
from the wall of epithelial cells and contain a doublewalled capillary system
• These protrusions elongate and thin, forming primitive
alveoli that at first resemble shallow cups and then
become deeper as development continues.
Postnatal Lung Development
• Continued growth of lungs and number
of alveoli
– 80% of alveoli develop after birth
• Factors affecting lung development
– Hypoxia or hyperoxia
– Nutrition
– Maternal smoking
Postnatal Lung Development
• During the postnatal phase, lung growth is
geometric, and there is no increase in airway
number. There is proportionately less growth
in the conducting airways in comparison with
alveolar-capillary tissue. Estimates of the
number of alveoli at birth vary widely, but an
average of 50 million is generally accepted
Postnatal Lung Development
• Alveoli greatly increase in number after birth, to
• reach the adult range of 300 million by 2 years of
age and the surface area of 75 to 100 m2 by
adulthood.
• There is substantial remodeling of the
parenchyma after birth, with morphologic
changes in the septa.
• Alveolarization occurs through the formation of
numerous short, blunt tissue crests or ridges, and
their protrusion into alveolar sacs increases the
internal surface of the lung.
Pulmonary Hypoplasia
• Causes of decreased lung development
– Compression
– Oligohydramnios
– Decreased respiration
– Metabolic disorders
Pulmonary hypoplasia
• Pulmonary hypoplasia is incomplete
development of the lungs, resulting in an
abnormally low number or size of
bronchopulmonary segments or alveoli. A
congenital malformation, it most often occurs
secondary to other fetal abnormalities that
interfere with normal development of the
lungs. Primary (idiopathic) pulmonary
hypoplasia is rare and usually not associated
with other maternal or fetal abnormalities.
Oligohydramnios
• The amniotic fluid is part of the baby’s life support system . It
protects your baby and aids in the development of muscles,
limbs, lungs and digestive system.
• Amniotic fluid is produced soon after the amniotic sac forms
at about 12 days after conception. It is first made up of water
that is provided by the mother, and then around 20 weeks
fetal urine becomes the primary substance. As the baby grows
he or she will move and tumble in the womb with the help of
the amniotic fluid. In the second trimester the baby will begin
to breathe and swallow the amniotic fluid. In some cases the
amniotic fluid may measure too low or too high. If the
measurement of amniotic fluid is too low it is called
oligohydramnios. If the measurement of amniotic fluid is too
high it is called polyhydramnios.
Oligohydramnios
• Oligohydramnios is the condition of having too
little amniotic fluid. Doctors can measure the
amount of fluid through a few different methods,
most commonly through amniotic fluid index
(AFI) evaluation or deep pocket measurements. If
an AFI shows a fluid level of less than 5
centimeters (or less than the 5th percentile), the
absence of a fluid pocket 2-3 cm in depth, or a
fluid volume of less than 500mL at 32-36 weeks
gestation, then a diagnosis of oligohydramnios
would be suspected.
Oligohydramnios
• About 8% of pregnant women can have low
levels of amniotic fluid, with about 4% being
diagnosed with oligohydramnios. It can occur
at any time during pregnancy, but it is most
common during the last trimester. If a woman
is past her due date by two weeks or more,
she may be at risk for low amniotic fluid levels
since fluids can decrease by half once she
reaches 42 weeks gestation. Oligohydramnios
can cause complications in about 12% of
pregnancies that go past 41 weeks.
Oligohydramnios Causes
• Birth defects – Problems with the development of the
kidneys or urinary tract which could cause little urine
production, leading to low levels of amniotic fluid.
• Placental problems – If the placenta is not providing
enough blood and nutrients to the baby, then the baby
may stop recycling fluid.
• Leaking or rupture of membranes –This may be a gush
of fluid or a slow constant trickle of fluid. This is due to
a tear in the membrane. Premature rupture of
membranes (PROM) can also result in low amniotic
fluid levels.
Oligohydramnios
• The risks associated with oligohydramnios often depend on
the gestation of the pregnancy. The amniotic fluid is
essential for the development of muscles, limbs, lungs, and
the digestive system. In the second trimester, the baby
begins to breathe and swallow the fluid to help their lungs
grow and mature. The amniotic fluid also helps the baby
develop muscles and limbs by providing plenty of room to
move around. If oligohydramnios is detected in the first half
of pregnancy, the complications can be more serious and
include:
• Compression of fetal organs resulting in birth defects
• Increased chance of miscarriage or stillbirth
• http://www.youtube.com/watch?v=nDQguqtooBM
Other Causes of Pulmonary Hypoplasia
• Prenatal and postnatal nutritional deprivation
• High concentrations of oxygen are toxic to
pulmonary tissue; leads to development of
bronchopulmonary dysplasia
• Cigarette smoke
• Chest wall compression (diaphragmatic
hernia)
• Metabolic issues
CDH
• http://www.youtube.com/watch?v=Q6pOL_S
R_8k
Leprechaunism
• a rare lethal familial condition marked by slow
physical and mental development, the elfin
facies suggested by the name (wide-set eyes,
low-set ears, and hirsutism), and severe
endocrine disorders, such as enlargement of
the clitoris and breasts in females and of the
phallus in males. Also called Donohue's
syndrome.
Down Syndrome
• Postnatal growth issues, fewer alveoli than
normal
Pulmonary Surfactant Development
• Type II pneumocytes
– Production, secretion, storage, reuse
• Prevents alveolar collapse
• Early stimulation of surfactant production
–
–
–
–
Beta agonists
Prostaglandins
Epidermal growth factor
Mechanical ventilation
– http://www.youtube.com/watch?v=TDrpPjQ1IPc
– http://www.youtube.com/watch?v=j9z3fb3dV1A
– http://www.youtube.com/watch?v=4VwdsdOBwtQ
Surface tension/surfactant
• Pascal's principle requires that the pressure is
everywhere the same inside the balloon at
equilibrium. But examination immediately
reveals that there are great differences in wall
tension on different parts of the balloon. The
variation is described by Laplace's Law.
• tension, pressure and radius have a definite
relationship and could be used to measure
tension or pressure.
La Place
• The larger the vessel radius, the larger the wall
tension required to withstand a given internal
fluid pressure.
• For a given vessel radius and internal pressure,
a spherical vessel will have half the wall
tension of a cylindrical vessel.
Assessing lung maturity
• Lecithin–sphingomyelin ratio (LS ratio)
• a test of fetal amniotic fluid to assess for fetal lung
immaturity.
• Lungs require surfactant, a soap-like substance, to
lower the surface pressure of the alveoli in the lungs.
This is especially important for premature babies
trying to expand their lungs after birth. Surfactant is
a mixture of lipids, proteins, and glycoproteins,
lecithin and sphingomyelin being two of them.
Lecithin makes the surfactant mixture more effective.
Lecithin–sphingomyelin ratio (LS ratio)
• The lecithin–sphingomyelin ratio is a marker of fetal
lung maturity. The outward flow of pulmonary
secretions from the fetal lungs into the amniotic fluid
maintains the level of lecithin and sphingomyelin
equally until 32–33 weeks gestation, when the
lecithin concentration begins to increase significantly
while sphingomyelin remains nearly the same.
• As such, if a sample of amniotic fluid has a higher
ratio, it indicates that there is more surfactant in the
lungs and the baby will have less difficulty breathing
at birth.
Lecithin–sphingomyelin ratio (LS ratio)
• An L–S ratio of 2 or more indicates fetal lung
maturity and a relatively low risk of infant respiratory
distress syndrome, and an L/S ratio of less than 1.5 is
associated with a high risk of infant respiratory
distress syndrome.
• If preterm delivery is necessary (as evaluated by a
biophysical profile or other tests) and the L–S ratio is
low, the mother may need to receive steroids such as
betamethasone to hasten the fetus' surfactant
production in the lungs.
Phosphatidylglycerol (PG)
• Not useful unless gestational age ≥35 weeks
• Rapid, sensitive
• The PG test is administered via an
amniocentesis that carries slight risks. There is
a chance it can induce labor when carried out
near term, as in the case of a PG test. This is
clearly undesirable if the lungs of the baby
have not matured.
Surfactant
Surfactant is a complex system of lipids, proteins
and glycoproteins which are produced in Type II
cells or Type II pneumocytes.
The surfactant is packaged by the cell in
structures called lamellar bodies, and extruded
into the air-spaces. The lamellar bodies then
unfold into a complex lining of the air-space.
This layer reduces the surface tension of the
fluid that lines the air-space. Surface tension is
responsible for approximately 2/3 of the elastic
recoil forces.
Immature surfactant
• Microscopically, a surfactant deficient lung is
characterized by collapsed air-spaces
alternating with hyper-expanded areas,
vascular congestion and, in time, hyaline
membranes. Hyaline membranes are
composed of fibrin, cellular debris, red blood
cells, rare neutrophils and macrophages.
• They appear as an eosinophilic, amorphous
material, lining or filling the air spaces and
blocking gas exchange.
Immature Surfactant = RDS
• Previously called hyaline membrane disease (HMD), is a
syndrome in premature infants caused by developmental
insufficiency of surfactant production and structural
immaturity in the lungs. MOST COMMON pathology of
prematurity; more severe under 30 weeks
• It can also result from a genetic problem with the production
of surfactant associated proteins. IRDS affects about 1% of
newborn infants and is the leading cause of death in preterm
infants.
• The incidence decreases with advancing gestational age, from
about 50% in babies born at 26–28 weeks, to about 25% at
30–31 weeks. The syndrome is more frequent in infants of
diabetic mothers and in the second born of premature twins.
Immature Surfactant = RDS
• RDS rarely occurs in full-term infants. The
disorder is more common in premature
infants born about 6 weeks or more before
their due dates.
• RDS is a common lung disorder in premature
infants. In fact, nearly all infants born before
28 weeks of pregnancy develop RDS.
• RDS might be an early phase of
bronchopulmonary dysplasia BPD
RDS
• Structural immaturity, as manifest by decreased number of
gas-exchange units and thicker walls, also contributes to the
disease process. Therapeutic oxygen and positive-pressure
ventilation, while potentially life-saving, can also damage the
lung.
• The diagnosis is made by the clinical picture and the chest
xray, which demonstrates decreased lung volumes (bellshaped chest), absence of the thymus (after about 6 hours), a
small (0.5–1 mm), discrete, uniform infiltrate (sometimes
described as a "ground glass" appearance) that involves all
lobes of the lung, and air-bronchograms (i.e. the infiltrate will
outline the larger airways passages which remain air-filled). In
severe cases, this becomes exaggerated until the cardiac
borders become inapparent (a 'white-out' appearance).
RDS prevention
• Most cases of infant respiratory distress syndrome
can be ameliorated or prevented if mothers who are
about to deliver prematurely can be given
glucocorticoids, one group of hormones.
• This speeds the production of surfactant. For very
premature deliveries, a glucocorticoid is given
without testing the fetal lung maturity. The American
College of Obstetricians and Gynecologists (ACOG),
have recommended antenatal glucocorticoid
treatment for women at risk for preterm delivery
prior to 34 weeks of gestation
RDS Detection
• In pregnancies of greater than 30 weeks, the fetal lung
maturity may be tested by sampling the amount of surfactant
in the amniotic fluid by amniocentesis
• include the lecithin-sphingomyelin ratio ("L/S ratio"), the
presence of phosphatidylglycerol (PG), and more recently, the
surfactant/albumin (S/A) ratio.
• For the L/S ratio, if the result is less than 2:1, the fetal lungs
may be surfactant deficient. The presence of PG usually
indicates fetal lung maturity. For the S/A ratio, the result is
given as mg of surfactant per gm of protein. An S/A ratio <35
indicates immature lungs, between 35-55 is indeterminate,
and >55 indicates mature surfactant production(correlates
with an L/S ratio of 2.2 or greater).
RDS treatment
• Oxygen is given with a small amount of continuous positive
airway pressure ("CPAP"), and intravenous fluids are
administered to stabilize the blood sugar, blood salts, and
blood pressure. If the baby's condition worsens, an
endotracheal tube is inserted and exogenous preparation of
surfactant, either synthetic or extracted from animal lungs, is
given into the lungs. One of the most commonly used
surfactants is Survanta 4ml/kg then 2 ml/kg; Curosurf 2.5
ml/kg/then 1.25ml/kg
• Chronic lung disease including bronchopulmonary dysplasia
are common in severe RDS. The etiology of BPD is problematic
and may be due to oxygen, overventilation or
underventilation. The mortality rate for babies greater than
27 weeks gestation is less than 10%.
• Other treatments: ECMO, HFV, Nitric Oxide
Surfactant Delivery
• Always given down ETT, research continues on
effectiveness of aerosolized surfactant
• Synthetic version no longer available in the US
• Can be given up to three times; typically
though 1 or 2 doses are suffice
• After delivery the patient is not to be
suctioned for at least 2 hours, a CXR should be
taken 1-2 hours after delivery. The first dose
should be given within the 1st hour of life and
the second within 12 hours and 3rd within 24
hours
Surfactant Delivery
• Typically the surfactant is delivered through a special adaptor
(looks like a inline suction ballard) that is used to push the
medication to the distal end of the ETT
• Usually it is bagged in, and given to 4 general areas of the
lungs: RUL, RLL, LUL and LLL.
• The neonate is positioned so that via gravity the medication
flows into the correct lung lobe (they are tilted up/down or
moved to one side during delivery)
• It is delivered slowly, to one lobe at a time, after each lobe
delivery the baby is placed in neutral position for 30 seconds
before delivering the next ¼ dose
Surfactant Delivery
• Surfactant is extremely frothy, do not mix or shake the
medication; it is also expensive, do not open the container
unless you are certain it will be used. Keep it refrigerated, but
warm it to at least room temp before use
• During delivery, the surfactant can in fact increase RAW,
increasing PIP and decreasing lung expansion.
• You may have to adjust the ventilator accordingly in the
immediate minutes following delivery to prevent collapse
• Watch for sudden increase in compliance as the surfactant
absorbs quickly, you will have to readjust your vent settings to
prevent over distension
• Assess/evaluate the neonate closely for 1 hour after delivery
for compliance changes
• Obtain a blood gas (CBG or ABG) about 1 hour after delivery
Surfactant Composition
Surfactant Hormonal Effects
• Antenatal steroids (speeds up
production)
• Thyroid hormones
Surfactant Dysfunction
Transient tachypnea of the newborn (TTN)
• Can be seen in the newborn shortly after delivery, typically after a
cesarean section, from retention of amniotic fluid due to the lack of
vaginal squeeze
• Amongst causes of respiratory distress in term neonates, it is the most
common
• It consists of a period of tachypnea >60, mild retractions and grunting. It is
likely due to retained lung fluid, and is most often seen in 35+ week
gestation babies who are delivered by caesarian section without labor.
• Usually, this condition resolves over 24–48 hours. Treatment is supportive
and may include supplemental oxygen, CPAP and antibiotics.
• The chest X-Ray shows hyperinflation of the lungs including prominent
pulmonary vascular markings, flattening of the diaphragm, and fluid in the
horizontal fissure of the right lung.
• http://www.youtube.com/watch?v=NBA9iigiDgk
Transient tachypnea of the newborn (TTN)
• Due to the higher incidence of TTN in newborns delivered by
caesarean section, it has been postulated that TTN could
result from a delayed absorption of fetal lung fluid from the
pulmonary lymphatic system. The increased fluid in the lungs
leads to increased airway resistance and reduced lung
compliance.
• It is thought this could be from lower levels of circulating
catecholamines after a caesarean section, which are believed
to be necessary to alter the function of the ENaC channel to
absorb excess fluid from the lungs.
• Pulmonary immaturity has also been proposed as a causative
factor.
• Mild surfactant deficiency has also been suggested as a
causative factor.
TTN
Fetal Lung Liquid
• Lungs’ secretion 250 to 330 ml/day
• Swallowed or expelled into amniotic
fluid
• Essential for normal lung development
• Removal after birth
– Blood and lymphatic vessels