Prematurity

and
Hyaline Membrane Disease

Hygeia Laurei M. Fernandez

 CLASSIFICATION OF PRETERM AND
LOW BIRTH WEIGHT BABIES

Different degrees of prematurity are defined by gestational age (GA) or birth weight.
Newborn classification based on gestational age
Preterm (premature) born at 37 weeks' gestation or less
Term born between the beginning of week 38 and the end of week 41 of gestation
Post-term (postmature) born at 42 weeks' gestation or more
Newborn classification based on birth weight
Low birth weight (LBW) less than 2500 g
Very low birth weight (VLBW) less than 1500 g
Extremely low birth weight (ELBW) less than 1000 g
 CLASSIFICATION ON GESTATIONAL AGE

premature baby Preterm baby Very preterm baby

baby born Babies born between the born between the

before 37 gestational ages of 32-36 weeks of gestational ages of 28-31
completed gestation weeks as calculated from
weeks of calculated from the mothers last the LNMP date
pregnancy normal menstrual period (LNMP Like very low birth weight
date). babies
can usually be managed safely have problems in
at home with some extra care and feeding and maintaining
support their body temperature
premature baby Preterm baby

Very preterm
baby

Term baby
INTRODUCTION

The late premature birth interrupts normal

utero fetal development during the last 6
weeks of gestation that represents a critical
period of growth and development of the
fetal brain and lungs.
INTRODUCTION

CRITICAL PERIOD: time-sensitive, irreversible

decision point in the development of a neural
structure or system in which deprivation of the
normal environment interrupts the maturational
trajectory of the structure/system.
 SURVIVAL

The neonatal mortality rate is 45 deaths per 1000

live births.
Preterm delivery accounts for 75-80% of all
neonatal morbidity and mortality.
 SURVIVAL

The mortality rate is high in developing countries,

especially those of Sub-Saharan Africa, LSEC, maternal
age.
Since the early 1960s, survival rates of premature infants
substantially increased because of technologic
advances.
SURVIVAL

Gestational age weeks Survival %

21 0-4
22 0-12
23 8-36
24 12-62
25 31-79
26 53-85
STATISTICS

Of babies born preterm:

84%: 32-36 wks AOG
10%: 28-31 wks AOG
6%: less than 28 wks AOG
STATISTICS

Late Preterms comprise about three-quarters of all

preterm births.
Between 1992 2002, there is a 16 % increase in
late preterm births.
Babies born at 34 weeks were 4.6 times more likely
to die than those at 40 weeks
SEQUELS

From 1979 to 1994 survival among preterm infants with BW 501-

800 gr increased from 20 to 59%.

The percentage of children with severe neurosensory injury was

however, unchanged. (OShea 1997)
 SEQUELS

Data from the Vermont Oxford Network in 1994-1996

Survival rate of infants born weighing less than 1000 g
was 74.9%.
Survival of infants born weighing less than 1000 g and
requiring cardiopulmonary resuscitation in the
delivery room was substantially decreased (53.8%).
PREDILECTION

Male infants born prematurely realized a higher risk of grade

III/IV intraventricular hemorrhage, sepsis, and major surgery
than premature females.
A greater risk of mortality and poorer long-term neurologic
outcome were also noted; however, sex-related differences
for these appeared to lose significance at 27 weeks
gestation.
Female sex is associated with increased rates of survival of
newborns born at 22-25 weeks' gestation.
 Identifiable Causes of Preterm Birth:

FETAL PLACENTAL OTHERS

Fetal distress Placental dysfunction PROM
Multiple gestation Placenta previa Polyhydramnios
Erythroblastosis Placenta abruptio Iatrogenic
Nonimmune hydrops Trauma

UTERINE MATERNAL
Bicornuate uterus Preeclampsia
Incompetent cervix (premature dilatation) Chronic medical illness
COMPLICATIONS OF LATE PRETERM BIRTH

A. Respiratory distress syndrome (RDS).

B. Length of stay.
C. Jaundice.
D. Poor feeding.
E. Temperature instability.
F. Hypoglycemia.
G. SIDS and apnea.
COMPLICATIONS OF PREMATURITY
 NEONATAL PROBLEMS ASSOCIATED WITH
PREMATURITY

RESPIRATORY
Respiratory distress syndrome (due to absence of surfactant)
Bronchopulmonary dysplasia (BPD)
Air leaks
Congenital pneumonia
Pulmonary hypoplasia
Pulmonary haemorrhage
Apnea
NEONATAL PROBLEMS ASSOCIATED WITH
PREMATURITY

HEMATOLOGIC
Anemia
Hyperbilirubinemia
Hemorrhage
Disseminated intravascular coagulation (DIC)
Vitamin K deficiency
Hydrops
NEONATAL PROBLEMS ASSOCIATED WITH
PREMATURITY

CARDIOVASCULAR
Patent ductus arteriosus (PDA)
Hypotension
Hypertension
Bradycardia with apnea
Congenital malformation
NEONATAL PROBLEMS ASSOCIATED WITH
PREMATURITY

GASTROINTESTINAL
Poor motility
Necrotizing enterocolitis (NEC)
Hyperbilirubinemia
Congenital anomalies
Spontaneous GIT isolated perforation
NEONATAL PROBLEMS ASSOCIATED WITH
PREMATURITY

CNS
Retinopathy of prematurity
Intraventricular hemorrhage (ROP)
(IVH)
Deafness
Paraventricular hemorrhage
(PVH) Hypotonia
Hypoxic-ischemic Congenital malformations
encephalopathy (HIE) Kernicterus
Seizures
NEONATAL PROBLEMS ASSOCIATED WITH
PREMATURITY

HEMATOLOGIC
Anemia
Hyperbilirubinemia
Haemorrhage
Disseminated intravascular coagulation (DIC)
Vit K deficiency
Hydrops
NEONATAL PROBLEMS ASSOCIATED WITH
PREMATURITY

RENAL
Hyponatremia
Hypernatremia
Hyperkalemia
Renal tubular acidosis
Renal glycosuria
Infant is prone to electrolyte imbalance
 HISTORY

Dating accurate gestational age by using the mother's history can be

unreliable because of uncertainty of the dates.
About 20% of women have an uncertain last menstrual period (LMP).
Gestational age assessment begins prenatally with obstetric
ultrasonography in the first trimester.
Discovery of many fetal anomalies, unsuspected multiple gestation,
location of the placenta, and an accurate dating of the pregnancy are
additional major benefits of early ultrasonography.
PHYSICAL EXAMINATION

The Ballard Scoring System, revised again to include

extremely low birth weight (ELBW) infants, remains
the main tool clinicians use after delivery to confirm
gestational age by means of physical examination.
The major parts of the anatomy for physical
characteristic markers are ear cartilage, sole
creases, breast tissue, and genitalia.
CRITERIA FOR RAPID GESTATIONAL
ASSESSMENT AT DELIVERY
EAR CARTILAGE
SOLE CREASES
 PHYSICAL EXAMINATION

This examination should be performed immediately after stabilization and

before the expected weight loss occurs on the first day.
Hittner et al reported that regression of the vascularity of the lens capsule is
an excellent tool to confirm a gestational age of 28-34 weeks.
Neurologic criteria include muscle tone of the trunk and extremities and
joint mobility.
Reassessing the neurologic criteria 18-24 hours after birth is best to allow for
recovery from maternal medication (eg, magnesium sulfate, analgesics),
which may decrease tone and responsiveness.
 DELIVERY ROOM MANAGEMENT

Ethics
Discuss the treatment options for the ELBW infant
Counseling should include discussions with the parents regarding survival
rate and both short- and long-term complications based on institutional
statistics and the National Institute of Child Health and Human
Development (NICHD) Neonatal Research Network calculator.
Communication regarding treatment options for the 2224 week
gestation infant is crucial.
THERMOREGULATION.

Apolyethylene wrap or bag.

Thermal-neutral environment in the neonatal
intensive care unit (NICU).
Thermoregulate temp. between 36.5-37.5 C.
 TEMPERATURE AND HUMIDITY CONTROL.

To maintain minimal evaporative heat loss, it is best if the

environmental humidity is 80%.
A.Incubators and hybrid incubators.
ELBW infants should be admitted into prewarmed double-
walled incubators.
 TEMPERATURE AND HUMIDITY CONTROL.

B. Humidification.
ELBW infants : increased insensible water loss secondary to large
body surface area and a greater proportion of body water to
body mass.
Transcutaneous water loss is enhanced by their thin epidermis and
underdeveloped stratum corneum.
Warm humidification within the incubator is recommended.
Double-walled incubators provide the best control for monitoring
humidity levels.
HYPOTHERMIA <36.0 C

If the infants temperature is <36.0C, set the warmer temperature 0.4C higher than
the infants temperature.
Do not rewarm faster than 1C/h.
When skin temperature of 36.5C is achieved, rewarming efforts should be gradually
discontinued and temperature maintenance should be monitored.
Rapid rewarming of ELBW infants must be avoided because core body temperatures
>37.5C cause increased insensible water losses, increased O2 consumption, apneic
episodes, increased incidence of intraventricular hemorrhage, deviations in vital
signs, and a detrimental effect on neurodevelopment.
HYPERTHERMIA >37.0 C

In case of hyperthermia, set the warmer temperature control to 0.4C

lower than the infants skin temperature.
If increased temperature persists, consider evaluation for pathologic
conditions such as sepsis, intraventricular hemorrhage, or mechanical
overheating by exterior lamps.
Do not turn off the warmer, as this may cause a sudden decrease in
the infants temperature.
RESPIRATORY SUPPORT

A. Endotracheal intubation
1. Type of endotracheal tube (ETT).
When possible, use an ETT with 1-cm markings on the side. The internal
diameter (ID) of the tube should routinely be 2.5 or 3.0 mm, according to
body weight:
a. <5001000 g. 2.5 mm ID.
b. 10001250 g. 3.0-mm ID.
RESPIRATORY SUPPORT

2. ETT placement.
Confirm proper placement by a chest radiograph study,
performed with the infants head in the midline position,
noting the marking at the gum. In ELBW infants, the carina
tends to be slightly higher than T4. As a means of
subsequently checking proper tube position, on every shift
the nurse responsible for the infant should check and record
the numbers or letters at the gum line.
RESPIRATORY SUPPORT

B. Mechanical ventilation.
With the advancement of ventilation technology, various
modes are available, including volume ventilation, pressure
support, and high-frequency ventilation. Ventilation applied
appropriately assists the clinician in avoiding overexpansion of
the lung or atelectasis.
CONVENTIONAL VENITILATION

a. Rate. 2060 (usually 30) breaths/min.

b. Inspiratory time. 0.250.35 seconds.
c. Peak inspiratory pressure (PIP). Select
PIP allowing optimal expansion
of lungs.
d. Fio2. As required to maintain O2
saturation 8892%.
e. Flow rate. 68 L/min.
OXYGENATION

It takes 710 minutes for oxyhemoglobin saturations

to rise to 90% after delivery.
The Neonatal Resuscitation Program recommends
availability of pulse oximetry and blended O2 for
resuscitation and low saturation protocol.
OXYGENATION

C. Monitoring respiratory status

1. Blood gas sampling.
Arterial catheterization either through percutaneous arterial
catheterization or for umbilical arterial catheterization should be
performed for frequent blood gas sampling. As the infant becomes
clinically stable, frequency of laboratory testing should be
decreased to minimize blood loss and the need for blood
transfusions.
OXYGENATION

Desirable arterial blood gas values

(a) Pao2. 4560 mm Hg.
(b) Paco2. 4560 mm Hg.
(c) pH. 7.257.32 is acceptable.
OXYGENATION

Abnormal blood gas values. Indicate the need for

assessment including ETT placement, chest wall movement,
effectiveness of ventilation, ventilator malfunction,
assessment for pneumothorax, and need for suction.
Actions may include immediate chest radiographs, chest
wall transillumination and repeat blood gas determinations.
 SUCTIONING

The need for suctioning can be determined with the use of flow-volume
loop monitoring, which can illustrate restricted airflow caused by secretions.
1. Assessment of the need for suctioning.
a. Breath sounds.
b. Blood gas values.
c. Airway monitoring.
d. Visible secretions in the ETT.
e. Loss of chest wall movement.
FLUIDS AND ELECTROLYTES

A. Intravenous fluid
therapy
1. First day of life.
FLUIDS AND ELECTROLYTES

3. Second and subsequent days of life.

Fluid management depends on changes in body
weight, renal function (blood urea nitrogen,
creatinine, urine output), and serum electrolyte
concentrations.
FLUIDS AND ELECTROLYTES

4. Additional fluid may be required if phototherapy is

used. The fluid volume should be increased by 1020
mL/kg/d.
 FLUID & ELECTROLYTES

Monitoring of fluid therapy.

Fluid status - evaluated at least twice daily
Monitored via measurement of body weight,
urine output, blood pressure measurements,
serum sodium, hematocrit, and physical
examination.
 FLUID & ELECTROLYTES

1. Body weight.
The most important method of monitoring fluid therapy.
If an in-bed scale is used, weigh the infant daily.
If unavailable, weighing may be delayed to every 48 hours,
depending on the stability of the tiny infant, to prevent
excessive handling and cold stress.
 FLUIDS & ELECTROLYTES

1. Body weight.
A weight loss of up to 15% of birthweight may be
experienced by the end of the first week of life.
If weight loss is excessive, environmental controls for
insensible fluid losses and fluid management must be
carefully reviewed.
 FLUIDS & ELECTROLYTES

2. Urine output
This is the second most important method of monitoring
fluid therapy.
For greatest accuracy, diapers should be weighed
before use and immediately after urination.
 FLUIDS & ELECTROLYTES

2. Urine output
a. First 12 hours. Any amount of urine output is acceptable.
b. 1224 hours. The minimum acceptable urine output is 0.5
mL/kg/h.
c. Day 2 and beyond. Normal urine output for the second
day is 12 mL/kg/h. After the second day of life, and during
a diuretic phase, urine output may increase to 3.05.0
mL/kg/h; values outside this range warrant reevaluation of
fluid management.
FLUIDS & ELECTROLYTES

Serum electrolyte levels should be

monitored at least twice daily or every 8
hours for the most immature infants.
FLUIDS & ELECTROLYTES

Sodium
Initially tiny infants have a sufficient sodium level (132138
mEq/L), and if there are no ongoing fluid losses, they will
not require additional sodium.
Serum sodium level may begin to decrease in the
postdiuretic phase (usually third to fifth days of life).
Subsequently, sodium chloride should be added to the IV
fluids (38 mEq/kg/d of sodium).
 FLUIDS & ELECTROLYTES

Hyponatremia Na+<130 mEq/L

Hyponatremia in the prediuretic phase usually indicates
fluid overload, and hypernatremia during the same
period usually indicates dehydration.
Differential diagnosis is (a) fluid overload, or (b)
inadequate Na+ intake, or (c) excessive Na+ loss.
 FLUIDS & ELECTROLYTES

Hypernatremia Na+ > 150 mEq/L.

Hypernatremia in the prediuretic phase is due to excessive insensible
water loss. This can be effectively treated with sterile water intragastric
drip. This avoids use of hyposmolar IV fluids. For subsequent monitoring of
the serum sodium levels:
Differential diagnosis is (a) premature addition of sodium in the
prediuretic phase, or (b) dehydration, or (c) excessive Na+ intake.
 FLUIDS & ELECTROLYTES

Potassium
During the first 48 hours after birth. During this time,
tiny infants are prone to increased serum potassium
levels of 5 mEq/L (range, 4.08.0 mEq/L).
 FLUIDS & ELECTROLYTES

Most clinicians recommend that no potassium be given during

the prediuretic phase. The increase is mostly a result of the
following:
(a) Relative hypoaldosteronism
(b) Shift of intracellular potassium to the extracellular space due to an
immature Na+, K+-ATPase pump
(c) Immature renal tubular function
(d) Lack of arginine, a precursor to insulin
FLUIDS & ELECTROLYTES

POTASSIUM
K+ >6 mEq/L mandates close ECG monitoring
T-wave changes and rhythm disturbances
along with electrolyte trends, acid-base
status, and urine output.
FLUIDS & ELECTROLYTES

Acidosis should be aggressively treated because

this tends to cause intracellular potassium to leak
out. Use of Kayexalate enemas is controversial in
this age group and best avoided if possible.
Albuterol metered-dose inhaler (MDI) (4 puffs every
2 hours; treated with insulin, NaHCO3, and calcium
gluconate
FLUIDS & ELECTROLYTES

36 days after birth. Usually by this time, the initially

elevated K+ level begins to decrease. When K+
levels approach 4 mEq/L, add supplemental K+ to IV
fluids. Begin with 12 mEq/kg/d. Measure serum K+
every 612 hours until the level is stabilized
 FLUIDS & ELECTROLYTES

Calcium.
Serum calcium should be monitored daily. Hypocalcemia
in preterm infants is a serum calcium <6 mg/dL.
Asymptomatic hypocalcemia is not treated with
additional calcium because it resolves with time.
Symptomatic hypocalcemia is treated with calcium salt.
This decrease usually happens on the second day of life.
 HEMODYNAMIC MONITORING

This is a valuable tool in assessing fluid status in the infant.

a. Heart rate.
Normal Limits: 140160 beats/min
Tachycardia, with a heart rate >160 beats/min, may be a sign of
hypovolemia, pain, inadequate ventilation, anemia, sepsis, or
hyperthermia.
Low heart rate (<100 beats/min) may be related to hypoxia or
medication.
 HEMODYNAMIC MONITORING

b. Arterial blood pressure.

This is most accurately measured via an indwelling arterial catheter and
transducer.
Cuff pressures are difficult to obtain because of the infants small size and
lower systemic pressures.
Maintain the infants mean arterial pressure at or equal to the gestational
age during the first 48 hours. Thereafter, mean blood pressure increases with
chronological age.
It is important to evaluate the infants perfusion, urine output, and acid-base
balance in conjunction with blood pressure monitoring.
 BLOOD GLUCOSE

ELBW infants should be supported with 46 mg/kg/min glucose

infusion.
Start with a 510% dextrose solution, depending on glucose
needs.
Amino acid used immediately after birth along with glucose
solutions achieves better glucose homeostasis. Bedside
glucose levels should be monitored frequently until a blood
glucose level of 5090 mg/dL has been established. Abnormal
values should be confirmed with serum glucose.
 BLOOD GLUCOSE

A. Hypoglycemia is <40 mg/dL for first 48 hours, thereafter < 50

mg/dL.
It may occur because of an inadequate glucose infusion rate or
a physiologic lack of glycogen stores. Additionally, pathologic
states such as sepsis, cold stress, or hyperinsulinemia need to be
considered.
 BLOOD GLUCOSE

B. Hyperglycemia >150 mg/dL.

This can cause osmotic glycosuria, resulting in excessive fluid loss.
Hyperglycemia may be secondary to increased glucose infusion rate or
pathologic causes such as sepsis, necrotizing enterocolitis (NEC),
intraventricular hemorrhage (IVH), or a stress response.
Treatment with insulin infusion is controversial. An alternative is to
decrease the glucose infusion rate (GIR); maintaining glucose infusion
as low as 1.5 mg/kg/min has been demonstrated to provide adequate
glucose for cerebral metabolism while not affecting proteolysis and
protein turnover.
RESPIRATORY DISTRESS SYNDROME - HMD
HYALINE MEMBRANE DISEASE

Currently termed as Respiratory Distress Syndrome

Commonly cause of morbidity and mortality associated with
premature delivery.
Incidence and severity generally increase with decreasing
gestational age at birth and are usually worse in male infants.
Infants born to mothers with co-morbidities
 DEFINITION

The Vermont Oxford Network definition for RDS requires

that babies have:
A.An arterial oxygen tension (Pao2) <50 mm Hg and
central cyanosis
B.A characteristic chest radiographic appearance
STAGES OF LUNG DEVELOPMENT

Embryonic stage - period between day 26, when

the lung bud first develops from the foregut, and
the next 7 weeks
Pseudoglandular stage - persists from 5 to 17
weeks of gestation and results in the formation of
20 of the 24 generations of airways lined by
glycogen-rich columnar epithelial cells
 STAGES OF LUNG DEVELOPMENT

Canalicular stage - marks the appearance of the pulmonary

acinus, abundant capillaries, and differentiation of airway
epithelial cells. This stage lasts from week 16 to week 26. By the
end of this period, a thinned epithelium provides marginal gas-
exchange capability allowing postnatal survival.
Terminal saccular stage - occurs from week 24 until term.
During this time, the peripheral airways widen into saccules,
forming the precursor of alveoli.
STAGES OF LUNG DEVELOPMENT

Alveolar stage - begins at approximately 36 weeks and

continues postnatally until about 18 months of age. In this
stage, low ridges protrude into the lumina of the saccules.
 METABOLISM OF
SURFACTANT
The components of pulmonary surfactant
are synthesized in the Golgi apparatus of
type II alveolar cells. Its production is
regulated by different hormones and
growth factor as glucocorticoids, insulin,
prolactin, thyroxine and trasforming growth
factor beta (TGF-). Its production
generally starts around the 24th to the 28th
week of pregnancy, and surfactant is
found in amniotic fluid between 28 and 32
weeks. By about 35 weeks of gestation,
most babies have developed adequate
amounts of surfactant.
 BASIC PATHWAYS FOR
SURFACTANT METABOLISM

synthesized in type II cells

stored in lamellar bodies
secreted into the alveoli where it forms a surface film
cleared from the airspaces by macrophages for catabolism or
taken back into type II cells where it is reprocessed and
resecreted, a recycling pathway
SURFACTANT FORMATION AND PHYSIOLOGY

Surfactant is a complex lipoprotein composed of 6

phospholipids and 4 apoproteins.
Surfactant recovered by alveolar wash from most mammals
contains:
1. 70- 80% phospholipids (DPPC, DDPG)
2. 8-10% protein
3. 10% neutral lipids, primarily cholesterol
Dipalmitoylphosphatidylcholine
(DPPC), or lecithin (50%), is
functionally the principle
phospholipid. About 1% of the
10% protein component
comprisessurfactant
apoproteins; the remaining
proteins are derived from
alveolar exudate.
SURFACTANT APOPROTEINS

1. SP-A is an innate host defense, hydrophilic lectin

coded on human chromosome 10 that regulates lung
inflammation. SP-A contributes to the biophysical
properties of surfactant primarily by decreasing protein-
mediated inhibition of surfactant function. SP-A facilitates
phagocytosis of pathogens by macrophages and their
clearance from the airways.
SURFACTANT APOPROTEINS

2. SP-B gene is localized on human chromosome 2,

and its primary translation product is 40 kd, which is
clipped to become an 8-kd protein in type II cells
before entering lamellar bodies to be co-secreted
with phospholipids.
 SURFACTANT APOPROTEINS

3. SP-C gene is on chromosome 8; its primary

translation product, 22 kd, is processed to an
extremely hydrophobic 4-kd protein that is
associated with lipids in lamellar bodies.
 SURFACTANT APOPROTEINS

4. SP-D is also a hydrophilic protein of 43 kd that is a

collectin with structural similarities to SP-A. SP-D is a
large multimer that is synthesized by type II alveolar
cells and Clara cells, in addition to other epithelial
cells in the body. It also binds pathogens and
facilitates their clearance.
 FUNCTIONS OF SURFACTANT

Reduce surface tension

smaller pressures for subsequent breaths
Maintain alveolar stability (surfactant lines the alveolar
cavity)
radius of cylindrical terminal bronchioles remain
enlarged
Preventing collapse of small air spaces at end expiration
EFFECT OF ABSENCE OF SURFACTANT

Failure of FRC to develop

Tendency of affected lungs to become
atelectatic
High surface tension
VOLUME - PRESSURE CURVE
PATHOLOGICAL FEATURES IN HYALINE
MEMBRANE DISEASE

Grossly, the lungs are

reduced in volume and
show a solid or liver-like
consistency. The neonatal
lungs appear congested,
with marked atelectasis.
 COMPLICATIONS

Major complications of RDS of the neonate, frequently observed at

autopsy, are:
intraventricular cerebral hemorrhage;
persistence of the patent ductus arteriosus;
necrotizing enterocolitis (NEC);
retinopathy of prematurity (ROP) or retrolental fibroplasia (RLF);
bronchopulmonary dysplasia (BPD).
DIFFERENTIAL DIAGNOSIS

meconium aspiration
neonatal pneumonia
pulmonary edema and hemorrhage
 CLINICAL PRESENTATION

History

The infant is often preterm or has a history of asphyxia in the

perinatal period. Infants have some respiratory difficulty at birth,
which becomes progressively more severe. The classic worsening
of the atelectasis seen on chest radiograph and increasing
oxygen requirement for these infants have been greatly modified
by the availability of exogenous surfactant therapy and effective
mechanical ventilator support.
CLINICAL MANIFESTATIONS

Appear within minutes of birth may not be recognized

for several hours in larger preterm
Tachypnea (>60 breaths/min), nasal flaring, subcostal
and intercostal retractions, cyanosis & expiratory
grunting
Breath sounds may be normal or diminished and fine
rales may be heard
CLINICAL MANIFESTATIONS

Progressive worsening of cyanosis & dyspnea. BP may

fall; fatigue, cyanosis and pallor increase & grunting
decreases.
Apnea and irregular respirations are ominous signs
In most cases, symptoms and signs reach a peak within
3 days, after which improvement occurs gradually.
CHEST X-RAY:

Findings can be graded according to the severity

Grade 1
Grade 2
Grade 3
Grade 4
HMD Grade 1

Grade 1 (mild cases):

The lungs show fine
homogenous ground
glass shadowing
HMD Grade 2

Grade 2:
Widespread air
bronchogram become
visible
HMD Grade 3

Grade 3:
Confluent alveolar
shadowing
HMD Grade 4

Grade 4:
Complete white lung
fields with obscuring of
the cardiac shadow
 MANAGEMENT

Prevention:
Lung maturity testing: lecithin/sphingomyelin (L/S) ratio
Tocolytics to inhibit premature labor.
Antenatal corticosteroid therapy:
 MANAGEMENT

Antenatal corticosteroid therapy:

They induce surfactant production and accelerate fetal lung
maturation.
Are indicated in pregnant women 24-34 weeks' gestation at high risk of
preterm delivery within the next 7 days.
Optimal benefit begins 24 hrs after initiation of therapy and lasts seven
days.
MANAGEMENT

Antenatal corticosteroid therapy consists

of either :
Betamethasone 12 mg/dose IM for 2 doses, 24 hrs apart,
or
Dexamethasone 6 mg/dose IM for 4 doses, 12 hrs apart
PREVENTION

Early surfactant therapy: prophylactic use of

surfactant in preterm newborn <27 weeks' gestation.
Early CPAP administration in the delivery room.
 TREATMENT

Administer oxygen
Initiate CPAP as early as possible in infants with mild RDS
Start MV if respiratory acidosis (PaCO2 >60 mmHg, PaO2 <50
mmHg or SaO2 <90%) with an FiO2 >0.5, or severe frequent
apnea.
Administer surfactant therapy: early rescue therapy within 2 hrs
after birth is better than late rescue treatment when the full
picture of RDS is evident.
 SURFACTANT THERAPY FOR RDS

Improvement in compliance, functional residual

capacity, and oxygenation
Reduces incidence of air leaks
Decreases mortality

110
 TYPES OF SURFACTANT

Natural Surfactants: contain appoproteins SP-B & SP-C

Curosurf (extract of pig lung mince)
Survanta (extract of cow lung mince)
Infasurf (extract of calf lung)

Synthetic Surfactants:do not contain proteins

Exocerf
ALEC
Lucinactant (Surfaxin)
 Mode of administration of Surfactant

Dosing may be divided

into 2 alliquots and
adminitered via a 5-Fr
catheter passed in the
ET.
Thank you!