Neonatal Respiratory Distress Syndrome (NRDS), also known as hyaline membrane disease (HMD), is caused primarily by a lack of pulmonary surfactant in premature infants. This leads to respiratory distress within hours after birth. The condition is characterized by rapid breathing, nasal flaring, and chest retractions. Treatment involves surfactant replacement therapy, respiratory support through CPAP or mechanical ventilation, maintaining proper acid-base balance and temperature control, and preventing infections. While treatment has improved survival rates, complications remain common in severe cases of NRDS.

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Neonatal Respiratory
Distress Syndrome, NRDS
(hyaline membrane disease, HMD)

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Aims
 To master the clinical manifestation and
treatment principles
 To understand the cause and
Pathogenesis
 To understand the differential diagnosis

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 Most common respiratory illness in NICU
 Primarily characterized by respiratory
distress
 Occur virtually exclusively in premature
neonate
 The shorter the gestational age and the
lower birth weight, the higher incidence,
the less likely survival.
High Spot

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Most infants with the disease die
from a complication , such as
 intracranial hemorrhage
 infection
 air leak syndromes
 bronchopulmonary dysplasia

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Etiology
 The main cause:
Pulmonary Surfactant (PS) Deficiency

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 lowers the surface
tension of the
alveolar membrane.
 maintains patent
distal lung units at
low volumes during
expiration.
 Increase in lung
compliance.
The Actions of pulmonary Surfactant:
normal abnormal
end expiratory

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Phosphatidylcholine (75%)
Phosphatidylglycerol (9%)
Apoproteins (13%)
Cholesterol
Pulmonary Surfactant
Constituent:

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Pulmonary Surfactant
 PS is produced by alveolar type Ⅱcells
 At 24thweeks : begin to increase progressively
with advancing gestational age
 At 34th-36thweeks : large increase

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The other factors
 Genetic factors: white race, history of
RDS in sibling, male sex.
severe RDS---can not be cured----die
 Hormones factors
(adrenergic and steroid hormones can
promote PS production and release )
elective cesarean section

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 Without surfactant the alveoli collapse at
the end of expiration.
 Pulmonary hypertension
So, absence of surfactant cause hypoxia,
acidosis, blood vessel contract , capillary vessel
and alveolus osmosis increase, blood plasma
leak, transparent membrane come into being,
dyspnea, RDS
Pathogenesis

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absence of surfactant hypoxia,
acidosis blood vessel contract
capillary vessel and alveolus osmosis
increase blood plasma leak
transparent membrane come into
being dyspnea.
So, absence of surfactant cause NRDS

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 This in turn leads to respiratory
failure .
 In older infants surfactant
deficiency can arise when they
develop asphyxia 、 shock and
acidosis.

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Pathology
 Generalized capillary leak and mucosal
necrosis leads to the small air filled
terminal airways.
 The respiratory bronchioles and alveolar
ducts, being surrounded by collapsed
alveoli filled with debris in a near
uniform distribution, and this leads to the
classic "ground glass" appearance on the
chest X-ray.

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 The NRDS affects the lung which is
not mature at delivery.
 Signs of respiratory distress appear
in 2-6hr after birth.
 Many of the patients appear signs
within minutes of birth---shallow
respirations are more than 60/min .
Sign

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 Infants have physical findings of
prematurity and present with
inspiratory supraclavicular ,
suprasternal and intercostals
retractions (three depression signs)

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Clinical Manifestations
 Tachypnea ( increasingly )
supraclavicular
 Three depression suprasternal
signs
intercostals
 Expiratory grunting (groan)
 Cyanosis
 Nasal flaring
 Apneic episode

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 progressing to a paradoxical seesaw
respiratory pattern in which the chest
sinks is on inspiration as the abdomen
balloons upward.
 Expiratory grunting, tachypnea, flaring
of the Nasal ala and requirement for
oxygen completes the clinical picture.

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 As the infant’s energy reserves
become depleted, there may be
cessation of grunting.

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 Hypoperfusion and poor capillary
filling may progress to hypotension
and shock unless intervention is
aggressive.
 In most cases, the signs and
symptoms may reach a peak within
3 days, followed by gradual
resolution over the next 5-7days.

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 If the condition is inadequately
treated, blood pressure and body
temperature may fall.
 Death is rare on the first day, usually
occurs between days 2-7.

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Complications
Complications of NRDS include
 infections (Sepsis)
 intracranial hemorrhage
 hyperbilirubinemia

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Complications
 PDA
 Cardiac failure caused by a left-to-
right shunt through a patent ductus
arteriosus.
 Pneumothorax
 Chronic lung disease

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Laboratory examination
1. Chest X-ray :
 changes usually appear shortly after
birth, but can be delayed for 12-24 hours.
The typical pattern at 6-12 hour.
 Ground glass appearance
 Air bronchograms
 White lung

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Ground glass

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Air bronchograms

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White lung

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 2. Gastric aspirate shake (Foam test):
Put 1ml gastric fluid and 1ml 95%
alcohol into a tube, shake 15 seconds
and keep still 15 minutes. If there is
foam around the wall of the tube, it is
positive. If not--negative.

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 3. Test of PS:
Test amniotic fluid or tracheal fluid
for lecithin / sphingomyelin. L/S ≥2
denotes mature lung, L/S ＜1.5
denotes immature lung, between 1.5
and 2 denotes doubtful.

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Acid base In NRDS
 pH
 PaCO2
 PaO2
 HCO3
-
 BE deficit

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Diagnosis Process
1. History of premature
2. Clinical signs: Respiratory distress
3. X-ray : ground glass , Air
bronchograms
4. Gastric aspirate shake: Negative
5. Blood gas and acid-base values:
hypoxemia, hypercarbia and metabolic acidosis.

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Differential Diagnosis of NRDS
1. GBS Infection pneumonia (Congenital pneumonia)
– Pneumonia causes by group B streptococcus (GBS).
Same signs of NRDS .
– The chest X-ray may be identical in both diseases.
The onset and the manifestations of respiratory
distress are often indistinguishable. Apnea in the
first few hours is more likely in GBS pneumonia.
– Bacterial culture

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 Sepsis risk factors
– Maternal fever, cough
– Leukocytosis or leukopenia with
neutropenia strongly suggests the presence
of GBS infection.
– Sometimes GBS can be found in gastric
fluid.

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2.Wet Lung
Usually lung fluid is cleared from the interstitial
space veins and lymphatics within 30 minutes
after birth.
Chest X-ray, usually has non-homogeneous
densities, may have interlobar effusion .
Clinical manifestations appear within several
hours after birth, but are milder than HMD.

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Lung
fluid
air
First breath Second btreath 30min later
Lung fluid clear away

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3.Meconium aspiration
 Common in full term infant or postterm infant
 Gasping cause is the aspiration
 Chemical diffuse pneumonitis
 Chest X-ray, patchy areas of decreased aeration
alternating with hyperventilation areas
 Treatment mainly supportive

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Treatment Principle
 Surfactant …1990s
– Prevention (100mg/Kg)
– Rescue (200mg/Kg)
 Supportive
– Thermal
– Fluid and nutrition
– oxygen
 Mechanical ventilation

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Therapy
1. General Comments
Therapy of hyaline membrane
disease (HMD) is complex.
Major responsibility befalls nurses.
Blood gases and pH should be check
according to necessary.

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2.Surfactant Replacement
Endotracheal instillation of surfactant
replacement has dramatically improved
survival and reduced the incidence of
pulmonary air leaks.
100-200mg/kg drop in bronchi of both sides 2-
4 times.
Curosurf (irrigating solution of piggy lung)
Calsurf (irrigating solution of calf lung)

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3. Other treatment
1) Respiratory Support
a. Nasal oxygen catheter (Flow: 0.5-1L/min)
Warm humidified oxygen should be provided
to maintain :
 PaO2 between 50 and 70 mmHg
 pH above 7.25
 PaCO2 between 45 and 50 mmHg.

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 b. CPAP(Continuos Positive Airway
Pressure ):
PEEP (positive end-expiratory pressure) :
4-10cm H2O.
rhinobyon
Air and
o2mixer
4-10cmH2O

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b. Mechanical ventilation : After CPAP (FiO2>60%),
if PaO2<6.7Kpa (50mmHg) or PaCO2>7.9Kpa
(60mmHg), ventilation should be used.
 SIPPV (Synchronized Intermittent Positive
Pressure Ventilation )
 SIMV (Synchronized Intermittent Mandatory
Ventilation )

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2) Acid-base Balance
– A metabolic acidosis can be prevented
by adding a small quantity of sodium
bicarbonate.
– Formula
 5% NaHCO3 3- 5ml/kg, one time, IV
 5%NaHCO3 (mmol) = -BE ×0.3× kg
 5%NaHCO3 (ml) = -BE × 0.5 × kg

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3) Keep Body Temperature
Maintenance of a neutral thermal
environment ( skin temperature
between 36.2-36.8℃) is of crucial
importance.

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4) Nutrition
– During the first 24 to 48 hours, caloric
needs are partially met by continuous
intravenous infusion. volumes are 60-80
ml/kg/d.
– Ensure that the blood sugar is maintained
within a normal range(＞2.5mmol/L).
– If bowel sounds are audible and meconium
has been passed, the milk should be fed.

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5) Antibiotic can be used to prevent
infection of lung.

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Preventive measures
1. Prevent Premature Deliveries.
Including :
 avoidance of unnecessary or pool timed
cesarean section
 appropriate management of high-risk
pregnancy and labor
 prediction possible in uterus acceleration
of pulmonary immaturity.

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2. Administration of Corticosteroids
There is good evidence that the
administration of corticosteroids to
mothers who are in premature labor to
diminish the incidence of NRDS. Their
effect is maximal at gestational ages
between 28 and 32 weeks. Steroids should
be administered between 24 hours and
7days before delivery.

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Thanks !