INFANT RESPIRATORY

DISTRESS SYNDROME
MIHAI CRAIU MD PhD

TERMINOLOGY
Hyaline membrane disease;
Infant respiratory distress syndrome
(IRDS);
Respiratory distress syndrome in infants;
RDS - infants

IRDS
Syndrome caused in
premature infants by
developmental
insufficiency of
surfactant production
and structural
immaturity in the
lungs.

IRDS
It can also result from a genetic problem
with the production of surfactant
associated proteins.
RDS affects about 1% of newborn infants
and is the leading cause of death in
preterm infants.

CRONOLOGY
The earlier a baby is born, the less
developed the lungs are and the higher
the chance of IRDS.
Most cases are seen in babies born
before 28 weeks.
It is very uncommon in infants born fullterm (at 40 weeks).

INCIDENCE 1
Frequency increases as gestational age
decreases:

GA < 30 weeks ~ 60%

GA 30 34 weeks ~ 25%
GA > 34 weeks ~ 5%
Term newborn << 1%

INCIDENCE 2
Frequency decreases with ante-partum
steroid treatment :

GA < 30 weeks ~ 35%

GA 30 34 weeks ~ 10%
GA > 34 weeks ~ 1%
Term newborn virtually no cases

SURFACTANT 1
The lungs of infants with respiratory
distress syndrome are developmentally
deficient in surfactant.
Surfactant is a complex system of
lipids, proteins and glyco-proteins which
are produced in specialized lung cells
called Type II cells or Type II
pneumocytes.

SURFACTANT 2
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.

SURFACTANT 3
Surfactant helps prevent collapse of the
terminal air-spaces throughout the
normal cycle of inhalation and exhalation.
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.

HYALINE MEMBRANE

HYALINE MEMBRANE

RISK FACTORS FOR IRDS

Prematurity (most frequent)
A brother or sister who had RDS
Diabetes in the mother
Cesarean delivery
Delivery complications that lead to
acidosis in the newborn at birth
Multiple pregnancy (twins or more)
Rapid labor

PROTECTIVE FACTORS FOR IRDS

Maternal prenatal stress
High BP
Toxemia

Maternal infection before birth

Intrauterine failure to thrive
Steroid treatment before labor

CLINICAL COURSE 1
Newborn has one or more of the physical
signs of respiratory distress
Tachypnoea
Chest retractions
Cyanosis
Grunting
Flaring of ala nasi
Thoraco-abdominal balance
Bobbing of the head

Tachypnoea & Chest retractions

Bobbing of the head

Flaring of ala nasi (nostrils)

CLINICAL COURSE 2
As the disease progresses, the baby may
develop
ventilatory failure (rising carbon dioxide
concentrations in the blood),
prolonged cessations of breathing ("apnea")

Whether treated or not, the clinical

course for the acute disease lasts about
2 to 3 days.

CLINICAL COURSE 3
During the first, the patient worsens
and requires more support.
During the second the baby may be
remarkably stable on adequate support
Usually resolution is noted during the
third-fourth day, heralded by a prompt
diuresis.
By day 7 complete resolution.

PREVENTION 1
Most cases of hyaline membrane disease
can be ameliorated or prevented if
mothers who are about to deliver
prematurely can be given glucocorticoids.
This speeds the production of
surfactant.
For very premature deliveries, a
glucocorticoid is given without testing
the fetal lung maturity.

PREVENTION 2
In pregnancies of greater than 30 weeks,
the fetal lung maturity may be tested by
sampling the amount of surfactant in the
amniotic fluid, obtained by amniocenthesis.
Several tests are available that correlate
with the production of surfactant.
The lecithin-sphingomyelin ratio ("L/S ratio"),
The presence of phosphatidol-glycerol (PG),
The surfactant/albumin (S/A) ratio.

PREVENTION 3
The lecithin-sphingomyelin ratio ("L/S ratio"),
if the result is less than 2:1, the fetal lungs may be
surfactant deficient.

The presence of phosphatidol-glycerol (PG),

The presence of PG usually indicates fetal lung maturity.

The surfactant/albumin (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,
>55 indicates mature surfactant production (correlates with
an L/S ratio of 2.2 or greater).

RADIOLOGY 1
Typically, diffuse groundglass opacification of both
lungs with air bronchograms
and hypoaeration
Fine granular pattern
Prominent air bronchograms
Bilateral and symmetrical
distribution

RADIOLOGY 2

Hypoaeration from loss of lung volume (may

be counteracted by respiratory therapy)

DIFFERENTIALS

RDS
Transient Tachypnea
Meconium aspiration
Other aspiration sy (milk,
amniotic fluid)
Pneumothorax
Pneumonia
Pulmonary hemorrhage
Atelectasis
Lung anomalies (cysts,
sequestration, adenomat m)

Diaphragmatic hernia
Choanal atresia
Congenit heart defects
Cardiac failure
Myocarditis
Persistent foetal circulation
Polycythemia
Anemia
Septicaemia / meningitis
Drugs to mother in labour

TREATMENT 1
Oxygen is given with a
small amount of
continuous positive
airway pressure
("CPAP").
Intravenous fluids are
administered to
stabilize the blood
sugar, blood salts, and
blood pressure.

TREATMENT 2
If the baby's condition
worsens, an endotracheal
tube (ET tube) is inserted
into the trachea and
intermittent breaths are
given by a mechanical device
(conventional of HF
ventilator).
In extreme cases ECMO

TREATMENT 3

Such small premature

infants may remain
ventilated for months.

TREATMENT 4
An exogenous preparation of surfactant,
either synthetic or extracted from
animal lungs, can be given through the ET
tube into the lungs.

TREATMENT 5
Commonly used surfactants are
SURVANTA derived from bovine lung
CUROSURF derived from porcine lung
EXOSURF artificial, from human lung

Dose:
100 mg/kg for natural surfactant
25-100 mg/kg for artificial surfactant

COMPLICATIONS 1
The mortality rate for
babies greater than 27
weeks gestation is less
than 10% in USA.
The disease is frequently
complicated by
prematurity-related comorbid diseases.

COMPLICATIONS 2
Complications include:
metabolic disorders
(acidosis, low blood sugar),
patent ductus arteriosus,
low blood pressure,
pulmonary hypertension
chronic lung changes,
intracranial hemorrhage,
alveolar hemorrhage

MECHANICAL
COMPLICATIONS

Surfactant decreases
PTX rate with 60% and death rate by 30-40%

PNEUMOTHORAX

CHRONIC COMPLICATIONS 1
Lobar emphysema
Localized interstitial
emphysema
Recurrent respiratory
tract infections

CHRONIC COMPLICATIONS 2
Rethinopathy of
prematurity (Retrolental
fibroplasia )- ROP
Subglottic stenosis from
intubation
Failure to thrive

CONCLUSSION
IRDS is caused in premature infants by
insufficiency of surfactant production.
Prenatal treatment with steroids
Postnatal treatment with surfactant
Ventilatory support is crucial
First week is crucial for survival
Sequelae : ROP, BDP, hiperreactive airway