RESPIRATORY DISTRESS SYNDROME, PREVIOUSLY HYALINE MEMBRANE DISEASE IS A COMMON COMPLICATION OF PREMATURITY WITH MORTALITY ALMOST 100% IN THE ABSENCE OF PULMONARY SURFACTANT ADMINISTRATION, ESPECIALLY IN LOW RESOURCE SETTINGS LIKE OURS.

1. RESPIRATORY DISTRESS
SYNDROME.
DR.ODONG RICHARD JUSTIN.
DEPARTMENT OF PAEDIATRICS.

2. DEFINITION.
 Respiratory distress syndrome(RDS) was
previously called hyaline membrane disease.
 The Vermont Oxford Network definition for RDS
requires that babies have:
 AN ARTERIAL OXGYEN TENSION(PaO2) <
50mmHg and CENTRAL CYANOSIS.
 A CHARACTERISTIC CHEST RADIOGRAPHIC
APPEARANCE.

3. AN ARTERIAL OXGYEN TENSION(PAO2) <
50MMHG AND CENTRAL CYANOSIS.
 Must be in room air.
 Requirement for supplemental oxygen to maintain
PaO2 > 50mmHg.
 Requirement for supplemental oxygen to maintain a
pulse oximeter saturation over 85%.

4. A CHARACTERISTIC CHEST
RADIOGRAPHIC APPEARANCE.
 Uniform reticulogranular pattern to lung fields with
or without low lung volumes and air bronchogram
within the first 24 hours of life.
 The clinical course of the disease varies with the
size of the infant, severity of disease, use of
surfactant replacement therapy, presence of
infection and degree of shunting of blood through
PDAs.

5. INCIDENCE.
 The incidence of RDS is as follows:
 91% at 23-25 weeks of gestation.
 88% at 26-27 weeks of gestation.
 74% at 28-29 weeks of gestation.
 52% at 30-31 weeks of gestation.

6.  The incidence and severity of RDS are expected to
decrease after the increase in use of antenatal
steroids in recent years.
 After the introduction of exogenous surfactant the
survival from RDS is at > 90%.
 During the surfactant era, RDS accounts for < 6%
of all neonatal death.

7. PATHOPHYSIOLOGY.
 Surfactant deficiency is the major cause of RDS,
often complicated by an overly compliant chest
wall.
 Both factors lead to progressive atlectasis and
failure to develop an effective functional residual
capacity.
 Surfactant is a surface active material produced by
airway epithelial cells called TYPE II
PNEUMOCYTES.
 This cell line differentiate and surfactant synthesis
begins at 24-28 weeks of gestation.

8.  Type II cells are sensitive to and decreased by
asphyxial insults in the perinatal period.
 The maturation of this cell line is delayed in the
presence of hyperinsulinemia.
 The maturity of Type II cells is enhanced by the
administration of antenatal corticosteroids and by
chronic intrauterine stress such as pregnancy
induced hypertension, intrauterine growth restriction
and twin gestation.

9. COMPOSITION OF SURFACTANT.
 Phospholipid (75%).
 Proteins (10%).
 This is produced and stored in characteristic
lamellar bodies of type II pneumocytes.
 This lipoprotein is released into the airways, where
it functions to decrease surface tension and
maintain alveolar expansion at physiological
pressure.

10. SURFACE TENSION.
 Law of Laplace as applied to alveoli.
P = 2 t / r where
P= Transpulmonary pressure.
R= Radius of an alveolus.
T= Tension in the wall of the alveolus.
Pulmonary surfactant reduces the surface tension
even at low volumes leading to a reduction in the
required pressure and maintaining alveolar stability.

11. LACK OF SURFACTANT:
 In the absence of surfactant the small airspaces
collapse.
 Each expiration results in progressive atelectasis.
PRESENCE OF AN OVERLY COMPLIANT CHEST
WALL:
 In the presence of a chest wall with weak structural
support secondary to prematurity, the large
negative pressures generated to open the
collapsed airways cause retraction and deformation
of the chest wall instead of inflation of the poorly
compliant lung.

12. DECREASED INTRATHORACIC PRESSURE:
 The infant with RDS who is < 30 weeks gestational age
often has immediate respiratory failure because of an
inability to generate the intrathoracic pressure
necessary to inflate the lungs without surfactant.
SHUNTING:
 The presence or absence of cardiovascular shunt
through a PDA or foramen ovale or both may change
the presentation or course of the disease process.
 Unfortunately this usually occurs when the infant is
starting to recover from RDS and can be aggreviated by
surfactant replacement.

13. RISK FACTORS THAT INCREASE OR DECREASE
RISK OF RDS.
INCREASE:
 Prematurity.
 Male sex.
 Familial predisposition.
 Cesarean delivery without labor.
 Perinatal asphyxia.
 Multiple gestation.
 Maternal diabetes.

14. DECREASE:
 Prolonged rupture of membranes.
 Female sex.
 Vaginal delivery.
 Narcotic/ cocaine use.
 Corticosteroids.
 Thyroid hormone.
 Tocolytic agents.

15. CLINICAL PRESENTATION.
HISTORY:
 Preterm, asphyxia in perinatal period, respiratory
difficulty at birth becoming progressively more
severe.
 Classic worsening of atlectasis seen on chest
radiograph.
PHYSICAL EXAMINATION:
 Tachypnea, grunting, nasal flaring, and retractions
of the chest wall, may have cyanosis.

16. DIAGNOSIS.
CHEST RADIOGRAPH:
 Reticulogranular pattern, reffered to as a ground-
glass appearance, accompanied by a peripheral air
bronchograms.
LABORATORY STUDIES:
 Blood gas sampling.
 Sepsis workup.
 Serum glucose levels.
 Serum electrolyte levels and calcium.

18. ECHOCARDIOGRAPHY:
 A valuable diagnostic tool in the evaluation of an
infant with hypoxemia and respiratory distress.
 Congenital heart disease can be excluded by this
technique.

19. MANAGEMENT.
PREVENTION.
ANTENATAL CORTICOSTEROIDS:
 A single course of antenatal steroids is
recommended between 24 and 34 weeks of
gestation to all women at risk of preterm delivery
within 7 days.
PREVENTIVE MEASURES:
 Antenatal ultrasonography for age assement.
 Continuous fetal monitoring during labor.
 Tocolytic agents.
 Assesment of lung maturity before delivery.

20. SURFACTANT REPLACEMENT.
 Standard care of intubated infants with RDS.
 Prophylactic surfactant to infants born at less than
31 weeks of gestation.
 Prophylaxis should also be given to all preterm
infants with RDS who require delivery room
intubation for stabilization.

21. RESPIRATORY SUPPORT.
 Endotracheal intubation and mechanical ventilation:
In apnea or hypoxemia with respiratory acidosis.
 Continuous positive airway pressure(CPAP) and
nasal synchronized intermittent mandatory
ventilation.
 Humidified high-flow nasal cannula system.

22.  Fluid and nutritional support.
 Antibiotic therapy: Should cover most common
neonatal infections are usually began initially.
SEDATION:
 Commonly used to control ventilation in these sick
infants. But there is significant controversy
surrounding such treatment.

23. OUTCOME.
 Although the survival of infants with RDS has
improved greatly, the survival with or without
respiratory and neurological sequelae is highly
dependent on birth weight and gestational age.
 Major morbidity and poor postnatal growth remain
high for the smallest infants.

24. SUMMARY.
 Respiratory distress syndrome is a common
respiratory condition in premature.
 The incidence decreases with increase in
gestational age.
 Surfactant deficiency is the primary cause of RDS.
 The incidence is expected to reduce after increased
use of antenatal steroids.
 With exogenous surfactant, the survival from RDS
is more than 90%.
 In the surfactant era, RDS accounts for less than
6% of all neonatal death.