RESPIRATORY DISTRESS

SYNDROME: NEWBORN
 Newborn respiratory distress syndrome (NRDS)
happens when a baby's lungs are not fully developed
and cannot provide enough oxygen, causing breathing
difficulties. It usually affects premature babies.
 It's also known as infant respiratory distress
syndrome, hyaline membrane disease or surfactant
deficiency lung disease.
 The primary cause of RDS is inadequate pulmonary
surfactant. The structurally immature and surfactant-deficient lung has ↓
compliance and a tendency to atelectasis;
SURFACTANT (ANTI SURFACE TENSION)

SURFACE TENSION IS A FORCE BETWEEN THE MOLECULES OF WATER, CAN CAUSE COLLAPSE
OF THE LUNG(DECREASE COMPLIANCE)
SURFACTANT
 Produced by type second(2) pneumocytes
 Made of phospholipids and some proteins
1)phosphatidylcholine(lecithine),
2) phosphatidylglycerol
Synthesis of surfactant starts in the 28 th week of gestation
Premature baby -> less surfactant->more surface tension-> more risk of collapse
Surfactant production is stimulated by:
1)cortisol
2)thyroxin
3)prolactin
Surfactant production is inhibited by:
1)insulin(diabetic mother)
 Greater risk factors:
 siblings that had RDS
 twin or multiple births
 C-section (cesarean) delivery
 mother that has diabetes
 Infection
 Premature babies
 cold, stress, or hypothermia.
Neonatal respiratory distress syndrome(Hyaline membrane
disease) - NRDS
Causes/risk factors:
1) prematurity<28 weeks of gestational age
2) Diabetic mother

(Mother has hyperglycemia -> glucose pass through the placenta(insulin cannot pass) ->baby(hyperplasia of the
pancreatic beta-cells) -> increased insulin secretion(baby’s) -> hypoglycemia and decreased surfactant production)
3) Asphixia
4)Maternal history of NRDS in previous infant
5) C-section (cesarean) delivery : no normal stress -> no increase in cortisol
(Vaginal delivery : the skull of the fetus is squeezed through the vaginal canal -> normal stress->
-> increased cortisol -> increased surfactant.)
 No surfactant -> increased surface tension -> lung collapse(atelectasis) ->
 Perfusion without ventilation;
 Alveoli are collapsed(due to atelectasis) -> damaged pulmonary vessels ->
leakage of proteins -> alveoli are lined by pink/hyaline membranes
THE AIR SPACES ARE LINED BY AN IRREGULAR LAYER OF HOMOGENOUS,
FINELY GRANULAR EOSINOPHILIC MATERIAL. IT IS MOST COMMONLY SEEN IN
PREMATURE INFANTS (LESS THAN 34 WEEKS GESTATION) WHO ARE DEFICIENT
IN ALVEOLAR SURFACTANT. THE ALVEOLAR DUCTS ARE DIFFUSELY LINED BY
HYALINE MEMBRANE COMPOSED OF FIBRIN WITH NECROTIC EPITHELIAL
CELLS. THE ALVEOLAR EPITHELIAL CELLS AND BRONCHIOLAR EPITHELIUM
ARE INJURED AND NECROTIC. THE ADMINISTRATION OF EXOGENOUS
SURFACTANT AT BIRTH IS VERY EFFECTIVE.
 Clinical manifestations
 Signs of RDS appear immediately after birth or within 4 h.
 RDS is characterized by tachypnea (>60 breaths/min),
 intercostal and subcostal retractions,
 nasal flaring, grunting, and cyanosis in room air.
 Respiratory difficulty
 Hypoxemia, hypercapnia -> respiratory acidosis
 Edema
 fine inspiratory crackles
 Progressive worsening of cyanosis and dyspnea
 Hypotension, apnea, irregular breathing
 Intraventricular hemorrhage
Diagnosis:
 Hypoxia, hypercapnia, respiratory acidosis
 Radiology:The typical chest radiograph shows low lung volumes and a bilateral, reticular granular
pattern (ground glass appearance) with superimposed air bronchograms.
 Biopsy: hyaline membrane(pink):protein

 The gastric aspirate shake test (GST) :

Methods: 
• Mix 0.5 ml of gastric aspirate & 0.5 ml of absolute alcohol
• Shake for 15 seconds & allow the solution to settle for 15 seconds
• If no bubbles – 60 % chances of RDS
• Small bubbles to the extent of 1/3rd of the circle of the test tube – 20% chances of RDS
THE GASTRIC ASPIRATE SHAKE
TEST
 The three most important advances in prevention and treatment of RDS
have been:
(a) antenatal glucocorticoids,
(b) continuous positive airway pressure (CPAP) and positive end-
expiratory pressure (PEEP),
(c) surfactant replacement therapy
 Treatment
Supportive care
 The supportive care of the infant with respiratory distress is similar regardless
of etiology.
 Infants with respiratory distress require: Frequent or continuous observations
of respiratory and heart rates, temperature, blood pressure and signs of
respiratory distress.
 Accurate fluid balance charts are essential.
 Adequate temperature control
 Adequate nutrition is essential part of respiratory care
 Oxygen is a useful and life-saving therapeutic agent, but is also potentially
dangerous, particularly in the preterm baby, as it may damage the eyes
(retinopathy of prematurity), or the lungs (bronchopulmonary
dysplasia).Oxygen should be warmed to 34–37°C and humidified.
 Fluids - In mild respiratory distress nasogastric feeding may be adequate. In
moderate to severe respiratory distress; babies should not be enterally fed.
 Intravenous fluids will be required. Usually a 10% dextrose and electrolytes or
total parenteral nutrition.

Blood gases and acid–base status

 Continuous transcutaneous monitoring of PO2 and PCO2 enables rapid
detection of fluctuations in clinical status.
 Prevention
 Antenatal glucocorticoids accelerate fetal lung maturity by increasing
formation and release of surfactant and maturing the lung morphologically.
 Administration of glucocorticoids(Dexamethasone, betamethasone) at least
24 to 48 h (and no more than 7 d) before preterm delivery decreases both
incidence and severity of RDS. They are most effective before 34 weeks