RESPIRATORY DISTRESS
SYNDROME
MIRITI M.D
MASTER OF CLINICAL MEDICINE: ACCIDENTS
AND EMERGENCY
June 2018
Specific Learning Objectives
• Definition
• Etiology
• Pathogenesis and Pathophysiology
• Clinical Features
• Management
• Complications
RESPIRATORY DISTRESS SYNDROME
• Respiratory Distress Syndrome (RDS) formerly
known as hyaline membrane disease, is a life
threatening lung disorder that results from
underdeveloped and small alveoli and
insufficient level of pulmonary surfactant that
leads to atelectasis.
• It is the leading cause of death in preterm infants
• Occurs in 50% babies born at26-28 weeks and
25% of babies born at 30-31 weeks
Etiology/ Causes
• RDS occurs as a result of insufficient production of surfactant
which is seen in:
Prematurity (more common)
Maternal diabetes (Inadequate utilization of glycogen for
surfactant production)
Meconium aspiration syndrome
Caesarian section (Due to lack of adrenergic and steroid hormones
released during labour)
Pulmonary Causes: Congenital malformation, pneumonia, edema
of lungs, bleeding from lungs, pleural effusion
Non Pulmonary causes: Sepsis, Exposure to cold, acute blood loss.
Pathogenesis and Pathophysiology
• Surfactant production starts at around 20 weeks of
gestation and peaks at 35 weeks. (Any neonate <35
weeks is prone to develop RDS)
• Surfactant is the substance produced by type II
alveolar cells composed of 90% phospholipids and
10 % protein. It has two major components: lecithin
(L) and sphingomyelin (S). Lecithin is a fatty protein
necessary for absorption of oxygen by lungs and
sphingomyelin, phospholipid helps to reduce surface
tension.
• After 35 weeks of gestation, normal L/S ratio
detected in amniotic fluid is 2:1 which indicates fetal
lungs are mature.
•Surfactant is a substance that has detergent properties,
thus reduce surface tension of the fluids that line the
alveolar and respiratory passages, resulting in increased
pulmonary compliance at low intra alveolar pressure.
Deficient surfactant production causes unequal inflation of
alveoli on inspiration and collapse of alveoli on end
expiration.
•Without surfactant, infants are unable to keep their lungs
inflated and thus produce widespread atelectasis. It has
been estimated that each breath requires as much negative
pressure (60-75cm H2O) as the initial lung expansion at
birth. Blood flow through the atelectatic portion of the
lungs is compromised leading to hypoperfusion to the
lung tissue and increased pulmonary vascular resistance.
•Inadequate pulmonary perfusion and ventilation
produce hypoxemia and hypercapnia which causes
pulmonary vasoconstriction, resulting to partial
reversion of fetal circulation (Right to left shunting of
blood through the ductus arteriosus and foramen
ovale).
•Prolonged Hypoxemia activates anaerobic glycolysis
which produce increased amount of lactic acid
eventually causing metabolic acidosis. Inability of
atelectatic lungs to flow off excess CO 2 produce
respiratory acidosis. Lower pH causes further
vasoconstriction.
•Deficient Pulmonary Circulation and Alveoli
perfusion, PO2 continues to fall, pH falls and
alveoli are necrosed, this further reduces surfactant
production. Ischemic damage to the alveoli, cause
transudation of proteins into the alveoli that forms
hyaline membrane which makes the lungs stiff and
inelastic, thereby inhibiting gas exchange in lungs
and is characterized by clinical triad of:
Tachypnea
Respiratory grunt
Inspiratory retractions
•Eventually the neonate goes into respiratory
Failure
Clinical Presentation
A) Initial manifestation B) Manifestation as
• Tachypnea and Labored disease progresses
breathing • Apnea
• Audible expiratory • Flaccidity
grunting
• Unresponsiveness
• Intercostal/ Substernal
retractions • Diminished breath
• Nasal Flaring sounds
• Cyanosis/ pallor • Mottling
• Fine respiratory crackles
Clinical Features
C) In severe Condition
• Shock like state
• X-ray shows reticulogranular pattern
( Ground Glass appearance) of lung fields
that represent alveoli atelectasis
Diagnostic measures
• Details of Antenatal and Prenatal History
• Assessment and Evaluation of Clinical manifestation
• Arterial Blood gas analysis:
PCO2 above 65mmHg
PO2 of 40mmHg
pH below 7.15
• X-ray shows ground glass appearance of lung fields that represent
alveolar atelectasis
• Pulse oximetry: Decreased SPO2
• Shake test
• Prenatal diagnosis of RDS can be made by determining
Lecithin/sphingomyelin ratio in amniotic fluid after 35 weeks of
gestation.
Diagnosis
Chest x-ray:
Grade 1 (mild cases): The lungs show fine homogenous
ground
glass shadowing.
Grade 2: Widespread air bronchogram
become visible.
Grade 3: Confluent alveolar
shadowing.
Grade 4: Complete white lung fields with obscuring
of the cardiac shadow.
Management
• Neonate should be placed in Newborn Unit (NBU)
and nursed in warm incubator. The infant must be
kept warm (36.50C).
• Oxygen administration- Adequate, warm and
humidified O2 in high concentration is given
through plastic hood to maintain arterial PO2
between 50-90mmHg is given.
• If oxygen saturation of blood cannot be maintained
at a satisfactory level and carbon dioxide level
rises, Infant will require ventilator support.
Management cont…….
• Mild distress can be managed without ventilator. Moderate
and severe RDS need ventilator support.
• Frequent monitoring of the PO2, PCO2,pH and arterial blood
gas are to be done to diagnose metabolic and respiratory
acidosis.
• Ventilator support- Infant with RDS are handicapped by
decreased lung compliance and alveolar collapse during
expiration. Administration of oxygen under positive pressure
would prevent alveolar collapse and ensure gas exchange
throughout respiratory cycle.
• Continuous Positive Airway Pressure (CPAP) is indicated and
useful in infant with decreased lung compliance.
Management cont…..
• After weaning from ventilator, Oxygen should
be administered via hood.
• Maintenance of nutrition and hydration by IV
route.
• Maintenance of acid base balance
• IV administration of 7.5% Sodium bicarbonate
in dose of 3-8 meq/kg in 24 hours in 1:1
dilution with distilled water.
Management cont…..
• Surfactant therapy-Via Endotracheal tube is indicated in all
neonates with RDS and prophylaxis can be given in all
premature infants. Adequate oxygenation, ventilation and
monitoring should be started before administration of
surfactant.
• Dose 100mg/kg body weight in 2 to 4 divided doses at 6 to
12 hours apart.
• Depending upon the babies condition, repeated dose of
surfactant need to be administered
• The adverse effect of surfactant therapy include: Apnea,
Hypotension, Pulmonary hemorrhage , lung tissue damage
from oxygen pressure and Bradycardia.
• Arterial Blood gases and CXR should be monitored .
Surfactant replacement therapy
Surfactant replacement therapy can reduce mortality
and incidence of Chronic pulmonary disease.
There are 2 types of surfactant :
1. Natural surfactant extract
Bovine(Survanta), Porcine(Curosurf)
Natural surfactants appear to be superior, perhaps of htrei
surfactant-associated protein content.
Natural surfactants have a more rapid onset and are
associated with a lower risk of pneumothorax and
improved survival.
Cont…
2. Synthetic surfactant
Exosurf and ALEC (Artificial Lung Expanding
Compound)
3. Newer surfactant
• Synthetic surfactants with synthetic peptides modelled
on surfactant proteins, Aerosolized surfactants.
Dose:
•Survanta 100mg/kg for the first and subsequent doses.
•Curosurf 200mg/kg for the first dose and 100mg/kg for
the subsequent doses or 100mg/kg for all the doses.
Management cont…..
• IV antibiotics
• Administration of Vitamin E- Low birth weight
or preterm babies receiving oxygen therapy
may be administered vitamin E at a dose of
100 IU/Kg/day IM from birth onwards.
Prognosis
• Prognosis is good with appropriate and timely
treatment
• Survival can be as 60-80% in infant >
1000grams. In the absence of ventilatory
support, neonate with severe disease will die.
• If there is no complication during the first 48
hours, infant begins to improve by 72 hours and
if they survive for 96 hours chances of survival
is higher.
Complications
• Patent ductus arteriosus
• Congestive cardiac failure
• Retrolental fibroplasia
• Intraventricular hemorrhage
• Bronchopulmonary dysplasia
• Neurological abnormalities
• Pneumonia
• Sepsis
REFERENCES
• Basic Paediatric Protocols: for ages upto 5 years.
(2016). Republic of Kenya Ministry of Health.
• Robert, N.R.C (1988) Textbook of neonatology (1st ed.)
Liberty of congress cataloguing publication, Singapore
(pp:274-306)
• Rodriguez RJ, Martin RJ, Fanaroff AA. Respiratory
distress syndrome and its management. In: Fanaroff
AA, Martin RJ, eds. Fanaroff and Martin’s Neonatal-
Perinatal Medicine: Diseases of the Fetus and Infant.
7th ed. St. Louis, MO: Mosby; 2002:1001–1011.
