Respiratory distress syndrome

1. CONTENT
UNIT 15.2 MAJOR PROBLEMS OF NEWBORN
RESPIRATORY DISTRESS SYNDROME
Definition:
Respiratory distress syndrome (RDS), formerly known as hyaline membrane disease, is life
threatening lung disorder that result from underdeveloped and small alveoli and insufficient level of
pulmonary surfactant.
Prevalence
Respiratory distress is leading cause of death in preterm infants. It occurs in 50% babies born at 26 to
28 weeks and 25% of babies born at 30-31weeks.
( Source: Sharma,R. (2013). Essential Paediatrics for Nurses( 2nd
ed.). Jyapee Brothers Medical
Publisher , New Delhi,India( pp:217).
Causes
RDS occur as a result of insufficient production of surfactant which is seen in:
-Prematurity (more common)
-Maternal diabetes (inadequate utilization of pulmonary glycogen for surfactant production.)
-Meconium aspiration syndrome
-Caesarean section (due to lack of adrenergic and steroid hormones which are release during labour)
-Pulmonary causes: Congenital malformation ,pneumonia , Pleural effusion , edema of lungs ,
bleeding from lungs
-Non pulmonary causes: Sepsis, exposure to cold, acute blood loss etc
Pathogenesis
Surfactant production starts at around 20 weeks of gestation and peaks at 35 weeks. Therefore, any
neonate <35 weeks is prone to develop RDS. Surfactant is the substance produce by type II alveolar
cells composed of 90% phospholipid and 10% protein .Surfactant 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.
Functionally the fetal lungs are deficient in surfactant in RDS. Acting most like detergent, these
substances reduces the surface tension of the fluids that line the alveolar and respiratory passages,
1

2. 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 produce wide spread atelectasis.
It has been estimated that each breath requires as much negative pressure (60-75 cm H2O) as the
initial lung expansion at birth. Blood flow through the atelectatic portion of the lungs is compromised
leading hypoperfusion to lung tissue and increased pulmonary vascular resistance. Inadequate
pulmonary perfusion and ventilation produce hypoxemia and hypercapnia which causes pulmonary
vasoconstriction resulting partial reversion of fetal circulation( right to left shunting of blood through
the ductus arteriosus and foramen ovale).
Prolong hypoxemia activates anaerobic glycolysis, which produce increased amount of lactic acid.
And increased lactic acid causes metabolic acidosis. Inability of atelectatic lungs to flow off excess
carbon dioxide produce respiratory acidosis. Lowered PH causes further vasoconstrictions. With
deficient pulmonary circulation and alveolar perfusion, PO2 continues to fall, PH falls, and alveoli are
necrosed that further reduces surfactant production. . Ischernic damage to the alveoli causes
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,
expiratory grunt and inspiratory retractions. Eventually the neonate goes into respiratory failure.
Hyopoxemia and hypercapnia
Increase pulmonary artery vasoconstriction
Right –to- left shunting through ductus arterious and foramen ovale as the neonates body attempts to
counteract the compromised pulmonary perfusion.
Metabolic acidosis that occur from a build of lactic acid that result from prolong period of
hypoxemia and respiratory acidosis that occur from the collapsed alveoli being unable to get rid of
excess carbondioxide
Alveolar necrosis and respiratory failure
Clinical Features
RDS usually occur within the 1st
6 hours of life. Clinical features include
A) Initial manifestation
2

3. -Tachypnea up to 80 -120 breath /min and labored breathing
- Audible expiratory grunting
- Intercoastal / substernal retractions
-Nasal flaring
-Cyanosis or pallor
-fine respiratory crackles
B) Manifestations as disease progresses
- Apnea
-Flaccidity
-Unresponsiveness
-Diminished breath sound
-Mottling
C) In severe condition
-Shock like state
-X- ray shows ground glass appearance of lung fields that represents alveolar atelectasis
Diagnostic Measures
• Details of antenatal and prenatal history should be collected which include gestational age,
maternal diabetes , intrapartum fever to mother, meconium stained liquor etc.
• Assessment and evaluation of clinical manifestations.
• Laboratory data :
Arterial blood gas analysis: PCO2 above 65mm of Hg(normal limit : 35-45mm of Hg)
PO2 of 40mm of Hg (normal limit:50-90mm of Hg)
PH below 7.15 (normal PH: 7.35 – 7.45)
• X- ray shows uniform reticogranular pattern known as ground glass appearance of lung fields
that represents alveolar atelectasis.
• Pulse oximetry : decrease SPO2
3

4. • Shake test : It is done on gastric aspirate withdrawn from the neonate in the first hour of life
.Normal saline 0.5ml is mixed with same amount of gastric aspirate and the resulting 1ml is
added to 1ml of 95% ethanol. The mixture is shaken well for 15 seconds and kept aside. After
15 minutes , the test tube is viewed against black background .If complete ring of bubbles is
seen on the meniscus ,this test is positive and indicates that surfactant is present and baby is
normal. If there is absence of bubbles on the meniscus ,it indicates test is negative i.e.
surfactant deficiency.
• Prenatal diagnosis of RDS can be made by determining lecithin / sphingomyelin ratio in
amniotic fluid after 30 weeks of gestation. L/S ratio of more than 2 indicates adequate lung
maturity which usually occurs after 35 weeks of geatation.
Management
 Neonate should be placed in intensive care unit and nursed in a warm incubator. The infant must
be kept warm (at around 36.50
C) because cooling increase acidosis in all newborn’s.
 Oxygen administration
- The goal of oxygen therapy are to provide adequate oxygen to the tissue, prevent lactic acid
accumulation resulting from hypoxia.
- Adequate warm and humidified O2 in high concentration is given through plastic hood to
maintain arterial PO2 between 50-90 mm of Hg. If oxygen saturation of blood cannot
maintained at a satisfactory level and carbon dioxide level rises , infant will required
ventilator support.
- Mild distress can be managed without ventilator. Moderate and severe RDS needs ventilator
support.
- Frequently monitoring of the PO2 , PCO2 , pH , and arterial blood gas are to be done to
diagnosis metabolic and respiratory acidosis.
 Ventilatory support
- Infants with RDS are handicapped by decrease lung compliance and alveolar collapse during
expiration. Administration of oxygen under positive pressure would prevent if alveolar collapse
and ensure gas exchange throughout the respiratory cycle.
- Continuous positive airway pressure is indicated and useful in infant with decrease lungs
compliance . CPAP(continue positive airway pressure) should be started if arterial oxygen
saturation remains below 50 mm 0f Hg even though the neonate getting oxygen more than
60%. While the baby is on CPAP,arterial blood gases should be closely monitored so that
oxygen concentration and CPAP pressures are adjusted.
4

5. - If despite of CPAP ,arterial PO2 remains below 50mm of Hg or PCO2 is greater than 50 mm of
Hg and PH can't be corrected then assisted ventilation with positive end expiratory pressure is
required. During ventilation ,transcutaneous saturation monitoring ,arterial blood gas and PH
should be checked 4-6 hourly and orophayngeal ,tracheal suctioning and chest physiotherapy
should be done properly.
- On recovery , the infant is gradually weaned to synchronised intermittent mandatory
(SIMV)mode followed by CPAP.
- After weaning from ventilator ,oxygen should be administered via hood.
 Maintenance of nutrition and hydration by IV route.
- It is advisable to start intravenous infusion in all newborn babies with respiratory distress
syndrome because the oral feeding may not be possible with the baby as oral feeding has
the risk of aspiration.Intravenous administration of 10% glucose in amount of 60 ml/kg
body weight per day may be given to a term baby on the first day through a catheter
inserted into peripheral or umbilical vein.
 Maintenance of acid base balance.
- Intravenous administration of sodium bicarbonate 7.5% sodium bicarbonate in dose of 3-8
meq/kg in 24 hours in 1:1 dilution with distilled water.
 Surfactant therapy
- Surfactant is indicated in all neonate with RDS. Prophylactic therapy is given in all
premature infant.
- Surfactant is administered via endotracheal tube directly into the infants trachea.
- Adequate oxygenation , ventilation and monitoring should be started before administration
surfactant.
- Dose -100mg/kg body weight in 2-4 divided doses at 6-12 hrs apart .Depending upon the
baby’s condition, repeated dose of surfactant need to be administered. The therapy leads to
improved oxygenation and reduction in oxygen dose required by patient.
- A blood gas should be checked within 15 - 20 minutes of the dose and the ventilator settings
should be weaned appropriately to minimize the risk of a pneumothorax. A chest radiograph
should be checked both 1 hour and 4 - 6 hours after the initial dose to avoid hyperinflation.
- The adverse effect of surfactant therapy include apnea, hypotension , pulmonary
hemorrhage and bradycardia, lung tissue damage from oxygen pressure.
 IV Antibiotics
5

6. - Antibiotics (aminoglycosides) are routinely administered to treat any pulmonary infection,
if present and due to continuous invasive procedure being done on the baby. Septic
screening and periodic cultures from endotracheal tube and blood are taken to guide
antimicrobial therapy.
 Administration of vitamin E
- Treatment of respiratory distress syndrome requires administration of high concentration of
O2 which may leads to bronchopulmonary dysplasia and retrolental fibroplasia. Vitamin E
being biological antioxidant ,inhibit perioxidation of membrane lipids there by reducing
chances of retrolental fibroplasia and bronchopulmonary dysplasia. So low birth weight or
preterm babies receiving O2 therapy may be administered vitamin E in dose of 100IU
/kg/day IM from birth onwards.
Nursing Management
 Assessment
Details of antenatal and prenatal history , assessment of clinical manifestations ,review of lab
investigations, monitoring general condition and respiratory status.
 Nursing diagnosis
-Ineffective breathing pattern related to surfactant deficiency , alveolar instability
-Impaired gas exchange related to immature pulmonary function.
-Risk of injury (brain injury) related to hypoxemia
-Ineffective thermoregulation related to immature temperature regulation mechanism.
-Risk of infection related to deficient immunological defence
 Nursing intervention
-Maintain airway and administer oxygen.
-The patient should be kept with the head elevated to reduce pressure on diaphragm.
-Endotracheal suctioning can be done as required using strict aseptic techniques. Monitor oxygen
saturation while suctioning (not more than 5 seconds) the baby.
-Assess the respiratory rate and general status of the neonate , O2 saturation, respiratory pattern ,
arterial blood gas and vital signs.
-Maintain neutral thermal environment.
- Preterm with respiratory distress syndrome should be prevented from infection by minimal handling
and using aseptic technique while handling.
6

7. -Skin care with use of water pillows, change of napkin if wet,clean skin folds with sterile swab and
with frequent position change.
-Provide necessary care to neonate in incubator and ventilator as per requirements.
Prognosis
Prognosis is good with appropriate and timely treatment. Survival can be as 60 -80% in infant
>1000gm. In the absence of ventilatory support neonate with severe disease will die.
If there is no complication during 48 hours , infant begins to improve by 72 hours and if survive for 96
hours, chance of survival is high.
Complication
- Patient ductus arterious
- Congestive cardiac failure
- Retrolental fibroplasia
- Intraventricular hemorrhage
- Bronchopulmonary dysplasia
- Neurological abnormalities
Summary
RDS is the life threatening lungs disorders that result from underdeveloped and small alveoli and
specially due to the deficiency of surfactant which occurs in newborn within 6 hours of life. Surfactant
is the substance produced by type II alveolar cells and start to produce at about 20 weeks of gestation
and till 36 weeks .It reduces the surface tension of the lungs and increases the pulmonary compliance
which prevent the alveoli from collapsing at the end of expiration. The main cause of RDS in
newborn is surfactant deficiency which is seen in prematurity , baby of diabetic mother , meconium
aspiration syndrome , caserian section baby, pleurai effusion etc. Sign and symptoms are tachypnea ,
expiratory grunting , chestwall retraction . nasal flaring , cyanosis or pallor. Mild distress can be
managed by Continuous positive airway pressure oxygen therapy, moderate and severe distress needs
ventilator support. frequently monitoring ABG , maintenance of nutrition hydration by IV route
surfactant therapy, antibiotic and vit E supplement. Prognosis is good with appropriate and timely
treatment. Several complications like patent ductus arteriosus ,retrolental fibroplasia , intraventricular
haemorrhage may arise.
7

8. References
 Subedi, D.& Gautam ,S.(2017) .Midwifery nursing part III ( 3rd ed.). Medhavi Publication
,Baneshwor, Kathmandu,Nepal (pp:257-260).
 Shrestha ,T.(2016).Essential child health nursing( 2nd
ed.). Apex Press Tinkune ,
Kathmandu,Nepal (pp:196-198).
 Adhikari,T. (2015) .Essentials of pediatric nursing (2nd
ed.). Vidhyarthi Pustak Bhandar,
Kathmandu,Nepal ( pp:53-55).
 Sharma,R. (2013). Essential Paediatrics for Nurses( 2nd
ed.). Jyapee Brothers Medical
Publisher , New Delhi,India( pp:217-22).
 Thakur, L .(2012).Advanced child health nursing (3rd
ed.).Ultimate Marketing ,Lazimpat
,Kathmandu,Nepal (pp: 77-79).
 Hocken., & Berry , J.M. (2011) , WONG’S Nursing care of infant and children’s (9th
ed.).
Libery of congress catologinia publication , United states of America (pp:347-354).
 Sing, M. (2008) , Essential paediatrics for nurses (2nd
ed.).CBS Publisher and Distributors ,
Daryaganj , New Delhi,India( pp:48-50).
8

9.  Lipincott, W .W. (2007), Maternal and child health nursing care of child bearing and child
rearing women(5th
ed.). Libery of congress catologinia publication , United states of America
(pp:777-784).
 Tuitui,R .(2007). Manul of midwifery C(4th
ed.).Vidyarthi Pustak Bhandar Publication,
Bhotahity ,Kathmandu ,Nepal(pp :179-182).
 Robert ,N.R.C. (1988).Textbook of neonatology (1st
ed.).Libery of Congress Cataloguing
Publication , Singapoor( pp:274-306).
 Durham ,R., & Cmapmam ,L Maternal newborn nursing(2nd
ed.) .Jyapee Brothers Medical
Publisher, New Delhi, India( pp:108-112).
SAMPLE QUESTION
Subject : Midwifery II Total Hour :30 min
Course no : BSN19 Total Mark :10
Pass Mark : 4
Candidates are required to give answers in their own words as far as practicable.
The figures in the margin indicates full marks.
Attempt all questions.
Objective Type of Question
1.Write 'T' for true and 'F' for false in the box . 1*2=2
a) RDS usually occur within the first 6 hours of life.
9

10. b) RDS is most common in post term baby than preterm.
2. Fill in the blanks. 1*2=2
a) Main cause of RDS in newborn is due to .................. deficiency.
b) PO2 is .......... in RDS.
Subjective Type of Question
Essay Type Question
Answer the following question.
a) Define respiratory distress syndrome.Explain the management of RDS. 2+4=6
10