Respiratory Distress Sydrome is a condition that affects the lungs of newborn infants predominantly. Not much is known about the condition in the tropics. In this presentation Daniel Faithful Miebaka provides detailed review of the condition that has fatal potential.

2. RESPIRATORY DISTRESS SYNDROME
BY DANIEL FAITHFUL MIEBAKA (MBBCH CALABAR)

3. OUTLINE
 Background
 Introduction
 Epidemiology
 Predisposing risk factors
 Aetiopathogenesis
 Pathophysiology
 Assessment of patients
 Investigations
 Management
 Complications
 References

4. BACKGROUND
It is important to provide a background on Respiratory Distress.
 Respiratory distress is among the predominant clinical features in the presentation of
neonatal illnesses.
 It is a common cause of morbidity in the infant age group, as it is the commonest
reason for hospital admission in preterm and term infants.
 The incidence of neonatal acute respiratory distress was reported to be 20.5% of
NICU admissions. These findings therefore provoke the need for deeper
understanding to mitigate the challenge.
 The increase in neonatal admissions, adoption of surgical deliveries, and preterm
birth have been implicated in the causality of the increase in the incidence.

5. BACKGROUND
 Even with the epidemiological interest in climes like ours, the
finding is less reported in developing countries; partly because of
poor records due to home deliveries and patronage of traditional
birth attendants thus limiting data on frequency, and most
premature infants are subjected to intrauterine stressors like
malnutrition and pregnancy induced hypertension.
 Respiratory diseases are a significant burden of ill-health,
morbidity and mortality in middle and low income countries(MLIC).
 If there is any chance at achieving the 2030 Sustainable
Development Goal 3 to reduce childhood mortality, there is need
to make concerted efforts to mitigate this condition.

6. INTRODUCTION
Respiratory Distress Syndrome refers to a severe lung disorder in new-borns that is
primarily associated with pulmonary immaturity., and can be a cause of neurological
complications and mortality.
It is a syndrome typically affecting premature neonates and is characterized by
progressive and fatal respiratory failure resulting from atelectasis or immaturity of the
lungs.
Respiratory distress syndrome is also known as HYALINE MEMBRANE DISEASE.
The gestational age of the new-born infant has been shown to be inversely related to
the incidence and severity of the disease. Surfactant plays a central role in the
pathology and usually starts at week 20 and peaks at 35 weeks of gestational age, thus
predisposing neonates born before 35 weeks to RDS. The neonates are unable to keep
their lungs inflated.

7. INTRODUCTION
 At the core of neonatal survival is the adaptation to extra uterine environment. The
pulmonary system adaptation plays the most critical role, however all systems undergo
physiological adaptations to varying degree.
 It is established that intrauterine perfusion and oxygenation is from umbilical vessels and
placenta, while waste products are excreted via maternal circulation.
 Emergency management of neonatal RDS involves the immediate reversal of hypoxia with
supplemental Oxygen, and the prevention of respiratory acidosis and correction where
necessary through pulmonary ventilation.
 Non-invasive respiratory support is the mainstay through continuous positive airway
pressure(CPAP), high flow therapy, or the adoption of tracheal intubation and mechanical
ventilation for more critical cases.
 An underlying diagnosis is required before feeding can be commenced and to initiate further
management.
 Respiratory infections feature strongly in the pathology of the condition, so antibiotics are
routinely administered.

8. EPIDEMIOLOGY
 This is a common preterm respiratory disorder and occurs
due to deficiency of surfactant in the lungs. About 7.5% of
term new-borns are also affected and are mostly babies
delivered via caesarean section.
 The incidence of the condition varies indirectly gestational
age among preterm new-borns. In infants of diabetic
mothers there is a positive relationship with risk of
developing RDS.

9. PREDISPOSING FACTORS
 Prematurity
 Asphyxia
 Hypothermia
 Maternal anaemia
 Pre-eclampsia
 Maternal diabetes
 Caesarean section

10. PULMONARY RISK FACTORS
Pneumonia
Pneumothorax
Congenital malformations
Upper airway obstruction e.g. meconium
aspiration syndrome

11. NON PULMONARY RISK FACTORS
Sepsis
Cardiac effect
Exposure to cold
Hypoglycaemia
Metabolic acidosis
Acute blood loss

12. AETIOPATHOGENESIS OF RDS
Schema showing the
pathology of RDS.
Infants may recover or
develop chronic lung
damage, resulting in
bronchopulmonary
dysplasia.
FIO2 fraction of Inspired
O2. HMD=hyaline
membrane disease.
V/Q= ventilation-
perfusion

13. AETIOLOGY OF RESPIRATORY DISTRESS SYNDROME
ROLE OF SURFACTANT IN RDS
 Surfactant is a phospholipid containing lipoprotein produced by type 2
pneumocytes from the 24th week of gestation, and continues increasing.
The alveolar pool size of surfactant phospholipid in a healthy term
infant is about100mg/kg body weight.
 In comparison with healthy term infants, neonates who develop RDS
have a surfactant concentration less than 10% of the normal.
 The surfactant among other things reduces the surface tension of the
fluid lining the alveoli. The underlying pathology is a failure to reduce
surface tension within the alveoli, Thus increasing the respiratory effort
needed for optimal lung expansion and increasing the risk of lung
collapse after expiration.

14. AETIOPATHOGENESIS
 NATURAL HISTORY
Signs of respiratory distress are evident in the
immediate post partum period. This worsens over the
first 2-3 days of life and stabilizes for another 2-3
days, before clinical resolutions which is usually
accompanied by a diuretic phase.

15. AETIOPATHOGENESIS
Diagram showing surfactant production and flow at the
alveolus. site of production, flow, complex lattice, tubular
myelin, reuptake, recycling and macrophages.
Bar chart
Showing composition of surfactant

16. AETIOPATHOGENESIS
SURFACTANT
PRODUCTION,
TRANSPORT, REUPTAKE,
AND RECYCLING
The production begins in
type 2 pneumocytes
Surfactant precursors are
produced in the
polyribosomes and
transported via multi-
vesicles to endoplasmic
reticulum
In the endoplasmic
reticulum they are
processed and packaged
and transported to the
Golgi Apparatus.
In the Golgi apparatus
surfactant proteins are
processed and transported
to the lamellar bodies for
storage.
The Lamellar bodies store
the surfactant proteins till
they are needed and
released by exocytosis not
the type 1 pneumocytes.
In the type 1
pneumocytes, they are
arranged into a complex
lattice and tubular myelin
sheath.
In this sheath the
phospholipids form a
monolayer between air
and fluid lining the alveoli
After use for a few hours,
they are taken up by
endosomes.
The endosomes take them
to the type 2
pneumocytes, for storage.
Macrophages also take up
some surfactants protein.
Surfactant proteins once
produced can be reused
10 times.

17. PATHOPHYSIOLOGY OF RESPIRATORY DISTRESS
SYNDROME(EXPIRATION)
Absence of
surfactant
Surface tension
increases
Alveoli
collapses

18. PATHOPHYSIOLOGY OF RESPIRATORY DISTRESS
SYNDROME(INSPIRATION)
More
negative
pressure is
needed to
keep the
alveoli
patent and
leads to the
following.
Inadequate
oxygenatio
n
Increased
work of
breathing
Hypoxemia
and acidosis
Pulmonary
vasoconstrict
ion right to
left shunting
across
foramen
ovale
Worsenin
g hypoxia
Respiratory
failure

19. ASSESSMENT OF A PATIENT WITH RESPIRATORY DISTRESS
HISTORY TAKING
 Adequate prenatal, intrapartum and immediate postpartum history
should be gotten.
 The following should be considered;
 History of Gestational Diabetes Mellitus
 Surgical delivery
 Twin birth, with emphasis on second born twins
 Family history of respiratory distress syndrome

20. ASSESSMENT OF A PATIENT WITH RESPIRATORY DISTRESS
Other things to consider
 Intrapartum asphyxia
 Meconium aspiration pneumonia
 Oxygen toxicity and pulmonary injuries from barotrauma or volutrauma from
overzealous ventilation.
 Congenital diaphragmatic hernia and pulmonary dysplasia
 Pulmonary Haemorrhage
 Pulmonary infections(example Group B, beta-haemolytic Streptococcal
Pneumonia)

21. ASSESSMENT OF A PATIENT WITH RESPIRATORY DISTRESS
PHYSICAL EXAMINATION
It is known that the physical findings elicited are consistent with the infants maturity assessment using Dubowitz
examination, or its modification by Ballard.
 These signs are in keeping respiratory distress and can be immediately noted after birth.
 Tachypnoea (</= 80-120cpm,Wong’s ) normal RR:30-60breaths per minute
 Auditory expiratory grunting, abrupt closure of the glottis during expiration to conserve functional residual capacity.
 Nasal flaring to increase the diameter of the upper airway
 Use of accessory muscles of respiration, chest wall recessions (suprasternal, intercostal, and subcostal)
 Cyanosis or pallor
 Apnoea (in extremely immature neonates)
 Hypothermia
 Tachycardia(heart rate >160bpm)
 Fine inspiratory crackles
 Downe’s scoring

22. ASSESSMENT OF A PATIENT WITH RESPIRATORY DISTRESS

23. ASSESSMENT OF A PATIENT WITH RESPIRATORY DISTRESS
 Flaccidity
 Absent spontaneous movement
 Unresponsiveness
 Diminished breath sounds
 Mottling
 In severe condition – shock like state

24. ASSESSMENT OF A PATIENT WITH RESPIRATORY(USING DOWNE’S
SCORE)
Normal infant: 0
Mild respiratory distress:1-3
Respiratory distress:4-7
Imprending respiratory failure: 8-10

25. INVESTIGATIONS
The goal of investigations is to establish the diagnosis, severity of illness,
identifying coexisting pathologies,
Common first line investigations include:
 Pulse oximetry
 Chest radiographing (useful in distinguishing underlying cause)
 Blood test (full blood count, C- reactive protein, blood culture, and arterial
blood gases).
 Pulmonary function test
 Shake test

26. INVESTIGATIONS
 Pulse oximetry is a non invasive tool to monitor oxygen
saturation, and should be maintained at 90-95%
Drawbacks
 Unreliable in determining hyperoxia, because of the flat
top portion of the S shaped oxygen-haemoglobin
dissociation curve.
Transcutaneous CO2 monitors are recommended for use in
infants with ongoing respiratory distress to monitor
ventilation if it correlates with PaCO2.

27. INVESTIGATIONS
SHAKE TEST
It is a simple, and cheap bedside test done to assess whether
sufficient surfactant is present in the infants lung a birth. By
evaluating its ability to generate stable foam in the presence of
ethanol(47.5%). Simple, reproducible and validated procedure
with 100% predictive value for surfactant sufficiency and 92%
for surfactant insufficiency.
Gastric aspirate is collected, mixed with 0.5mls of absolute
alcohol in a test tube. The solution is shaken for 15 seconds.
Positive finding of bubbles indicate adequate surfactant and
less chance of RDS.

28. INVESTIGATIONS
Why Ethanol?
 Because it is a non-foaming competitive surfactant,
eliminates the contribution of proteins, bile salts, salts of
free fatty acids to the formation of a stable foam.
 If a foam appears, it is due to amniotic fluid lecithin
 Positive tap test can also be used to assess for surfactant
sufficiency is the formation of a complete ring of bubbles
at the meniscus with a 1;2 dilution of amniotic fluid is
rarely associated with neonatal RDS.

29. INVESTIGATIONS (SHAKE TEST)

30. INVESTIGATIONS
CHEST RADIOGRAPHS
It reveals bilateral, diffuse, reticular, granular or ground-glass appearances, air
bronchograms, poor lung expansion.
The bronchograms represent aerated bronchioles superimposed on a background of
collapsed alveoli.
The cardiac silhouette maybe normal or enlarged.
Causes of cardiomegaly: prenatal asphyxia, maternal diabetes, patent ductus arteriosus
(PDA), congenital cardiac anomalies, poor lung expansion.
It is important to note that early initiation of surfactant therapy and mechanical
ventilation can alter radiologic findings

31. INVESTIGATIONS
Chest radiograph
showing an infant
with RDS.

32. INVESTIGATIONS
Chest radiograph interpretation
 Ground glass appearance is a radiologic feature characterized by the haziness
of the lung fields and suggests consolidation. Borrowed from grinding glass
to make it less clear.
 Air bronchograms are another r feature of consolidation (can also occur in
collapse). The airway and lungs (alveoli) carry air and appear lucent in a
normal radiograph. However, in this cases the alveoli have fluid or pus or
infiltrate so are opaque, the lucent airway over this backdrop is the air
bronchogram. The Y tracing of the trachea and the bronchi

33. INVESTIGATIONS
Chest radiograph
showing how
radiographs can be
altered after initiation
of surfactant . Done
in the first 30 minutes
before surfactant
therapy, and the
second film 3 hours
post delivery.

34. INVESTIGATIONS
ECHOCARDIOGRAPHY
This is used in assessing patients with cardiac anomalies like PDA. PDA features
commonly in RDS, and in most cases as a coincidence. This is because of the
prematurity. There is reported incidence of 80% in preterm born before 26
weeks and 20% in those born after 32 weeks. All views except the four chamber
view can be used to detect a ductal defect.
GOALS
 Assists in diagnosing of PDA
 Determining the direction and degree of shunting on Doppler study.
 Useful in diagnosing pulmonary hypertension
 Assessing cardiac function
 R/O structural heart diseases

35. INVESTIGATIONS (ECHOCARDIOGRAPHY0

36. MANAGEMENT
 TREATMENT AND PROGNOSIS
 Antenatal maternal corticosteroids(Dexamethasone)induces foetal lung maturation
by promoting maturation of the antioxidant system and of surfactant production and
also prepares the foetal lung for breathing and preventing or reducing the severity of
respiratory distress.
 Exogenous surfactant therapy to preterm infants who require tracheal intubation at
birth to prevent Respiratory Distress Syndrome.
 There are innovations in surfactant administration with reduced intubation time, and
non-utilization of endotracheal intubation in preterm infants at risk of developing
RDS.
 Surfactants can be used subsequently in management of established cases of RDS,
However, little is known about the optimal time for the administration of rescue
doses of surfactant.

37. MANAGEMENT
 In patients who are less severely affected, maintenance can be done with positive
end respiratory pressure with continuous positive airway pressure (CPAP) and
supplemental oxygen.
 Administration IV fluids, and oxygen therapy @4-6l/min
 Antibiotics: aminoglycosides, amoxicillin, ampicillin, cotrimoxazole, and procaine
penicillin usually given 7-10 days.
 Muscle relaxants: Pancuronium.
 Diuretics: Furosemide
 Antacids: sodium bicarbonate, sodium citrate
 Indomethacin: if PDA
 In resource poor settings “high flow’ nasal oxygen therapy is used as an alternative to
CPAP, however this requires careful evaluation.

38. PROGNOSIS
 Prognostication depends on the severity on the disease
which directly correlates with gestational age and birth
weight.
 Data shows that mortality is as high as 50% in infants with
birth weight <1000g, and as low as 0% with those with
birth weight >4000g.

39. SUPPORTIVE MANAGEMENT
 Maintain adequate hydration and electrolyte status
 Administer antipyretics to reduce fever
 Maintain acid base balance
 No nipple or gavage feeding: increase respiratory rate and chance
of aspiration.
 IV line for fluid/hydration, nutrition and medication.

40. COMPLICATIONS
Acute
 Patent ductus arteriosus
 Alveolar rupture
 Congestive cardiac failure
 Intraventricular haemorrhage
 Periventricular leukomalacia
 Pulmonary hemmorhage
 Apnea of prematurity
 Necrotizing enterocolitis and or gastrointestinal perforation
 Pneumonia
 Sepsis

41. COMPLICATIONS
Chronic
 Bronchopulmonary dysplasia
 Neurologic sequelae
 Retinopathy of prematurity

42. REFERENCES
 West JB., (2010) Respiratory Physiology : The Essential.
 Hibbard JU., Wilkins I., Sun L., et al(2012) Consortium on Safe Labor. Respiratory Morbidity In
Late Preterm Births.
 Bahadue FL., Soll R.,(2012) Early versus delayed selective surfactant treatment for neonatal
respiratory distress syndrome. Cochrane Database System.
 Edwads MO., Kotecha SJ., Kotecha S. (2013) Respiratory Distress of The Term Newborn Infant.
 Reuter S., Moser C., Baack M.,(2014)
 Ghimire N., Poudel S., Poudel A., Rana D., Karki N.,(2017) Respiratory Distress Syndrome
 Arlettaz R.,(2017) Echocardiographic Evaluation Of Patent Ductus Arteriosus In Preterm Infants
 Nelson Textbook Of Paediatrics
 Pramanik KA (2020) Respiratory Distress Syndrome
 Okorie E(2022) Lecture presentation on Respiratory Problems In The Newborn

43. THE END

44. THANK YOU FOR LISTENING
 Hopefully, I didn’t take your breath away?