DR. ROOPAM JAIN, Professor & Head, Department of Pathology & Blood Bank

1. respiratory distress syndrome
(RDS)
(HYALINE MEMBRANE DISEASE)
Dr. ROOPAM JAIN
PROFESSOR & HEAD

2. ACUTE respiratory distress syndrome
(RDS)
(HYALINE MEMBRANE DISEASE)

3. • a severe, at times life-threatening, form of progressive respiratory
insufficiency which involves pulmonary tissues diffusely
• ARDS exists in 2 forms: neonatal and adult type.
• Both have the common morphological feature of formation of hyaline
membrane in the alveoli and hence is also termed as HMD.

4. CLINICAL FEATURES & CONSEQUENCES
• Neonatal ARDS
• newborn infants
• begins with dyspnoea
• within a few hours after birth with tachypnoea, hypoxia and cyanosis;
• in severe cases death may occur within a few hours.

5. CLINICAL FEATURES & CONSEQUENCES
• Adult ARDS
• (shock lung syndrome,
• diffuse alveolar damage (DAD),
• acute alveolar injury,
• traumatic wet lungs
• post-traumatic respiratory insufficiency.
• presents clinically by sudden & severe respiratory distress,
tachypnoea, tachycardia, cyanosis & severe hypoxaemia

6. respiratory distress syndrome
(RDS)

7. Neonatal ACUTE respiratory distress syndrome
(ARDS)

8.  Neonatal respiratory distress syndrome:
 It is most common cause of respiratory distress in newborn
 Also known as Hyaline Membrane Disease because of deposition of a
layer of hyaline protein in the peripheral airspaces of infants
Neonatal respiratory distress syndrome
(ARDS)

9. Neonatal ARDS is primarily initiated by hypoxia
• 1. Preterm infants
• 2. Infants born to diabetic mothers
• 3. Delivery by caesarean section
• 4. Infants born to mothers with previous premature infants
• 5. Excessive sedation of the mother causing depression in respiration
of the infant
• 6. Birth asphyxia from various causes such as coils of umbilical cord
around the neck
• 7. Male preponderance (2 t) due to early maturation of female lungs
• 8. Finally, many cases of neonatal ARDS remain idiopathic

10. Causes of Adult ARDS
• a) Direct lung injury:
• 1. Diffuse pulmonary infections, chiefly viral pneumonia
• 2. Oxygen toxicity
• 3. Inhalation of toxins and irritants e.g. smoke, war gases,
nitrogen dioxide, metal fumes etc.
• 4. Aspiration of gastric contents
• 5. Near drowning
• b) Indirect lung injury:
• 1. Shock due to sepsis, trauma, burns 2. Narcotic overdose
• 3. Pancreatitis 4. Drugs e.g. salicylates, colchicines
• 5. Fat embolism 6. Radiation 7. Multiple transfusions

11. Schematic outline of the pathophysiology of RDS

12. NEONATAL RESPIRATORY DISTRESS
SYNDROME
Pathogenesis: Prematurity
Reduced synthesis of surfactant
Deficiency of Alveolar surfactant
Increased Alveolar surface tension
Collapse of lung
Damage to endothelium and epithelium
Pulmonary hypoperfusion
Plasma leaks into alveoli
Deposition of Fibrin & Necrotic cells (Hyaline)

13. Pathogenesis
NEONATAL RESPIRATORY DISTRESS SYNDROME
• Immaturity of the lungs is the most important substrate on which RDS
develops
• The fundamental defect in RDS is a deficiency of pulmonary surfactant.

14. sequence of events
leading to the
formation of hyaline
membrane in
neonatal acute
respiratory distress
syndrome (ARDS).

15. NEONATAL RESPIRATORY DISTRESS
SYNDROME
Morphology of lungs:
Gross:
Solid, Airless, Reddish purple
Sink in water
Microscopically:
Poorly developed alveoli or Collapsed alveoli
Necrotic material incorporates in hyaline membrane and is seen in:
• Terminal bronchioles
• Alveolar ducts
• Alveoli

17. NEONATAL RESPIRATORY DISTRESS SYNDROME
Clinical features:
Infant is almost always preterm
Males are affected more
Maternal diabetes is a contributing factor
Resuscitation may be required at birth
Within 30 minutes, breathing becomes difficult
Within few hours, Cyanosis becomes evident
On auscultation, crepitations heard
X-ray shows ground glass appearance (granular densities)

18. • Surfactant synthesis is modulated by a variety of hormones and growth
factors, including cortisol, insulin, prolactin, thyroxine, and TGF-β.
• The role of glucocorticoids is particularly important.
• Conditions associated with intrauterine stress and FGR that increase
corticosteroid release lower the risk of developing RDS

19. Adult ARDS

20. sequence of events
leading to the
formation of hyaline
membrane in adult
acute respiratory
distress syndrome
(ARDS).

21. • The imbalance between proinflammatory and anti-inflammatory cytokines:
• i) Activated pulmonary macrophages release proinflammatory cytokines
such as IL8, IL1, and TNF,
• Neutrophils on activation release products which cause active tissue injury
e.g. proteases, platelet activating factor, oxidants and leukotrienes.
• ii) injury to the capillary endothelium leads to increased vascular
permeability while injured pneumocytes, especially type 1, undergo
necrosis. - oedema, congestion, fibrin deposition and formation of hyaline
membranes.
• As a result of coating of the alveoli with hyaline membranes, there is loss of
surfactant causing collapse resulting in ‘stiff lung

22. Histological
appearance of HMD.
There are alternate
areas of collapsed and
dilated alveolar
spaces, many of which
are lined by
eosinophilic hyaline
membranes.

23. Histological
appearance of HMD.
There are alternate
areas of collapsed
and dilated alveolar
spaces, many of
which are lined by
eosinophilic hyaline
membranes.

24. CONSEQUENCES
• 1. Death The mortality rate in
neonatal ARDS is high (20 to 30%) and is still higher in babies under 1 kg
of body weight
• 2. Resolution Milder cases of neonatal ARDS recover with adequate oxygen
therapy by ventilator-assist methods in a few days, while in adult ARDS
control of the trigger which initiated it may result in resolution.

25. CONSEQUENCES
• 3. Other sequelae Besides the two extremes—death and recovery,
• i) may develop broncho pulmonary dysplasia later on.
• ii) there may be development of desquamative interstitial pneumonia
(DIP) due to pneumocytes proliferation supervened with infl
ammation.
• iii) Patients of adult ARDS who survive acute episodes may develop
widespread interstitial fibrosis later and progress to diffuse fibrosing
alveolitis (Hamman-Rich syndrome)