A seminar I made during my first year of medical college on the pathophysiology of RDS. feel free to tell me what you think.

1. Pathophysiology of
respiratory distress
syndrome [RDS].
(In adults and neonates)
By Alan E. Mizwari 1

2. We’re going to talk about:
• The surfactant, its’ functions and relation to RDS.
A brief description as well as pathophysiology, symptoms and
treatment of:
• Infant respiratory distress syndrome. Some statistics to
showcase it’s importance in pediatrics.
• Adult respiratory distress syndrome.
2

3. But first, to make sure we’re on the
same page..
Pathophysiology: The physiology of abnormal states;
specifically the functional changes that accompany a syndrome or
disease.
Syndrome: a group of signs and symptoms that occur
together and characterize a particular abnormality or condition.
3

4. Pulmonary surfactant
Neonate RDS is caused by the lack of sufficient amounts of
pulmonary surfactant mostly due to under development of the
neonate. Decreased surfactant is also a secondary to Adult RDS.
The pulmonary surfactant is a lipoprotein (with a polar and non
polar part) produced by type II alveolar cells that coats the inner
surface of the alveolus and has the following functions:
• facilitates its expansion during inspiration
• lowers alveolar surface tension at end-expiration, and,
thereby, prevents lung collapse.
• contributes to control of lung inflammation and innate and
adaptive immunity. 4

5. Illustrationofthestructureofanalveolus.
Notice how the fluid surface is occupied by the surfactant
5

6. Lung collapse prevention
mechanism
• The absence of sufficient surfactant leads to lung collapse at
the end of expiration due to the surface tension of the fluid.
• Surface tension occurs at any gas-liquid interface and refers to
the tendency for liquid molecules that are exposed to air to
adhere to one another.
• Surface tension increases the pressure needed to inflate the
alveolus according to the law of Laplace (P = 2T/r).
• The pulmonary surfactant coats the fluid surface and
therefore reduces the gas-liquid interface, thus effectively
reducing surface tension. 6

7. Surfactantandfluidsurfaceinterface
Notice how the polar part of the part faces the fluid while the non polar
part faces the air space.
Non polar part
Facing air space
Polar part
facing fluid
surface
7

8. To make things clear..
The surfactant is actually a liquid that exhibits surface tension
too however, the intermolecular bonds that cause surface
tension in the surfactant are much weaker than the molecular
bonds in the fluid.
8

9. Infant Respiratory distress
syndrome
Is very important in pediatrics since it’s a common cause of mortality
Extra details are provided later on.
Also known as Neonatal Respiratory Distress Syndrome [NRDS] and
hyaline membrane disease*, is a common cause of neonatal deaths,
particularly in premature infants (infants with a gestational** age of
less than 37 weeks are considered premature). In other words, most
NRDS cases are of premature neonates .
The mortality rate of NRDS neonates has fallen in the past decade due
to advances in treatment and prevention.
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*explained later
**Gestation refers to the length of time since the first day of the last monthly period. Gestational age is 2
weeks longer than the actual age of the child from the time of fertilization.
9

10. Some statistics.
Preterm births makeup 12% of all births. About 50-60% of
neonates with a gestational age of less than 29 suffer from RDS
The percentage declines with the increase of the gestational
age. So NRDS is fairly common.
In a study published in the International Journal of Clinical and
Experimental Medicine, out of 232 neonates diagnosed with
NRDS the following percentages of gestational age groups were
obtained:
• 37.07% (86) were full-term neonates (≥ 37 weeks)
• 15.52% (36) were late-term neonates (34 to less than 37
weeks)
• 47.41% (110) were early-preterm neonates (less than 34
weeks)
This means that 37.07% of the cases were term neonates
while 62.93% of the cases were premature neonates. Yielding
approximately a 5:3 ratio of premature to term.
10

11. Agraphshowing thedistributionofcasesamonggestationalages
inthe study
(thecaseswereobtainedoverthecourseoftwoyears)
11

12. So again.. The primary cause of NRDS is premature birth,
however it may also occur due to:
• Surfactant deficiency during disease
• Probable inadequate hormonal (corticoid) stimulus in
utero
• DPL synthesis impaired and/or destruction increased
• Autonomic dysfunction
12

13. • Infants of diabetic mothers and those with cesarean delivery
(especially elective C-section) are more likely to develop RDS.
• Premature Neonates.
• More common in boys than girls.
• More common in white infants.
• Family history of RDS.
Who’s at a greater risk?
13

14. Pathophysiology of NRDS.
Normally the first few inspirations after birth are difficult as the
lungs are first inflated; then breathing becomes easier as
residual air volume increases. But this is not the case with NRDS.
• inadequate surfactant causes heavily labored breathing
because the lungs totally collapse during each expiration.
• Increased use of accessory muscles to overcome the lung
collapse leading to chest retraction, which is a clinical sign
indicating RDS.
• Increased usage of accessory muscles increases the demand
for oxygen which is already insufficient. 14

15. 15

16. • inadequate blood and oxygen supply further deters the
production of surfactant by type II alveolar cells.
• Diffuse atelectasis results which decreases pulmonary blood
flow and leads to reflex pulmonary vasoconstriction and
severe hypoxia.
• Poor lung perfusion and lack of surfactant lead to increased
alveolar capillary permeability, with fluid and protein (fibrin)
leaking into the interstitial area and alveoli, forming the
“hyaline membrane”. This is why NRDS Is also known as
hyaline membrane disease
• The formation of the “hyaline membrane” further impairs
lung expansion and decreases oxygen diffusion. Some of the
surviving neonates experience brain damage due to severe
hypoxia.
16

17. • A vicious cycle results from metabolic and respiratory acidosis,
acidosis causes pulmonary vasoconstriction and impairs cell
metabolism, reducing the synthesis and secretion of
surfactant.
Respiratory acidosis is due to hypoventilation that increase the
partial pressure of CO2 leading to increased hydrogen and
bicarbonate formation according to the following equation:
The metabolic acidosis is caused by the hypoxia in the skeletal
muscles. since oxygen is not available to the skeletal muscle the
skeletal muscles resort to anaerobic respiration as an energy
source for their contraction. Lactic acid is a product of anaerobic
respiration. 17

18. Clinical signs
Respiratory difficulty may be evident at birth or shortly after
birth.
Initial signs include:
• A persistent respiratory rate of more than 60 breaths per
minute.
• nasal flaring (nostrils widen breathing).
• On auscultation, rales are heard (crackling sounds).
• Chest retractions .
• Low body temperature.
18

19. As the sickness progresses the following signs appear:
• Breathing becomes shallower and more rapid.
• frothy sputum.
• expiratory grunt develops.
• blood pressure drops.
• Cyanosis becomes evident (bluish discoloration of skin).
• peripheral edema.
As hypoxemia (lowed blood O2) reaches a severe state it’s signs
will appear, the signs include:
• Decreased responsiveness of the neonate.
• Apnea (temporary cessation of breath especially during
sleep).
• Decreased breath sounds. 19

20. Prevention
Ultimate treatment forNRDS would be prevention of premature
birth.
Lung maturity can be assessed during intra-uterine life by
amniocentesis to measure the lecithin/sphingomyelin ratio.
There is extensive evidence that when there is risk of preterm
labor antenatal corticosteroid therapygiven to the mother
between 26 and 34 weeks of gestation reduces the incidence of
RDS and death.
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*Amniocentesis: a process in which amniotic fluid is sampled using a hollow needle inserted into the uterus,
to screen for abnormalities in the developing fetus.
20

21. Figureillustrating amniocentesis
The needle is guided with the help of ultrasonography to avoid damaging the fetus.
21

22. Treatment
includes:
• Synthetic surfactant administered to the high-risk neonate
both as prophylaxis (postnatally) and as necessary therapy.
• Supportive care includes oxygen administration and
mechanical ventilation. However both have risks, as increased
intrapulmonary oxygen pressure can cause pulmonary damage
(Bronchodysplasia *) and permanent damage to the retina of
the eye and loss of vision.
• Most infants survive RDS. Recovery may be complete
within 10 to 14 days in some cases.
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*may also be caused by mechanical ventilation
22

23. Adult respiratory distress
syndrome
Also known as Acute Respiratory Distress Syndrome [ARDS]. Has many
causes, it’s also known as shock lung, wet lung, stiff lung,
postperfusion lung, and a variety of other names related to specific
causes.
ARDS has a wide variety of causes. However, All the different causes of
ARDS share the same effect of eliciting lung inflammation by causing
acute injury to the alveolocapillary membrane.
Causes include but are not limited to: inhalation of toxic chemicals or
smoke; excessive oxygen concentration in inspired air; severe viral
infections in the lungs; toxins from systemic infection (sepsis and
septic shocks; fat emboli; explosions; aspiration of highly acidic gastric
contents; or lung trauma. cancer, and acute pancreatitis.
23

24. Pathophysiology
Injury to the alveolocapillary membrane causes iflammation
leading to:
• Increased permeability of alveolocapillary membrane which in
turn leads to leakage of fluid and proteins into the interstitial
space as well as damage to the surfactant producing cells.
• Leakage of proteins also leads to the formation of hyaline
membrane (which reduces compliance and oxygen diffusion).
• Diffuse atelectasis (lung collapse) due to the increased fluid
within the alveoli and reduced surfactant production.
• Decreased vital capacity and tidal volume (ARDS is actually
classified as a restrictive lung disease).
24

25. 25
• aggregation and microthrombi develop in the pulmonary
circulation, causing stiffness and decreased compliance.
• Excess fluid in the lungs predisposes to pneumonia as a
complication. Congestive heart failure may develop.
• As more neutrophils migrate to the lungs, lung tissue
damage increases.
• Metabolic and respiratory acidosis

26. 26
Yep.. The prognosis is generally poor,
with a case fatality rate of 30% to
40%, but depends on the underlying
problem (with infection, the case
fatality rate is 80% to 90%).

27. Clinical symptoms
• Early signs may be masked by the effects of the primary
problem.
• Onset is usually marked by dyspnea, restlessness, rapid,
shallow respirations, and increased heart rate. significant
decrease in Po2. As lung congestion increases, the accessory
muscles are used, rales can be heard, cough with frothy
sputum may be evident, and cyanosis and lethargy with
confusion develops.
27

28. Treatment
• The underlying cause must be successfully treated
• supportive respiratory therapy such as oxygen therapy and
mechanical ventilation.
• Administration of fluid may be limited to minimize alveolar
edema
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29. 29

30. Sources..
1. Pathophysiology for health professionals 4th edition. By
Barbara E. Gould and Ruthanna M. Dyer
2. Pathophysiology The biologic basis for disease in adults and
children 7th edition
3. A study published in the International Journal of Clinical and
Experimental Medicine. Study online link:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4659032/#
__ref-listidm140548358134896title
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