1) The document discusses three lung conditions: atelectasis, ARDS, and interstitial pneumonia. It provides details on the causes, symptoms, diagnosis, and pathogenesis of each condition. 2) ARDS is characterized by diffuse pulmonary edema and hypoxemia. It develops due to acute lung injury from direct or indirect causes like sepsis, trauma, pneumonia, etc. There are three stages: exudative, proliferative, and fibrotic. 3) The pathogenesis of ARDS involves damage to lung endothelial and epithelial cells by cytokines and neutrophils, leading to accumulation of fluid in the lungs and impaired gas exchange. This results in hypoxemia and reduced lung compliance.

1. Atelectasis, ARDS, Interstitial
Pneumonia
Dr. Vinita Singh

2. CASE -1
A 7yr old boy accidentally inhales a small
peanut , which lodges in one of the bronchi.
A chest X – ray reveals the mediastinum to be
shifted towards the side of the obstruction .
What is the diagnosis?

3. Atelectasis
Definition : Refers either to incomplete
expansion of the lungs ( neonatal atelectasis)
Or to the collapse of previously inflated lungs ,
Producing areas of relatively airless pulmonary
Parenchyma .

4. Types
1. Resorption ( obstructive ) : Mucus plugs ,
exudates , Foreign bodies aspiration,
2. Compression : CHF, pneumothorax
3. Contraction : Fibrosis of lung

5. CASE - 2
A 26 yr old man barely survives a house fire .
He is taken unconscious to the hospital where
over next several days he develops worsening
signs of respiratory failure .
A chest X- ray on third hospital day reveals a
complete “ White - Out ‘’ of both lungs .
Laboratory evaluation finds severe hypoxemia
that does not improve with 100% oxygen.

6. Cont’
1. What is the probable diagnosis?
2. What is the etio - pathogenesis ?

7. ARDS
Definition: Manifestation of severe ALI.
( Acute Lung Injury )
ALI( k/n as noncardiogenic pulmonary edema)
is characterized by the abrupt onset of
significant hypoxemia and bilateral pulmonary
infiltrates in the absence of cardiac failure.

8. Aetiology
Direct Precipitating Cause
• Pneumonia
• Aspiration
• Pulmonary embolism
• Pulmonary contusion
• Inhalation injury
• Reperfusion injury
• Chest trauma with lung contusion
• Near-drowning

9. Indirect (Systemic) Precipitating Cause
• Sepsis
• Blood transfusions with transfusion-related acute lung
injury (TRALI)
• Trauma with multiple fractures and the fat-emboli
syndrome
• Burns
• Acute pancreatitis
• Post-cardiopulmonary bypass
• Toxic ingestions, e.g., aspirin, tricyclic antidepressants

10. • Over 60 possible causes have been identified
but the four most frequent causes include:
» Sepsis (Most common cause )
» Aspiration
» Pneumonia
» Severe Trauma

11. Pathogenesis
Initiated by injury of pneumocytes and
pulmonary endothelium .
Viscous cycle of inflammation and pulmonary
damage .

12. Cont’
1. Endothelium activation
2. Adhesion and extravasation of neutrophils
3. Accumulation of intraalveolar fluid and
formation of hyaline membrane.
4. Resolution of injury.

13. Pathology and Pathophysiology
• In normal, healthy lungs there is a small
amount of fluid that leaks into the
interstitium. The lymphatic system removes
this fluid and returns it into the circulation
keeping the alveoli dry.

14. • ARDS is a consequence of an alveolar injury
which produces diffuse alveolar damage. The
injury causes the release of pro-inflammatory
“cytokines”.
• Cytokines recruit neutrophils to the lungs, where
they become activated and release toxic
mediators (eg, reactive oxygen species and
proteases) that damage the capillary
endothelium and alveolar epithelium.

15. • Damage to the capillary endothelium and
alveolar epithelium allows protein to escape
from the vascular space.

16. Breakdown of the alveolar epithelial barrier allows the air
spaces to fill with bloody, proteinaceous edema fluid and
debris from degenerating cells. In addition, functional
surfactant is lost, resulting in alveolar collapse.

17. • Healthy lungs regulate the movement of fluid
to maintain a small amount of interstitial fluid
and dry alveoli.
• Lung injury interrupts this balance causing
excess fluid in both the interstitium and
alveoli.

18. Results of the excess fluid include impaired gas exchange, decreased
compliance, and increased pulmonary arterial pressure.

19. NORMAL ALVEOLUS
Type I cell
Endothelial
Cell
RBC’s
Capillary
Alveolar
macrophage
Type II
cell

20. ACUTE PHASE OF ARDS
Type I cell
Endothelial
Cell
RBC’s
Capillary
Alveolar
macrophage
Type II
cell
Neutrophils

21. • Three distinct stages (or phases) of the
syndrome including:
» Exudative stage
» Proliferative (or fibroproliferative) stage
» Fibrotic stage

22. Exudative Stage (0-6 Days)
Characterized by:
• Accumulation of excessive fluid in the lungs due to
exudation (leaking of fluids) and acute injury.
• Hypoxemia is usually most severe during this phase of
acute injury, as is injury to the endothelium (lining
membrane) and epithelium (surface layer of cells).
• Some individuals quickly recover from this first stage;
many others progress after about a week into the
second stage.

23. Proliferative Stage (7-10 Days)
• Connective tissue and other structural elements
in the lungs proliferate in response to the initial
injury, including development of fibroblasts
• The terms "stiff lung" and "shock lung" frequently
used to characterize this stage.
• Abnormally enlarged air spaces and fibrotic tissue
(scarring) are increasingly apparent.

24. Fibrotic Stage ( >10-14 Days)
• Inflammation resolves.
• Oxygenation improves and extubation becomes
possible.
• Lung function may continue to improve for as long as 6
to 12 months after onset of respiratory failure,
depending on the precipitating condition and severity
of the initial injury.
• Varying levels of pulmonary fibrotic changes are
possible.

25. • Because cardiogenic pulmonary edema
must be distinguished from ARDS,
carefully look for signs of congestive
heart failure or intravascular volume
overload, including jugular venous
distention, cardiac murmurs and gallops,
hepatomegaly, and edema.

26. Approach to Clinical Diagnosis
• Chest Radiograph -diffuse, bilateral alveolar
infiltrates consistent with pulmonary edema
• Early in the course of the disorder, the infiltrates
associated with ARDS may be variable: mild or
dense, interstitial or alveolar, patchy or confluent
• Initially, the infiltrates may have a patchy
peripheral distribution, but soon they progress to
diffuse bilateral involvement with ground glass
changes or frank alveolar infiltrates

27. Morphologic Feature
GROSS: Lungs are heavy , firm , red and boggy.
MICROSCOPIC: Interstitial and intra-alveolar
edema , inflammation , fibrin deposition ,
Diffuse Alveolar Damage .
The alveolar walls lined by hyaline membrane.

28. Acute Interstitial Pneumonia
ALI of unknown etiology associated with a
rapidly progressive clinical course.
Occurs at 5- 6 decades .
Pt. presents with acute respiratory failure often
Following an illness of less than 3 weeks
duration.

29. THANKS