1. Atelectasis, acute respiratory distress syndrome & pulmonary edema
Morphology will be discussed in the lab
Ali Al Khader, M.D.
Faculty of Medicine
Al-Balqa’ Applied University

2. Atelectasis = Collapse
= Inadequate expansion and subsequently: No lung volume
It will cause hypoxia and may be complicated by infection of the collapsed lung tissue
3 main types:
1-Resorption atelectasis…reversible
2-Compression atelectasis…reversible
3-Contraction (cicatrization) atelectasis…irreversible

3. Types of atelectasis Fibrosis of the lung or the pleura -Postoperative
-Bronchial tumor
-Foreign body
-Asthma
-Chronic bronchitis
-Bronchiectasis
Types of atelectasis
-Pneumothorax
-Hydrothorax/
pleural effusion
-Hemothorax
-Mesothelioma
-Metastates to pleura
-Basal atelectasis: in
the bedridden and in
ascites
Fibrosis of the lung or the pleura

4. Acute respiratory distress syndrome (ARDS)
The severe end of acute lung injury (ALI) spectrum…but no more use of the term “Acute lung injury”
Defined as: respiratory failure occurring within 1 week of a known clinical insult with bilateral opacities on chest imaging, not fully explained by effusions, atelectasis, cardiac failure, or fluid overload
It is an extensive bilateral alveolar damage with resultant bilateral non-cardiogenic edema due to the material spilled from the blood to the alveolar spaces

5. ARDS, cont’d
…graded based on the severity of the changes in arterial blood oxygenation …rapid onset of life-threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia that is refractory to oxygen therapy ***Diffuse alveolar damage (DAD) is the histological manifestation***
Remember: hyaline membranes

6. ARDS, causes Pneumonia Sepsis Aspiration
Trauma (including brain injury, abdominal surgery, and multiple fractures)
Pancreatitis
Transfusion reactions
The most common
Respiratory distress syndrome of the newborn is different from ARDS and is caused by surfactant deficiency

7. ARDS, pathogenesis
Alveolar-capillary membrane damage due to endothelial and epithelial injury with loss of surfactant
Mainly by an inflammatory reaction due to pro-inflammatory mediators
A role of IL-8, IL-1 & TNF…especially neutrophil recruitment

8. ARDS, clinical features
In 85% of cases, it develops within 72 hours of the initial insult
The overall hospital mortality rate is 38.5%...high mortality
Most patients who survive the acute insult recover normal respiratory function within 6 to 12 months
…the rest develop diffuse interstitial fibrosis leading to chronic
respiratory insufficiency

9. Pulmonary edema
*Left-sided heart failure Venous congestion (a passive process) in lung veins Increased hydrostatic pressure Pulmonary edema
Acute pulmonary congestion
Chronic pulmonary congestion
Blood-engorged alveolar capillaries
Thickened & fibrotic alveolar septa
Alveolar septal edema
Numerous hemosiderin-laden macrophages (“Heart failure cells”) in the alveolar spaces
Intra-alveolar hemorrhage

10. Thank You