patoloji-ders-notlari

Atelectasis and Acute Lung Injury

Serdar Balcı

Atelectasis and Acute Lung Injury

Serdar BALCI, MD

Lungs

• Bronchi
• Bronchioles
• Terminal bronchioles
• Acinus
  • Respiratory bronchioles
  • Alveolar sacs
  • Alveoli
• Bronchi
• Bronchioles
• Terminal bronchioles
• Acinus
  • Respiratory bronchioles
  • Alveolar sacs
  • Alveoli

Basement membranes

Robbins and Cotran Pathologic Basis of Disease

Basement Membranes

Capillary

Pneumocytes

Robbins Basic Pathology

Pulmonary interstitium

Fine elastic fibers

Small bundles of collagen

Few fibroblast-like cells

Smooth muscle cells

Mast cells

Rare mononuclear cells

Robbins Basic Pathology

• Alveolar epithelium
• Type I pneumocytes
  • Flattened, platelike
  • 95% of the alveolar surface
• Type II pneumocytes
  • Rounded
  • Synthesize pulmonary surfactant
  • Main cell type involved in repair

Robbins Basic Pathology

Alveoli

• Alveolar walls
  • Not solid
  • Perforated by numerous pores of Kohn
  • Permit passage of air, bacteria, and exudates between adjacent alveoli
• Alveolar macrophages
  • Lie free within the alveolar space
  • Phagocytosed carbon particles

ATELECTASIS

Atelectasis

Collapse

Loss of lung volume

Inadequate expansion of air spaces

Shunting of inadequately oxygenated blood from pulmonary arteries into veins

Ventilation-perfusion imbalance

Hypoxia

Resorption atelectasis

Obstruction prevents air from reaching distal airways

Air already present gradually becomes absorbed

Alveolar collapse follows

Robbins Basic Pathology

Entire lung

A complete lobe

One or more segments

Robbins Basic Pathology

Obstruction of a bronchus by a mucous or mucopurulent plug

Postoperative

Bronchial asthma

Bronchiectasis

Chronic bronchitis

Tumor

Foreign body aspiration

Robbins Basic Pathology

Compression atelectasis

• Passive or relaxation atelectasis
• Accumulation within the pleural cavity
  • Fluid
    • Transudate
    • Exudate
  • Blood
  • Air
    • Pneumothorax
• Mechanical collapse of adjacent lung

Robbins Basic Pathology

• Pleural effusion
  • Most commonly by congestive heart failure
• Leakage of air
  • Pneumothorax

Robbins Basic Pathology

• Basal atelectasis
  • Bedridden patients
  • Ascites
  • During and after surgery

Robbins Basic Pathology

Contraction atelectasis

Cicatrization atelectasis

Local or generalized fibrotic changes in the lung or pleura

Cannot expand

Increase elastic recoil during expiration

Robbins Basic Pathology

PULMONARY EDEMA

Pulmonary Edema

Leakage and accumulation of excessive interstitial fluid in the alveolar space

Caused by:

Hemodynamic disturbances

Microvascular injury

ACUTE LUNG INJURY

Acute lung Injury

• Endothelial and epithelial pulmonary damage
• Clinically
  • Acute onset of dyspnea
  • Decreased arterial oxygen pressure
    • Hypoxemia
  • Development of bilateral pulmonary infiltrates on the chest radiograph
• No primary left-sided heart failure

Acute Respiratory Distress Syndrome (ARDS)

• Diffuse alveolar capillary and epithelial damage
  • Rapid onset
  • Life-threatening respiratory insufficiency
  • Cyanosis
  • Severe arterial hypoxemia
  • Refractory to oxygen therapy
  • Progress to multisystem organ failure
• Histology → Diffuse alveolar damage (DAD)

Robbins Basic Pathology

Respiratory distress syndrome of the newborn

Caused by a primary deficiency of surfactant

Acute Respiratory Distress Syndrome (ARDS)

• The alveolar-capillary membrane has two separate barriers
  • Microvascular endothelium
  • Alveolar epithelium
• In ARDS
  • integrity of this barrier is compromised
  • either endothelial or epithelial injury
  • more commonly, both
• Acute consequences
  • Increased vascular permeability
  • Alveolar flooding
  • Loss of diffusion capacity
  • Widespread surfactant abnormalities caused by damage to type II pneumocytes

Robbins Basic Pathology

1. Endothelial activation

• 30 minutes after acute insult
• Macrophages
  • Proinflammatory cytokines
  • IL-8, IL-1, TNF
• Neutrophil attraction

Robbins Basic Pathology

2. Adhesion and extravasation of neutrophils

• Neutrophils
  • sequestration in the pulmonary microvasculature
  • Margination
  • Go to alveolar space, undergo activation
• Increased numbers of neutrophils
  • Vascular space
  • Interstitium
  • Alveoli

Robbins Basic Pathology

3. Accumulation of intraalveolar fluid and formation of hyaline membranes

• Activated neutrophils release
  • Leukotrienes
  • Oxidants
  • Proteases
  • Platelet-activating factor
• Local tissue damage to endothelium and epithelium
• Accumulation of edema fluid in the air spaces
• Surfactant loss
  • Inability to expand
• Hyaline membrane formation

Robbins Basic Pathology

4. Resolution of Injury

• Macrophage
  • TGF-β, PGDF
  • Stimulate fibroblast growth
• Collagen deposition
• Fibroblasts → Fibrosis
• Bronchiolar stem cells → pneumocytes
• Uninjured endothelial cells → endothelial restoration

Robbins Basic Pathology

Acute phase of ARDS

• Lungs are dark red, firm, airless, and heavy
• Microscopic examination
  • Capillary congestion
  • Necrosis of alveolar epithelial cells
  • Interstitial and intra-alveolar edema and hemorrhage
  • Collections of neutrophils in capillaries
    • Abundant in sepsis
• Characteristic finding → Hyaline membranes, lining the distended alveolar ducts

Diffuse alveolar damage

Lungs are heavy, firm, boggy, red parenchyma

Alveolar remodeling, interstitial fibrosis, cyst formation

Autopsy Pathology: A Manual and Atlas

Robbins Basic Pathology

Diffuse alveolar damage

Some of the alveoli are collapsed, others are distended

**Many lined by hyaline membranes **

Hyaline membranes

Fibrin-rich edema fluid

Remnants of necrotic epithelial cells

Similar to respiratory distress syndrome in the newborn

Resolution of Injury and Organizing stage

Proliferation of type II pneumocytes

Organization of the fibrin exudates

Intra-alveolar fibrosis

Thickening of the alveolar septa

Proliferation of interstitial cells and deposition of collagen

Robbins Basic Pathology