Atelectasis, ARDS, Interstitial Pneumonia

Dr. Vinita Singh

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?

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 .

Types

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

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.

Cont’

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

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.

Aetiology

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

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

• Over 60 possible causes have been identified but the four most frequent causes include:

» Sepsis (Most common cause )» Aspiration» Pneumonia» Severe Trauma

Pathogenesis

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

Cont’

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

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.

• 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.

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

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.

• 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.

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

NORMAL ALVEOLUS

Type I cell

EndothelialCell

RBC’s

Capillary

Alveolarmacrophage

Type IIcell

ACUTE PHASE OF ARDS

Type I cell

EndothelialCell

RBC’s

Capillary

Alveolarmacrophage

Type IIcell

Neutrophils

• Three distinct stages (or phases) of the syndrome including:

» Exudative stage

» Proliferative (or fibroproliferative) stage

» Fibrotic stage

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.

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.

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.

• 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.

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

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.

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.

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