Acute Respiratory Distress Syndrome ARDS Pathology,Pathophysiology

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Results

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

Lab Investigations and Pathophysiology

Related topics

Introduction Predisposing Factors and Clinical Features

Management and Prognosis

Dr Vishal Dublish, Dr Ira Shah

Continued...

Pathophysiology:

Pathology of ARDS: 3 distinct phases:

Exudative phase: Starts within few days after lung injury. It is characterized by:
- Extensive epithelial cell injury especially to type I pneumocytes and basement membrane denudation.
- Swelling of endothelial cells with widening of intercellular junctions.
- Formation of hyaline membrane composed of fibrin and other matrix protein in alveolar ducts and airspaces.
- Neutrophilic infiltration
- Fibrin thrombi in alveolar capillaries and small pulmonary arteries.
Proliferative phase: This phase is most prominent in second or third week after onset of symptoms and is characterized by :
- Resolution of neutrophilic infiltration
- Cuboidal type II cells and squamous epithelium cover over denuded alveolar basement membrane.
- Migration of fibroblast and myofibroblasts through breaks in alveolar membrane.
Fibrotic phase: After few weeks. It is characterized by :
- Architectural resolution of lung tissue
- Type III elastic collagen is replaced by Type I rigid collagen causing stiff lung.
- Interstitial fibrosis with or without cystic and honeycomb changes leading to chronic pulmonary dysfunction and/or death.

Statistical facts of ARDS and sepsis:

Sepsis especially gram negative with shock is the most common and frequent risk factor.
Frequency of ARDS with sepsis is 18-38%.
18-25% of patients with gram negative sepsis develop ARDS.
Bacteremia with sustained hypotension is the harbinger for development of ARDS.
30% of patients with septic shock develop ARDS while only 14% of patients with sepsis without shock develop ARDS.
When DIC is present, 38% patients developed ARDS, while only 17% developed ARDS when DIC was not present.

Figure 1: Pathophysiology of ARDS

SEPSIS

Release of inflammatory mediators (lipopolysaccharide, Cytokines, TNF-a, IL-1ß, IL-8 etc.)

Acute systemic inflammatory response

Neutrophil sequestration
(More immature, less deformable and less motile)

Increased adhesiveness of neutrophils to endothelium

Initially loose adhesion (Rolling effect)
Later on firm adhesions

Neutrophil migration (chemotaxis) from vascular space into pulmonary interstitium or alveoli

Neutrophil activation and release of oxidative metabolites and proteolytic enzymes

Epithelial and endothelial cell injury
Loss of barrier function
Increased capillary permeability
Impaired gas exchange

Acute lung injury / ARDS

Next : Management and Prognosis

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