000 ARDS

ARDS is characterized by an
- acute and diffuse inflammatory damage
- into the alveolar-capillary barrier
  - increased vascular permeability increase and
  - Caused by
    - direct (pulmonary ARDS) or
    - indirect (nonpulmonary ARDS),
    - Most Common

Patient with ARDS HIV Fournier Gangrene
CXR shows diffuse ground glass and multifocal subsegmental infiltrates consistent with ARDS
Ashley Davidoff MD The CommonVein.net

Patient with ARDS HIV Fournier Gangrene
CTscan shows diffuse ground glass and multifocal subsegmental infiltrates consistent with ARDS
Ashley Davidoff MD The CommonVein.net

Patient with ARDS HIV Fournier Gangrene
CTscan shows diffuse ground glass and multifocal subsegmental infiltrates consistent with ARDS. Noted also are moderate bilateral effusions
Ashley Davidoff MD The CommonVein.net

DAD
- Diffuse alveolar damage (DAD) is manifested by
  - injury to alveolar lining and
  - endothelial cells,
  - pulmonary edema,
  - hyaline membrane formation and
    - later by proliferative changes involving
      - alveolar and
      - bronchiolar lining cells and
      - interstitial cells
DAD is the stereotypical morphology of ARDS,
Clinical syndrome of ARDS is not synonymous with the pathologic diagnosis of DAD
DAD pattern is often characterized by hyaline membranes in acute phase but shows a wide variety of findings that makes the diagnosis challenging
Buzz in a Nutshell
- Acute
- Diffuse
- Extensive
- bilateral
- without upper or lower lobe predominance
- Can be regional,
  - depending on the degree and cause of the inflammation
Alveoli
Causes either
pulmonary or
severe systemic disease

Cellular Makeup of the Normal Alveolus
The diagram shows the lining of the normal alveolus composed of type 1 pneumocyte squamous in nature and the cuboidal cell (type pneumocyte) which rest on a lamina propria, and basement membrane (not shown) shared with the inner endothelial layer of the capillary. Intra-alveolar macrophage lies within the alveolar lumen
Ashley Davidoff
TheCommonVein.net

ARDS – Causes
The lung is injured either by direst causes most commonly pneumonia, aspiration or from inhalation of toxic substances. Severe systemic illnesses, most commonly sepsis with shock, and severe trauma are considered indirect causes.
Ashley Davidoff
TheCommonVein.net

- Exudative (acute) phase: 1 – 7 days
  - Early Events in the Pathophysiology of the ARDS
    The initial injury results in an acute severe inflammatory response consisting hyperemia , edema with migration initially of neutrophils in the first 6-24 hours followed by monocytes (24-48hours). The intra -alveolar macrophages are activated.
    Ashley Davidoff
    TheCommonVein.net
    
    Result of Cellular Response
    The cells of the immune system release cytokines, chemotactic agents and proteases. Immune cells , macrophages and fibroblasts are attracted to the interstitium. Some of proinflammatory agents are toxic to the cell lining causing damage to the surfactant, type 1 pneumocytes and the capillary endothelium. There is progressive edema.
    Ashley Davidoff
    TheCommonVein.net
    
    Result of Cellular Response and Associated Tissue Injury
    The damage to the endothelium of the capillary results in bleeding into the alveoli. The severe tissue damage and fluid exudation results in protein rich intra-alveolar fluid . The fibroblasts start to lay down collagen as part of the early repair process
    Ashley Davidoff
    TheCommonVein.net
    
    Hyaline Membrane
    A hyaline membrane evolves covering the damaged surface of the alveolus. This impedes gas exchange
    Ashley Davidoff
    TheCommonVein.net
    
    Acute exudative phase of diffuse alveolar damage with prominent hyaline membranes (DAD)
    Courtesy Dr Yale Rosen
    
    ARDS
    Acute Exudative Phase
    Ashley Davidoff
    TheCommonVein.net
    
    ARDS
    Ashley Davidoff
    TheCommonVein.net
  - Neutrophil mediated inflammation
    - neutrophils predominate in the first 6 to 24 hours
      - (monocytes predominate in 24-48 hours)
    - Neutrophils destroys the alveolar capillary barrier (alveolar epithelium and endothelium),
    - increases its permeability
    - results in intra-alveolar hemorrhage and
    - edema
    - interacts with alveolar surfactants,
    - resulting in decreased pulmonary compliance
    - hyaline membranes develop in the alveolar wall
- Proliferative / organizing (subacute) phase: 8-14 days
  - restoration of type II pneumocytes a
  - differentiation into type I pneumocytes
  - proliferation of myofibroblasts

Pale eosinophillic polypoid proliferation of myofibroblasts protruding into the alveolar spaces
Courtesy Akira Yoshikawa

Masson body exhibits weak staining on elastic van Gieson
Courtesy Akira Yoshikawa

CXR
diffuse coarse reticular opacities
does not imply irreversible fibrosis,
- - opacities may resolve
- Fibrotic (chronic) phase: after 3 weeks
  - Collagenous fibrosis in
    - alveolar spaces and
    - interstitium
  - rigidity of alveoli due to architectural remodeling
  - Extensive interstitial and intra-alveolar fibroblastic proliferation
    Courtesy Dr Yale Rosen
    
    Dense collagenous fibrosis with destruction of the alveolar architecture
    Courtesy Akira Yoshikawa

53 F ARDS

Diffuse Ground Glass with Basilar Infiltrates

Acute Exudative Phase

Acute exudative phase of diffuse alveolar damage with prominent hyaline membranes (DAD)
Courtesy Dr Yale Rosen

ARDS
Acute Exudative Phase
Ashley Davidoff
TheCommonVein.net