The Common Vein

• Etymology
  Derived from Latin: “diffusus” (spread out), “alveolus” (small cavity), and “damnum” (harm or loss).
• AKA
  DAD
• What is it?
  Diffuse Alveolar Damage (DAD) is the histopathological hallmark of acute lung injury, characterized by widespread damage to the alveolar-capillary barrier. It involves alveolar edema, hyaline membrane formation, and interstitial inflammation, commonly associated with Acute Respiratory Distress Syndrome (ARDS) and Acute Interstitial Pneumonia (AIP).
•  While DAD is a pathological term, ARDS is a clinical syndrome diagnosed based on imaging, hypoxemia, and exclusion of cardiac causes. Radiologists should use the term ARDS when interpreting imaging in a clinical context and reserve DAD for pathological discussions or biopsy-based findings.
• Caused by
  • Direct lung injuries
    • Pneumonia
    • Aspiration of gastric contents
    • Inhalational injuries (e.g., smoke, toxic gases)
    • Pulmonary contusion
  • Indirect lung injuries
    • Sepsis
    • Severe trauma or burns
    • Pancreatitis
    • Transfusion-related acute lung injury (TRALI)
  • Other causes
    • Viral infections (e.g., COVID-19, influenza)
    • Autoimmune diseases (e.g., systemic lupus erythematosus, rheumatoid arthritis)
    • Drug-induced lung injury (e.g., chemotherapy, amiodarone)
• Resulting in
  • Impaired gas exchange due to alveolar flooding and reduced compliance
  • Acute hypoxemic respiratory failure
  • Fibrosis in severe or unresolved cases
• Structural changes
  • Alveolar flooding with protein-rich fluid
  • Hyaline membrane formation along alveolar ducts
  • Interstitial inflammation and edema
  • Fibroblast proliferation and fibrosis in chronic phases
• Pathophysiology
  • Injury to alveolar epithelium or capillary endothelium disrupts the alveolar-capillary barrier.
  • Increased permeability allows fluid and proteins to flood alveoli, leading to hyaline membrane formation.
  • Impaired gas exchange occurs due to alveolar collapse, interstitial thickening, and inflammation.
• Pathology
  • Exudative phase
    • Alveolar edema
    • Hyaline membranes
    • Infiltration by neutrophils and macrophages
  • Proliferative phase
    • Type II pneumocyte hyperplasia
    • Interstitial fibroblast proliferation
    • Alveolar septal thickening
  • Fibrotic phase
    • Collagen deposition
    • Honeycombing
    • Pulmonary hypertension due to vascular remodeling
• Diagnosis
  • Clinical
    • Acute onset of dyspnea and hypoxemia
    • Bilateral pulmonary infiltrates
    • Absence of cardiogenic pulmonary edema
  • Radiology
    • CXR
      • Bilateral diffuse opacities
      • Air bronchograms
    • CT
      • Ground-glass opacities
      • Consolidation
      • Dependent atelectasis
  • Labs
    • Arterial blood gases indicating hypoxemia
    • Elevated inflammatory markers
• Management
  • Supportive care
    • Mechanical ventilation with lung-protective strategies
    • Prone positioning to improve oxygenation
  • Treat underlying causes
    • Antibiotics for infections
    • Immunosuppressants for autoimmune causes
• Radiology Detail
  • CXR
    • Findings
      • Diffuse bilateral opacities with sparing of lung apices
    • Associated Findings
      • Air bronchograms
  • CT
    • Parts
      • Involves alveolar spaces and interstitium
    • Size
      • Diffuse or focal involvement depending on severity
    • Shape
      • Consolidation with ill-defined borders
    • Position
      • Dependent lung zones are often more involved
    • Character
      • Ground-glass opacities with superimposed consolidation
    • Time
      • Progresses from exudative to fibrotic phases over days to weeks
    • Associated Findings
      • Subpleural sparing in some cases
  • Other relevant Imaging Modalities
    • MRI: Rarely used for acute conditions but can help in chronic phases.
    • PET-CT: Can detect inflammation or infection in atypical cases.
  • Pulmonary function tests (PFTs)
    • Severe restrictive pattern with reduced lung volumes.
• Recommendations
  • Early recognition and treatment of underlying causes.
  • Optimize oxygenation and minimize ventilator-induced lung injury.
  • Follow-up imaging to assess resolution or progression to fibrosis.
• Key Points and Pearls
  • DAD is the hallmark of ARDS and represents a spectrum of acute lung injuries.
  • Ground-glass opacities and consolidation are typical imaging findings.
  • The progression from acute to fibrotic phases requires close monitoring, as it may result in irreversible damage.
  • Early intervention can significantly improve outcomes in reversible cases.

Distinction Between Diffuse Alveolar Damage (DAD) and Acute Respiratory Distress Syndrome (ARDS)

What is DAD?

• DAD is a pathological term used to describe the histological findings of acute lung injury.
• It is characterized by hyaline membrane formation, alveolar edema, type II pneumocyte hyperplasia, and interstitial inflammation.
• DAD is the underlying histopathologic correlate of ARDS and Acute Interstitial Pneumonia (AIP).

What is ARDS?

• ARDS is a clinical syndrome defined by a set of criteria (e.g., Berlin definition), including:
  • Acute onset of respiratory failure.
  • Bilateral pulmonary infiltrates on imaging.
  • Hypoxemia not fully explained by cardiogenic causes.
• ARDS is diagnosed based on clinical presentation and radiologic findings, not pathology.

When Should a Radiologist Use the Term DAD vs. ARDS?

• Use DAD:
  • When discussing histopathological features, either in the context of biopsy findings or theoretical explanations of lung injury patterns.
  • In academic or research settings where the focus is on lung pathology.
• Use ARDS:
  • When describing clinical-radiologic syndromes with bilateral pulmonary infiltrates and hypoxemia.
  • When correlating imaging findings with a clinical diagnosis made by the treating team.
  • For imaging reports, ARDS should be used instead of DAD, as it aligns with clinical terminology.

Incorporation into the DefinitionWhat is it?