Lab investigations:

There are no characteristic abnormalities in ARDS, except related to a specific underlying condition e.g. leucocytosis in sepsis, raised serum amylase in pancreatitis etc.

Chest X-Ray: Initially may be normal but soon diffuse bilateral interstitial or alveolar infiltrates develop.

CT scan (Chest): Heterogeneous pattern with a predominance of infiltrates in the dependent regions of lungs.

Pathophysiology:

ARDS may be the pulmonary manifestations of a systemic process and is the consequence of an over expression of the normal     inflammatory response. There are 3 overlapping phases in inflammatory cascade (Figure 1):

1. Initiation: Any precipitating event (e.g. sepsis) causes production of variety of mediators and cytokines (TNF - a, IL-1) by immune or non-immune cells.
   
   
2. Amplification: Effector cells e.g. neutrophils are activated recruited and retained in specific target organs such as lungs. Interleukin - 8 (IL-8) is important for activation and released by monocytes.
   
   
3. Injury: Production of reactive oxygen metabolites and proteases causing cellular damage.

Pathophysiologic hallmark of ARDS is increased vascular permeability to proteins. Even mild increase in pulmonary capillary pressure (because of increased intravascular fluid or myocardial depression) causes increased interstitial and pulmonary edema.

• Alveolar damage occurs also because of:
  
  
  • Quantitative reduction of surfactant synthesis due to injury to type-II pneumocytes
    
    
  • Qualitative abnormality in size, composition and metabolism of the remaining surfactant pool causing alveolar collapse.
    
    
  
  
• There is increased pulmonary airway resistance due to:
  
  
  • Bronchial wall edema
    
    
  • Cytokine mediated bronchospasm.
    
    
  
  

Effect on pulmonary vasculature: Pulmonary artery pressure and pulmonary vascular resistance may be increased due to following reasons:

• Increased pulmonary vascular smooth muscle tone
  
  
• Perivascular edema
  
  
• Microvascular thrombosis
  
  
• Humoral factors e.g. - leukotrienes, thromboxane-A2 causing vasoconstriction.