#RESPIRATORY DISEASES- “ARDS”( ACUTE RESPIRATORY DISTRESS SYNDROME).!!

Helloo steemians and my dear friends,

Today i want to tell you about ACUTE RESPIRATORY DISTRESS SYNDROME. But what does it mean??

First of all ARDS is not a disease entity, its a clinical condition. Any syndrome is a condition which might be caused by a single disease or a group of various diseases.

image source: OAWhealth

It is charecterised by

1. Abrupt onset of significant HYPOXEMIA and
2. Bilateral pulmonary infiltrates in the absence of cardiac failures.

UNDERLYING FACTORS

Image source: Robbinn textbook of pathology

PATHOGENESIS

There are 4 stages in the pathogenesis of ARDS which were intiated by *injury of Pneumocytes and pulmonary Endothelium.

1. Endothelial Activation:
   This can be directly by tissue injury and by sepsis or secondarily due to pneumocyte injury.
   In both of the cases, inflammatory mediators plays a crucial role in activating the endothelium. Hence it is good to say that ARDS IS A CONDITION RELATED TO INFLAMMATION.
   Inflammatory mediators like TNF factor and other circulating mediators activates the endithelium and this is the first step in the pathogenesis.

2. Adhesion and Extravasation of Neutrophils:
   As we previously said ARDS is condition due to abnormality in INFLAMMATION and the most important agent that cause damage in ARDS are NEUTROPHILS.
   They migrate to the alveoli and interstium - release some mediators like Proteases, reactive o2 species, cytokines and most importsnt one is MIF ( Macrophage migration Inhibitory Factors).
   This is the important step in the Endothelial Injury.
   
   Image source: Robbins textbook of Pathology

3. Accumulation of intra alveolar fluid and Hyaline membrane formation.
   Endothelial injury leads to pulmonary capillary leak and further keads to intra alveolar oedema. And Damage to type 2 Pneumocytes leads to accumulation of dead epithelium.
   Both these together helps in the formation of Hyaline Membrane which looks Hyaline disease of neonates.

4. Resolution of Injury:
   As there is both the Endothelial damage and the Epithelial necrosis, resolution is impeded.
   But in case if ghe inflammatory stimulus lessens there is a chance of resolution by a series of events where the macrophages clears away the debris and release fibrogenic cytokines which stimulate the deposition of collagen.
   Bronchilar stem cells proliferate to replace pneumocytes and Endothelial restoration by proliferation of uninjured capillary Endothelium.

MORPHOLOGY:
GROSS appearance:

1. Lungs look heavy, red and boggy and they are congested with intra alveolar edema.
2. There is wide spread inflammation, fibrin deposition and Diffuse alveolar damage
   
   Image source: wikimedia commons.

Histology:

1. Alveolar walls are lines with waxy hyaline membrane
2. In the organising stage, type 2 pneumocyte proliferation and granulation in the alveolar walls can be seen.

Image source: wikipedia

CLINICAL FEATURES:

1. Hospitalised mainly due to the underlying condition which predisposes to ARDS
2. Dyspnea and Tachyonea.
3. Diffuse alveolar Damage in radiological Examination.
4. Hypoxemia may be seen in oxygen therapy which is due to ventilation-perfusion mismatch. This may also leads to respiratory acidosis.
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   Image source: Pinterest.

TREATMENT:
Treating the underlying condition is the effective way and no other strategies will give good results.
The underlying factors which can be treated are Trauma and Sepsis.

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