Friday, June 23, 2017

Pathophysiology and Radiologic patterns of Atelectasis


Hey guys!

This post will be on the classification of Atelectasis based on its pathophysiology and a brief overview of its radiology patterns. 

Let us deal with the radiology aspects first:

1. Opacification of airless lobe and displacement of fissures,

2. displacement of hilar and cardiomediastinal structures toward the side of collapse,

3. narrowing of the ipsilateral intercostal spaces,

4. elevation of the ipsilateral hemidiaphragm,

5. compensatory hyperinflation and hyperlucency of the remaining aerated lung and

6. obscuration or desilhouetting of the structures adjacent to the collapsed lung (eg, diaphragm and heart borders).

Google the Chest X ray scans for atelectasis to consolidate the above points.


Now the lengthy part, The Pathophysiology. Let us start with active or obstructive atelectasis. 

1. Active/Obstructive Atelectasis.

Obstructive atelectasis is a consequence of blockage of an airway. Air retained in the alveoli distal to the occlusion is absorbed into the pulmonary capillary blood since the pressure of gases in the blood plasma (PvO2) is lower than that in the alveoli. For this reason, it is also called absorptive atelectasis. This causes the affected regions to become totally gasless and then collapse. 
Obstruction of a segmental bronchus is less likely to result in segmental atelectasis than obstruction of a lobar bronchus is to produce lobar atelectasis. This difference is because of collateral ventilation between bronchopulmonary segments within a lobe. 
Collateral ventilation occurs via the age-old physiologic adaptive process of recruitment and distension of neighbouring bronchioles. But three are three other players here, or brothers as I like to call them. A small anecdote to remember these three brothers:
Once there was a priest named Kohn who decided to help out a fellow bronchopulmonary segment in aeration. Brother Kohn being eldest and hence weak could only manage to dig a pore. His work was carried on by Brother Boren who bored (as his name suggests) and made this pore into a fenestration. There was still some work left. And for that Brother Boren asked the help of the engineer Brother Lambert. Brother Lambert, after much hard work was eventually able to dig up a canal all the way upto the neighbouring segment so that they can share the aeration bestowed upon them by Lord Almighty!
So we have three distinct collateral connections: 1. Pores of Kohn, 2. Fenestrations of Boren and 3. Canals of Lambert.
So you need to defeat these three if you want to cause obstructive atelectasis.
Let's dig a bit deeper into Fenestrations of Boren. These collateral channels are extensively prominent in an emphysematous lung. Now take a case of a 60 year old male smoker with emphysema who has now developed small cell carcinoma. Suppose there is a tumor mass obstructing the right bronchus, this patient will take a lot of time to develop obstructive atelectasis in the right lung because of the presence of extensive network of fenestrations of Boren. Hence, this patient will become symptomatic late and thereby will be diagnosed late. Blessing or Curse!
One more thing, it has been observed that atelectasis occurs more rapidly in patients on oxygen therapy. Why? There is a simple reason behind this. Oxygen is more soluble than nitrogen in water, when you give inhalational O2 with a FiO2 take 50%, you are altering the partial pressures of gases in the alveoli, Nitrogen which was 79% will fall down to below 50% and O2 which was 20% will rise upto 50%. Hence overall solubility rises, this elevates the tendency and spontaneity of gases diffusing into the blood plasma.

Honestly speaking, rest of the causes are nowhere as important as the one mentioned above so let us try to ace them quickly. 
2. Nonobstructive Atelectasis

A. Relaxation (ie, passive) atelectasis ensues when contact between the parietal and visceral pleurae is eliminated. While this is usually due to a pleural effusion or pneumothorax, a large emphysematous bulla can have a similar effect. In this case, the residual physiologic elastic recoil of normal lung parenchyma allows the normal lung to collapse away from the chest wall with consequent loss of volume.
The middle and lower lobes may shrink more than the upper lobe in the presence of a pleural effusion, while the upper lobe may be affected more by a pneumothorax.

B. Adhesive atelectasis is a consequence of alveolar instability due, in part, to surfactant deficiency or dysfunction. As its name suggests, the alveoli walls will collapse into the alveolar space sticking with each other. In the normal lung, surfactant reduces the surface tension of alveoli and decreases the tendency of alveoli to collapse. Decreased production or inactivation of surfactant leads to alveolar instability and collapse. Adhesive atelectasis is a major problem in respiratory distress syndrome of premature infants(IRDS), acute respiratory distress syndrome (ARDS) in adults, acute radiation pneumonia, and posttraumatic lung contusion.

C. Cicatrization (ie, cicatricial atelectasis) results from diminution of lung volume due to severe parenchymal scarring. Common underlying etiologies include granulomatous disease (eg, sarcoidosis), necrotizing pneumonia, and radiation pneumonia.
D. Acceleration Atelectasis- This type of atelectasis has been described in pilots subjected to very high, vertical accelerative forces between 5G and 9G: at 5G, up to 50 percent of pulmonary airways are distorted and closed due to gravitational forces. The atelectasis is exacerbated by breathing a high fractional concentration of oxygen. Decreases in vital capacity are a reflection of this type of atelectasis in pilots. Acceleration atelectasis can cause symptoms like chest pain, coughing, and dyspnea.
E. Rounded atelectasis (also called folded lung, Blesovsky’s syndrome, or atelectatic pseudotumor) is a distinct form of atelectasis associated with pleural disease, particularly following asbestos exposure and in India following pleural tuberculosis. Asbestosis is associated with pleural plaques and diffuse pleural thickening while pleural TB will have pleural thickening alongwith pleural effusion which eventually resolves with or without organization and pleural septations(Harbingers of Fibrothorax). 
In this condition, there is a subpleural mass mainly in the middle or lower lobes from which bronchi and blood vessels arise and they form a structure like a comet tail which traverses through the underlying atelectatic lung parenchyma to join at the hilum. Some un-astronomical sources compare this to a Vacuum Cleaner, with the dirt box as the subpleural mass and the hose as the comet tail. 

P.S. Blesovsky's Syndrome is not the only syndrome connected to pneumoconiosis, there is also Caplan's syndrome(Rheumatoid pneumoconiosis); which has a well-known mnemonic CAPlaN;
C- Coal workers' pneumoconiosis
A- Rheumatoid Arthritis
PlaN- Pulmonary nodule

That's all! 
-VM

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