Panlobular emphysema is depicted by permanent destruction of the entire acinus distal to the respiratory bronchioles with no “obvious” associated fibrosis.
Panlobular emphysema is characterized by permanent destruction of the alveoli distal to the respiratory bronchioles.
The pathogenesis involves an intrinsic imbalance in the activity of protease/elastase released and an inhibitor of protease – alpha-1 antitrypsin.
Microscopical depiction involves abnormally enlarged alveoli with floating alveolar septa, but, as the disease progress, the lung parenchyma is further destroyed, and intervening alveoli walls become harder to find.
“Panlobular” refers to the involvement of the entire acinus of the lung, in contrast to the centrilobular distribution in a smoker’s lung.
Macroscopically, the lower lobes are affected more severely in panlobular emphysema,
Panlobular emphysema may involve the entire lung in a homogeneous manner, or it may show lower lobe predominance.
Two distinct patterns have been described:
1. Localized form: Multilobular distribution
2. Diffuse form: Distribution not related to the zonal anatomy of the lung
- Ritalin lung
- Obliterative bronchiolitis
- Alpha-1 antitrypsin deficiency: classical cause that may show a lower zone predominance
- Swyer-James syndrome: Affects one lung
- The condition can also manifest as a normal senescent finding in non-smokers
On the computed tomography, The entire lung appears darker with attenuation of bronchovascular markings.
The lung volumes are seen to be increased, and distinct spaces of low attenuation may not be seen.