When the disease follows upon an attack of croupous pneumonia the change principally involves the alveoli. The walls of the air-cells become greatly thickened, and in some cases, at least, as in an instance reported by Dr. Sidney Coupland, the exudation products filling the alveoli become or ganised into a fibrillated and at first vascularised mesh-work. By this means the alveoli are either compressed or filled up, and in either case ef faced ; and as the tissue shrinks, the new vessels which had been devel oped in the growing tissue become obliterated.
If the cirrhosis originate in a bronchopneumonia the alveolar walls are thickened as in the former case ; but in addition there is great develop ment of fibroid tissue in the walls of the bronchi and in the connective tissue between the lobules. In these cases whitish bands are seen radia ting from the thickened walls of the air-tubes.
When the morbid process starts from the pleura, dense fibrous bands pass inwards from the surface. The pleura itself is greatly thickened, and the lung-tissue underlying it may be converted after a time into a dense fibrous substance. At first, however, the fibroid degeneration is more partial than in cases where the disease is the consequence of pneumonia.
Microscopic examination discovers closely packed wavy fibres in the denser portions, or even a homogeneous or faintly fibrillated material with a few small round or fusiform cells.
The alveoli, where not completely compressed and effaced, are either empty or are filled with nucleated and epithelial cells, granular corpuscles, and granules.
The bronchi are either obliterated or are greatly thickened and dilated, especially in parts where the disease is most advanced. The tubes are in some cases regularly enlarged, but sometimes more local dilatations are seen forming cavities of various sizes. The lining mucus membrane may be ulcerated, and in very advanced cases ulcerative destruction of tissue may have penetrated from these spots into the lung. This form of the disease has been called "fibroid phthisis" by Sir Andrew Clark.
Fibroid induration is usually limited to one lung, the other being healthy or emphysematous. It may occupy any part of the organ but more commonly affects the base than the apex.
In addition to the mischief in the lung, disease is often found in other parts. The liver, spleen, and sometimes the kidneys may be the seat of amyloid degeneration. In some cases the liver has been found to be cir
rhotic and the kidneys to be granular.
Symptoms.—In the early stage of the disease the development of fibroid_ tissue in the lung is accompanied by no special symptoms. The process most commonly begins at the end of an attack of catarrhal pneumonia. In some children we find a peculiar tendency to recurring attacks of this form of pneumonia of very unusual duration. Between the attacks the child seems almost well, and an examination of the back detects merely a slight impairment of resonance on one side (best detected by "broad percus sion " upon three fingers at once), with perceptible increase in the resist ance. The respiratory sounds, however, are normal. When an attack of catarrhal pneumonia comes on, the symptoms and signs are those peculiar to that form of inflammation of the lung. If death occur after a prolonged attack of bronchopneumonia, we may find one of the lungs small, shrunken, and particularly firm to the touch ; and notice on section that the inter lobular septa and walls of the bronchioles are much thickened, especially at the base of the organ, and that the bronchi are dilated. Such a con dition constitutes an early stage of the fibroid change in the lung. The incipient fibrosis, beyond conferring a certain high-pitched quality upon the percussion note--and this sign is but an indefinite one—gives rise to no symptoms. Nutrition is not interfered with, the appetite is good, and the temperature is normal. Pyrexia, cough, loss of appetite, and impairment of nutrition only occur as a result of an intercurrent inflammatory attack ; and at these times only are any pronounced physical signs to be detected on examination of the chest. Dulness is then marked and extensive ; the breathing becomes blowing or tubular ; and coarse bubbling or sub-crepi tant rhonchus—more or less metallic and ringing according to the degree of acute dilatation of the tubes—is to be heard with the stethoscope. After each of these attacks the lung is left in a distinctly worse condition than before. The fibroid overgrowth increases in the lung ; the bronchi get to be permanently dilated ; and the lining membrane of the air-tithes becomes the seat of more or less persistent catarrh.