This is essentially a disease of the lung alveoli, and the most prominent feature is an exudation of fibrine, from which the name croupous pneumonia is derived.
The Causation of pneumonia has been already considered at pp. 346, 347. Certain forms of microbes, of which the diplococcus of Fraenkel is the chief, are the active agents. These microbes are often present in enormous numbers in the exudation contained in the lung alveoli. The fact that the diplococcus is frequently present in the normal sputum, and consequently in the lung, points to the existence of other contributing causes. It is probable that certain conditions of the body, such as exposure to cold or a preceding attack of true influenza, may give occasion to the specific microbe and enable it to overcome the resistance of the tissues. It is to be remembered also that an acute pneumonia may be produced by an irritant in the blood, as indicated by the fact that it has been met with in cases where carbolic acid has been administered in considerable quantity by mistake.
Pneumonia is to be regarded as one of the acute specific fevers in which the infective agent has a local seat. The lungs present the more direct effects of the agent, but the general febrile disturbance is clinically the more important part of the phenomena. The fever has a distinct periodicity, and, consistently with this, there is an antitoxine produced, which has the power of conferring immunity (see pp.289-290).
Many epidemics of pneumonia have been observed in various quarters of the globe (see Hirsch). It is an interesting fact that occasionally epidemic outbreaks of fever of peculiar and unusual characters have been associated with acute pneumonia. Amongst these may be mentioned an epidemic which occurred in an industrial school in Glasgow, which in some of the earlier cases caused death within twenty-four hours of the onset, and which, in many of the cases which lived for a longer period or survived, was accompanied by a typical pneumonia. This epidemic could not be referred to any of the recognized forms of fever (see Eussell). Strain has also described an epidemic of pneumonia in South America.
The disease is an acute inflammation, and as the lung alveoli possess merely a single layer of pavement epithelium which is soon desquamated, the inflammation resembles that of serous rather than of mucous membranes. As in the former we have here a fibrinous exudation, and though this occurs primarily and mainly in the alveoli, the fibrine, as we shall see, generally extends to the finer bronchi, forming casts of them.
Pneumonia is divisible into several stages, which, however, to some extent merge into each other.
In the first stage, that of Engorgement, there is an active inflammatory hyperemia; the lung capillaries are highly injected, and there is an exudation of serous fluid into the air vesicles. To the naked eye the affected portion of lung is of a dark red colour, to the touch it is inelastic, and the finger applied to the surface leaves a pit behind. On section a reddish serum flows out, and the tissue does not crepitate under the knife so much as in the natural state. This state, from the resemblance of the cut surface of the diseased lung to the spleen, has been called Splenization. So far as the merely anatomical condition is concerned the lung is very much in the same state as in passive hyperemia and oedema, to which also the term splenization is applied. In pneumonia, however, the splenization is not localized in the dependent parts, but it affects a definite region of lung, generally the lower lobe as a whole, along with, perhaps, a portion of the upper. Like other inflammatory exudations, the serous fluid contains leucocytes and also red blood-corpuscles, sometimes in large numbers. As the alveoli are filled with serous fluid, the air, bubbling in and out among the fluid during respiration, produces the fine crepitation which is the characteristic auscultatory sign of this stage.
In the second stage, that of Red hepatization, we have fibrine deposited in the alveoli. In consequence a coagulum (Fig. 359) comes to occupy the lumen of the vesicles and infundibula, instead of the mixture of serous fluid and air which is present in the first stage. The coagulum, like the fluid, contains abundant leucocytes and some red corpuscles, the former often so abundantly as almost to conceal the fibrine. The fibrine may be detected as a coarse network of interlacing fibres (Fig. 360). The capillaries of the lung are in much the same state of over-distension as in the first stage, and the lung parenchyma is likewise little altered.
On microscopic examination of an ordinary section of the lung in this stage the lung alveoli are found to be occupied by solid plugs, to the entire exclusion of the air, as in Fig. 361. On closer examination of an unstained section, or by means of special staining, the fibrine will be detected as in Fig. 360.
The red corpuscles are present in the alveoli in very varying proportion. They are never entirely absent, but they form generally the minority of the total cells present; in some cases they are equal to the leucocytes, in some more abundant. In very rare cases they are so abundant that the exudation has more the character of an ordinary clot than of a fibrinous exudation. In these latter cases, which may be described as Haemorrhagic pneumonia, the lung itself has a deep red colour.
Fig. 359. - Cast of small bronchus, infundibula, and air vesicles in pneumonia, x 40. (Cornil and Ranvier).
Fig. 360. - A lung alveolus in acute pneumonia.
These are mostly very severe cases, and imply a previous state of debility in the patient, very commonly referable to alcoholic excess. In accordance with this exudation of red blood-corpuscles we have, in this and in the preceding stage, the rusty tinge of the sputum which is characteristic of pneumonia.