The blood is hyperinotic in croupous pneumonia, and, while the amount of fibrin is only slightly increased at the very onset, the amount obtainable goes on increasing until the eighth or ninth day; i.e. as the amount of fibrinous exudation within the alveoli augments, so does the same factor appear in greater quantity in the blood—a circumstance whose opposite condition we should expect to observe. In infectious diseases—e.g. variola—as the temperature rises the hyperinosis increases. In pneumonia, however, the pyrexia and fibrin increase in the blood and bear no relationship to each other. The amount varies greatly in every case; it has reached 10.5 in 1000.
Around the zone of pneumonic inflammation it is not infrequent to discover pulmonary oedema; and in many fatal cases extensive oedema seems to be the direct mode of death.
Temporary compensatory emphysema may occur in the neighborhood of the inflamed lobe or lobes. It may be mentioned that when emphysema has previously existed the pulmonic granules observable in the second stage are of unusually large size.
The bronchial glands are enlarged and congested, and in rare instances they may suppurate. The lymphatics of the lung are choked with fibrin and with red and white blood-corpuscles, and the deeper lymphatics contain products identical with those in the pulmonary alveoli. In both lymphatic vessels and in the lymph-glands (bronchial) at the root of the lung there are always well-marked evidences of inflammation.
The liver and spleen are congested, the latter organ especially presenting the characteristics which are found in it in cases of death from fevers.
Finally, gastro-intestinal catarrh is occasionally observed, and in rare cases it is attended by ulceration and hemorrhage. But there seems no good reason for believing that there is any connection between pneumonia and these intestinal changes. Indeed, most of the observations bearing on this point were made during cholera epidemics. Still, analogous influences might induce both at the same time.
No change in the brain accompanies pneumonia, except congestion. Pus and inflammatory products when found in the meshes of the pia-mater are in all probability due to coexisting meningitis or cerebro-spinal meningitis of an epidemic character.
ETIOLOGY.—The specific cause of croupous pneumonia is as yet undetermined, and the very existence of such a cause is still a matter of conjecture.
Among the predisposing causes age ranks first. There are three distinct periods of life in which the liability to pneumonia is greatest—viz. in early childhood, between the ages of twenty and forty, and after sixty.
Notwithstanding the fact that catarrhal pneumonia is a very common disease in childhood,9 the statement that croupous pneumonia is rare at this period cannot be received.10 From a number of statistical tables it appears that it is five times more frequent during the first two years of life than in the succeeding eighteen.11 It is met with most frequently between the ages of twenty and forty, and after a lapse of twenty years the predisposition to it increases, pneumonia being the most fatal of all acute diseases after the sixtieth year. Nine-tenths of the deaths from acute diseases after the age of sixty-five are from pneumonia. Each year after sixty the liability to it is greatly increased.