Senile Emphysema is that occurring in old age from atrophy of the intervesicular septa. The lung is smaller than normal and frequently accompanied by edema, congestion or even infarction. Vicarious emphysema is that found in one part of the lung as a result of obstruction in some other portion. The uninvolved portions of the lung in bronchopneumonia may show a temporary dilatation.

Pneumonia

Pneumonia, or inflammation of the lungs, can be divided into various forms according to the nature of the inflammatory exudate, to the mode of entrance of the etiologic material, and to the portion of the lung involved. Fibrinous pneumonia when the exudate into the air-sacs and bronchioles is rich in fibrin; catarrhal when the exudate contains an albuminous fluid in which are desquamated epithelial cells and erythrocytes; purulent when pus cells are numerous; caseous when there is cheesy necrosis, and fibrous when there is extensive fibrous connective-tissue formation.

It may be lobar or lobular.

Aërogenic when the infecting substance is conveyed by the air through the bronchi; hematogenic when carried by the blood; lymphogenic, by the lymphatics; pleurogenic, by extension from the pleura.

Inspiration pneumonia, when a large amount of infecting substance gains entrance by the bronchi.

Hypostatic, when the blood, on account of weakened circulatory efforts, settles in the dependent portions of the lung and consolidation takes place.

Pneumonias may also be acute or chronic.

Lobar, fibrinous, or croupous pneumonia is an acute infectious disease, generally caused by the diplococcus of Fränkel. Although usually primary it may follow in the course of other infectious diseases. It usually involves one or more lobes, an entire lung, or rarely both lungs. It is characterized by an exudation, rich in fibrin, into the air-spaces and bronchioles.

Morbid Anatomy

The lower lobe of the right lung is most frequently first involved, then the lower left, the apices seldom primarily. An entire lobe is generally involved.

The course of the disease can be best studied by arbitrarily dividing it into three stages - that of congestion, of red and gray hepatization, and of resolution. It must be remembered that all of these conditions may be present in one lung at the same moment.

Fig. 141. - Lung. Lobar Pneumonia (Mallory).

Alveolus filled with an exudation of serum and polymorphonuclear leukocytes. Much fibrin has formed. At two points it runs through openings in the alveolar wall.

Stage Of Congestion

The lung is actively hyperemic, dark red in color, enlarged, and firm. Unlike the healthy lung it is very friable and contains but little air. The air-vesicles are filled with fluid in which are found pneumococci, numerous red cells, a few leukocytes, epithelial cells, and bacteria. The capillaries are greatly distended.

Stage Of Red Hepatization

In this the exudate has undergone coagulation and there is complete absence of air from the involved area. The lung is solid and resembles the liver in consistency. It may weigh as much as 1500 to 2500 gm. Is swollen, dark red in color, and pits on pressure. From the cut surface, which is quite dry, there project minute plug-like bodies formed largely of fibrin, leukocytes, red cells and epithelium, which give a granular appearance to the tissue. They are formed by the coagulated exudate in the alveoli being pushed outward by the contraction of the elastic fibers. The pleura generally shows some fibrinous exudate. Microscopically the air-vesicles are seen to be filled with red cells entangled in a network of fibrin; leukocytes and epithelial cells are also present. The capillaries are less prominent. The diseased tissue will sink when placed in water. The expectoration in this stage is blood-streaked, or rusty.

Stage Of Gray Hepatization

With the beginning of this stage recovery is indicated. The red cells lose their hemoglobin, the exudate softens and the lung becomes gray or yellowish. This is shown microscopically to be due to changes taking place within the alveoli. The blood-supply being interfered with, the exudate undergoes fatty degeneration, probably due in large part to the greatly increased autolytic processes. The erythrocytes have broken down, the fibrin has disappeared in part, and leukocytes are now present in great numbers. The exudate no longer closely adheres to the walls, but leaves space for the entrance of air.

Stage Of Resolution

The broken-down exudate is removed by absorption and by expectoration, which is no longer rusty, but is purulent. The leukocytes also carry off much of the debris. The lung becomes more moist, is less solid, and crepitation returns. The epithelium of the alveoli and bronchioles proliferates and the lung returns to the normal. There is sometimes a delay in the return of the normal elasticity of the alveolar walls.

Instead of the lung returning to the normal various complications may arise. Infection by pyogenic bacteria may take place, with abscess-formation. Gangrene may also follow, particularly if the circulation is weak. Resolution may be delayed and proliferation of connective tissue occur, giving rise to fibrous pneumonia. Microscopically there is seen an extensive cellular infiltration and proliferation. The septa become much thickened and masses of connective tissue extend into the air-vesicles. In alcoholics there is a marked hemorrhagic tendency.

There may be serious conditions associated with lobar pneumonia. The uninvolved portions may be emphysematous and congested, and sometimes edema develops. The infecting organism may gain entrance into the blood and cause inflammations of the serous membranes, particularly endocarditis, pericarditis or meningitis. Cardiac disturbances may occur, probably due to the action of toxins. There is also usually some involvement of the kidneys. Leukocytosis is generally marked. Tuberculosis may follow the pneumonia.

The symptoms in this disease would seem to depend more upon a toxic condition than upon mechanical obstruction to breathing by the filling of the alveoli. This would seem to be shown by the fact that on the fall of temperature, the crisis, the alarming objective symptoms subside. Yet a physical examination made at that time shows no changes in the lung itself.

Death may result from the action of the toxins, from overburdening of the heart, or from some of the associated conditions, as edema or gangrene.