walls. The air-cells immediately about this tubercle are always found to exhibit more or less catarrhal inflammation.

The increase in the size of the original lesion might go on indefinitely if certain accidental factors did not cooperate against it. Thus we find with the infiltration of the interalveolar septa destruction and obstruction of the capillaries. In the tuberculous tissue no new capillary blood vessels are formed, so that there soon comes a time when the nutrition of the inflammatory tissue is outgrown, and coagulation necrosis sets in and both cells and micro-organisms at the center of the tubercle die, the younger tubercle bacilli being found in large numbers only in the newly invaded tissue. The tubercle bacilli are in all probability frequently picked up by leukocytes or other phagocytic cells, and carried to the lymphatics, where they seem to overpower their captors, grow, and produce secondary tubercles. It may also be true that the lymph-currents themselves occasionally detach and carry away the tubercle bacilli, and remembering the great blood vascularity and equally great lymph vascularity of the pulmonary tissues, it is easy to understand how a focus of tuberculous disease may become a center from which the process extends in all directions, and leads to an extensive invasion of the lung.

While this is going on the size of the original lesion continues to increase by the incorporation of outlying tubercles as they are reached. The center is continually degenerating-that is, caseating. Cavities are formed of tuberculous tissue in various ways: for example, from a large, caseous, primary lesion, or from a similar secondary lesion, the extension of the tuberculous disease into the bronchial tube may offer an opportunity for the escape of the softened, necrotic center of the tuberculous mass. In this way a ragged hole is formed, small in the beginning but continually tending to increase in size. Such a cavity presents an irregular wall of yellowish or yellowish-gray, cheesy, tuberculous tissue. The bronchial vessel from which its contents escape may appear to enter at one side and leave it at the other, or may enter and apparently not leave it, the proximal portion having been obliterated by the tuberculous inflammation or plugged by inhaled secretions. If thick-walled blood vessels occur in the immediate surroundings, they may appear as ridges upon the walls of the cavity, or may extend as cords directly through it. The distending influence of the inspired air will always aid in increasing the size of cavities. The entering air brings into the cavity mucous secretion from the inflamed bronchioles with which it connects, and with this secretion, bacteria of putrefaction or of suppuration, which, by developing in the necrotic material within the cavity, cause a rapid destruction of the tissue and somewhat change the natural order of events, by the production of purulent or even gangrenous lesions. At other times the wall of a bronchial vessel is weakened, without being perforated or eroded by the tuberculous process, when bronchiectasis occurs.

The erosion of blood vessels within tuberculous cavities not infrequently causes hemorrhage. If capillaries are eroded, the hemorrhage is slight and the sputum blood-stained. If large vessels rupture, the hemorrhage may be large or even fatal. Blood vessels with tuberculous, weakened walls dilate, with the formation of small aneurysms, which, should they rupture, produce severe and sometimes fatal hemorrhage. The presence of escaped blood into the tuberculous cavity facilitates the growth of saprophytic bacteria, and thus aids the further progress of the secondary infections. The pulmonary tuberculosis is invariably associated with bronchitis, the mucopurulent discharges from the inflamed tubes, mixed with the necrotic material from the cavities, forming the sputum so characteristic of the affection.

During the time that the cheesy material is being discharged from the

cavity into the tube with which it communicates, and while the tuberculous area is disseminating its infectious micro-organisms through the lymphatics and thus invading new tissue, there is a continual backward and forward movement of infectious material in the air-passages of the lung, constantly invading new parts of the bronchial tree. With each expiratory effort the infectious matter is carried outward; with each succeeding inspiratory effort

FIG. 281.-Tuberculosis of the lung: the upper lobe shows advanced cheesy consolidation with cavity-formation, bronchiectasis, and fibroid changes; the lower lobe retains its spongy texture, but contains numerous miliary tubercles.

it is carried back again into deeper and heretofore uninvaded air-passages, so that a triple infection is continually in progress: (1) By continuity of tissue; (2) through the lymphatics; (3) through the air-tubes. Thus, from a single primitive lesion of the lung, the whole organ may become involved and transformed into an almost unrecognizable, consolidated, cheesy, eroded, and cavernous mass of diseased tissue.

The disease of the lung usually does not progress very far before tuberculous changes are inaugurated within the bronchial lymphatic glands. It is interesting that the disease of these organs is subordinate to that of the lungs, and only in rare cases progresses more rapidly than the original lesion. Occasionally the erosion of a blood vessel enables infectious material to enter the blood-stream, and, by disseminating the bacilli through the systemic circulation, occasions general miliary tuberculosis.

Hematogenous Pulmonary Tuberculosis.-In this form of tuberculosis the primary lesion, instead of occurring within air-cells, takes place within capillary blood vessels. The bacilli are not inspired, but carried to the lung from tuberculous foci elsewhere, in the form of minute emboli. They probably enter the thoracic duct by way of the lacteals with the products of digestion, reach the venous circulation, and are then conveyed to the lungs. Should a single embolus containing a tubercle bacillus thus enter the lung, a miliary tubercle will be formed, differing from other miliary tubercles only in that its primitive cells have been derived from the endothelium of the capillary blood vessels and from the cells of the surrounding interalveolar tissue. Before the tubercle attains visible dimensions it encroaches upon the air-cells and occasions within them a catarrhal inflammation identical with that already described in connection with the aërogenic tubercles. One by one the neighboring cells are filled up and included, and thus in a short time a lesion similar to that already described will be formed.

It often happens that great numbers of tubercle bacilli are carried to the lung by the venous blood from tuberculous lesions of the spinal column, testicle, joints, etc., in a short time causing the formation of a great number of miliary tubercles. Sometimes both lungs appear filled with equally distributed, minute tubercles, originating in this manner. This is called miliary tuberculosis of the lung.

Lymphogenic Pulmonary Tuberculosis.-The lymphatic form of pulmonary tuberculosis most frequently succeeds tuberculosis of the bronchial glands and pleura, the tubercle bacilli being carried from these tissues into the lung tissue itself via the lymphatics. In tuberculous bronchial lymphadenitis the perforation of the enlarged, softened, and ulcerating glands into a bronchus or even into the lung itself, followed by discharge of their contents into the air-passages, causes what is really a form of secondary aërogenic tuberculosis.

Tuberculous extension takes place from the pleura both by continuity of tissue and by distribution of the bacilli along the lymphatic vessels of the pulmonary septa and those about the bronchial vessels. There is usually little difficulty in detecting the pleurogenic pulmonary tuberculosis, as the diseased pleura is so altered in appearance as to be quite characteristic.

The tubercle formation or eruption is accompanied by more or less hyperemia of the surrounding lung and by alveolar and bronchial catarrh. The bronchi usually manifest signs of inflammation; the mucous membrane is red, may contain a mucopurulent, sometimes a bloody, material. When many tubercles are present, the lung is consolidated and denser and contains less air than normal. The exclusion of air from the lung is always in proportion to the amount of consolidated pulmonary tissue. When the tuberculous areas are of large size, the tissue appears solid, yellowish or grayish, sometimes friable, sometimes softened, and creamy or even purulent. Cavities when present appear as irregular spaces in the consolidated tissue. Sometimes neighboring cavities communicate with one another.

The tuberculous disease may be confined entirely to one lung, but it is somewhat unusual to find advanced tuberculosis of one lung without some involvement of the other. The lungs are rarely uniformly affected, the dis

ease usually being much more advanced in one than the other. The disease is rarely limited to the natural divisions of the lung, several or all of the lobes of the diseased lung being simultaneously, though not equally, affected.

In advanced cases the disease may transform an entire lung into a consolidated mass of yellowish tissue, riddled with cavities, divided up by dense bands of connective tissue, and covered with a thickened pleura, and devoid of any resemblance to normal pulmonary tissue.

The remaining air-containing portions of the lung are rarely normal in appearance, because of an acute or chronic distention (compensatory emphysema). Along the free borders of the lung, and here and there upon its surface, one finds groups of distended air-cells. The plugging of the bronchial vessels with secretions and cheesy matter from the cavities, and the obliteration of the smaller bronchial tubes by the development of tubercles in and around them and the swelling of their lining membrane, predispose to atelectasis. Fresh atelectasis in the tuberculous lung is common.

Bronchopneumonia is a common secondary process in tuberculosis of the lungs, depending upon the entrance of infectious material. It is usually, but not always, tuberculous in nature, and tends to diminish the air-space by increasing the amount of consolidated tissue.

Tuberculous Pleuritis.-Tuberculosis of the lung rarely progresses to any considerable extent without affecting the pleura, which is at first likely to undergo a simple local inflammation over the tuberculous area, but very frequently becomes agglutinative, so that the parietal and visceral pleuræ unite. When this does not occur, the pleura over the tuberculous lung almost invariably becomes much thickened, and not infrequently exhibits a number of miliary tubercles upon its surface, or immediately beneath it. In the more chronic cases the thickening of the pleura probably aids the progress of the disease by keeping the lung from properly expanding.

According to the course of the disease different appearances are presented. Thus, when the progress is extremely rapid, the lung may consolidate so quickly and uniformly as to bear a close resemblance to the stage of gray hepatization of croupous pneumonia. In such lungs there may be no excavations or cavities. This is sometimes spoken of as tuberculous pneumonia. When less rapid and accompanied by consolidation with numerous small excavations, the condition which leads to a rapid fatal termination is spoken of as phthisis florida. The ordinary form, which is familiar to every practitioner and soon becomes familiar to every student, is that in which the disease is of months' and sometimes of several years' duration. It is usually called caseofibroid phthisis, and seems to indicate some resisting power on the part of the patient.

In the caseofibroid tuberculosis of the lungs, together with cheesy areas, excavations, fresh miliary tubercles, bronchiectasis, emphysema, atelectasis, etc., one finds also new formation of connective tissue, sometimes surrounding tuberculous areas, sometimes taking on the form of a hyperplasia of the pulmonary trabecula and peribronchial tissue, which seems to indicate a tendency of nature to shut off, encapsulate, or organize the specific inflammatory lesions. Extensive areas of tissue may show marked connective-tissue formation, but though healing is in progress in some parts of the organ, the destructive lesions are steadily gaining upon it elsewhere, and ultimately the individual is obliged to succumb.

Rarely the disease takes an essentially chronic course in which the multiplication and dissemination of tubercles are held in abeyance for years by an enormous hyperplasia of connective tissue, surrounding, encapsulating, and isolating the tuberculous areas. Unfortunately, however, in fibroid phthisis the connective-tissue formation is itself far from benign, and the isolating and encapsulating bands, when they subsequently contract, deform the lung, diminish its size, distort the chest (especially when pleuritic adhesions exist), and diminish the breathing space.

Recovery from Pulmonary Tuberculosis.-Recovery occurs when the immunity of the patient checks the further spread of the disease. It takes place by organization, encapsulation, isolation, and subsequent calcification of the lesions already present. It is quite probable that it is not less the encapsulating barrier formed to limit the disease than that peculiar resisting power of the individual which enables the barrier to be formed that predisposes to recovery. The isolated and encapsulated tuberculous tissue undergoes caseation, and in it both cells and tubercle bacilli seem to die. In the molecular débris lime-salts are usually deposited. It is quite common to find firm fibroid and calcified tuberculous nodules in the apices and sometimes in the lower lobes of the lungs of individuals dying from other affections. In size they vary from that of a pin-head to that of a pigeon's egg. They are firmly encapsulated in the connective tissue, and when incised, are found to consist entirely of chalky material, which the knife penetrates with difficulty. These are in all probability healed tubercles, although it is not always possible to differentiate between the healed tubercle and a healed abscess or gumma.

Complications of Pulmonary Tuberculosis.-Pleuritic Adhesions.-These are extremely common. When extensive, they diminish the respiratory movements and probably thus facilitate the spread of the tuberculous disease. In fibroid phthisis, by uniting the lung with the wall of the chest, they enable the contracting bands of tissue to draw upon the chest-wall so as to deform the thorax. The adhesions result from pleuritic inflammations secondary to the tuberculosis, but not always themselves tuberculous. The pleuritic adhesions found in tuberculosis pulmonalis may at times be independent of the tuberculosis and subsequent to prior simple pleuritis.

Suppuration and Gangrene.-These two processes depend upon the accidental entrance of septic micro-organisms into a tissue of diminished vital resistance. The appearances are quite typical and need no repeated description.

Empyema.-The occasional discharge into the pleural cavity of pyogenic micro-organisms or tubercle bacilli from subpleural tuberculous lesions not infrequently causes suppuration of the pleura, or empyema. The empyema is, however, frequently preceded by pneumothorax.

Pneumothorax.-This results from the rupture of a tuberculous cavity, permitting air to enter the cavity of the pleura. It causes collapse of the lung, with great embarrassment of respiration and compression of the lung. As the escape of air is usually accompanied by the escape of septic organisms, the development of pneumothorax is almost invariably followed by suppuration and forms a pyopneumothorax.

Hemorrhage.-Hemorrhage from the lung-hemoptysis-may occur from the oozing of the blood from eroded capillaries, usually situated in the walls of the cavities. It may occur from the direct erosion of a blood vessel of considerable size, but is usually preceded by aneurysmal dilatation resulting from weakening of the walls of the vessel. The hemorrhages are of all degrees of severity-sometimes only sufficient to tinge the expectoration slightly red, sometimes large enough to cause the death of the patient from loss of blood. When large hemorrhages are not fatal, they are usually distinctly detrimental, in that the blood which escapes by way of the air-vessels is sucked back into the bronchioles and air cells with each inspiratory effort, thus lessening the already diminished breathing space, increasing the amount of effete matter contained within the lungs, and paving the way for the development of any septic and putrefactive organisms that may be present. For this reason hemorrhages are sometimes followed by gangrene of the lung.

It.

Syphilis of the Lung.-Syphilitic disease of the lung is rare. may be either congenital or acquired. The congenital form is by far the more common. Its usual appearance is that known as white pneumonia, a form resembling bronchopneumonia.

White pneumonia is characterized by the occurrence of consolidated patches which may unite and form lobar areas of inflammation. The disease is so called because of the whitish or grayish color of the inflamed patches, which are completely consolidated. When examined with the microscope, desquamation of the epithelial cells of the alveoli, similar to that seen in catarrhal pneumonia, is observed. There are marked infiltration of leukocytes and a characteristic proliferation of cells in the interalveolar tissue. The blood vessels of the alveolar walls show thickening of the intima. In the lung tissue immediately surrounding the patch there is imperfect devel