109 Thèse de Paris, 1869.
110 E. Moutard-Martin.
PATHOLOGICAL ANATOMY.—This is shown by an examination of the effused liquid, the different solid detritus that it contains, the false membranes, the pleura, the lung, and the thoracic wall itself. The liquid effused is purulent in character. It contains a greater or less number of leucocytes, some red globules, and voluminous granular cells, besides crystals of the fatty acids and plates of cholesterin. The pus is mixed with the serosity in varying quantities. The liquid may be slightly opaline or greenish-yellow, and sometimes gray. It may be thin or thick, with heavy flocculi, so as to pass with difficulty through a canula. The liquid is, ordinarily, inodorous, but it may be strong, and even fetid, where it has been in contact with air. In very few cases of old standing can the pus be regarded as active, the corpuscles being, as a rule, dead or having undergone fatty degeneration. Active suppuration is also more readily set up in a pleura which has already yielded pus.
Purulent effusions, independent of contact with air, may become in a short time the seat of putrid transformations. False membranes undergo alterations which produce fetid gases. The air, with its germs, its humidity, and heat, the three grand factors in putrefaction, is thrown in contact with substances of a putrescible composition. Marshall111 holds that sero-fibrinous effusions appear to have a greater tendency to quick decomposition when air is admitted into the pleural sac than the sero-purulent or purulent products. Pus, he considers, is more stable and less inclined to rapid putrefaction than sero-albuminous fluid. In quantity it varies from a very small number of grammes to five or even six liters. By examining the fluid first drawn out we can predict, by the number of leucocytes present, whether the pleurisy will continue to be serous or will become purulent. If subjected to the influence of ammonia, it will become thready, just as happens when pus is suspended in water, if the fluid contains many of these pus-elements. The purulent fluid may fill the whole or occupy but a small part of the cavity, or again the interlobular spaces only may contain the fluid, the cavity itself being empty. False membranes are almost constantly present and adherent to the parietal or pulmonary pleura; we find them also floating in the liquid. These false membranes may be more or less voluminous. The flocculi, which may be as large as an egg, undergo transformation when air is admitted, and become horribly fetid. They may give rise to septicæmic symptoms. When we see these enormous masses in the cavity, and are unable to get rid of them by suction, we do not wonder that their presence should poison the patient and the case become incurable. Pleurotomy is the only effective mode of getting rid of these dangerous masses, with sometimes gangrenous portions of pleural or lung-tissue. These false membranes frequently form pouches and divisions for isolated quantities of fluid. The false membranes are partly adherent and partly free, especially in cases where there are pulmonary or thoracic fistula. These false membranes differ in acute purulent pleurisies from those found in pleurisies of long standing. They are but feebly adherent to the pleura, and have a slight rose coloration. In old pleurisies the false membranes are of greater density, sometimes from 6 to 8 mm. in thickness. They are more adherent, and cannot be separated, and have a grayish color. The physical state and position of the lung and disposition of the adjoining structures are very similar to what they are in serous effusions. In but few cases do the false membranes envelop the whole of the lung. They pass over one part, and on to the costal pleura. The pulmonary tissue is condensed, sometimes absolutely impermeable to air, so that it will actually sink when dropped in water, being in a state of atelectasis. In cases of shorter duration it is found crepitant throughout its structure. Brouardet112 called attention to the inflammation in the under-pleural cellular tissue, as well as in the interlobular connective tissue, forming interstitial pneumonia, which determines condensation of this tissue and its retraction after the manner of cicatrices, and afterward its inextensibility. These explain the retraction of the thoracic walls and the narrowing of the chest.
111 Loc. cit.
112 "Interstitielle Pneumonie," Soc. Méd. des Hôp. Bullétin, 1872.
The most serious complication of this disease is the pleuro-bronchial fistula113 by which the fluid escapes through the lung. The firm adhesions between the lungs and walls, forming enclosed pockets, contribute in no small degree to the incurability of purulent pleurisy. These pockets cannot be emptied thoroughly, nor can the washings be made to penetrate them. The purulent secretion exercises a destructive action over the tissues surrounding it, as well as upon the viscera and walls of the chest: the soft parts become inflamed and abscesses form; the intercostal muscles suffer atrophy and undergo fatty degeneration, external openings occurring from ulceration. The latter are found less frequently than pleuro-bronchial fistula. This external perforation is habitually in front, in the upper intercostal spaces, which, near the sternum, are very wide and not protected by external intercostal muscles. The fifth intercostal is the most frequent locality. There may be one or several openings. They may be caused by the pus ulcerating through the parietal walls, or abscesses may be produced in the walls and burst externally. Exceptionally, the emptying of the liquid is by ulceration of the diaphragm into the abdomen, causing fatal peritonitis. Some years since the author saw, in consultation, a patient where the autopsy proved this condition. Rare cases have been reported where the fluid escaped into the pericardium, into the mediastinum, and into the opposite pleural cavity (Fernet114). Bouveret115 relates a number of cases in which the discharge of pus took place through such unusual channels as the oesophagus, the stomach, the intestines, and the pelvis of kidneys; also where the pus perforated the posterior cul-de-sac of the pleura and appeared in the posterior walls of the abdomen. In the last cases, he states, it may point in the groin, the lumbar region, the buttocks, or even in the thigh.
113 See section on [Pneumothorax].
114 Loc. cit.
115 Journal de Méd., Dec. 16, 1882; N.Y. Med. Rec., March, 1883.