Pathological anatomy of pleurisy

Acute pleurisy. Serous effusion is rare. When fibrinous pleurisy (dry P.) pleural plaques appears first tender, easily removable fibrinous incrustation. Later formed fibrinous film (Fig. 1) yellowish or yellowish-gray color. Serous, sero-fibrinous and fibrinous P. seen in various diseases (tuberculosis, lobar pneumonia, rheumatism, disseminated lupus erythematosus, tularemia, psittacosis, blastomycosis, koktsidiomikoz, abscesses and heart attacks the lungs, uremia).

Fig. 1. Fibrinous pleurisy.

Purulent pleurisy (empyema), rarely from the beginning occurs pus-like, often develops after sero-fibrinous inflammation of the pleura. The process usually happens mostly one-sided and is located in the basal or the back of the pleural cavity. Purulent P.
observed at the break, lung abscess in the pleural cavity, septic heart attacks, bronchopleural fistula, etc. In sowing find various microorganisms: streptococci, staphylococci, Diplomatie Friedlander, etc. Sometimes there aseptic purulent P. (for example, when autolytic the collapse of the lung, heart attacks).
Putrid pleurisy occurs when released into the pleural cavity putrefactive microorganisms of the seats of gangrenous tissue decomposition (gangrene, septic heart attack, disintegrating cancer and so on). In the pleural cavity accumulates exudate with an unpleasant smell, dirty grey colour, often with symptoms of gassing.
Hemorrhagic effusion is accompanied by prepodavanie into the pleural exudate containing significant admixture of red blood cells (for example, malignant tumors, tuberculosis). Exudate can also take the bloody character of diseases involving hemorrhagic diathesis (anemia, leukemia, scurvy and other).
The outcomes of acute pleurisy can be different. Serous exudate can be established. In most cases fibrinous exudate resolved only in part, and is mainly exposed organization that leads to the development of adhesions (Fig. 2), fibrous thickening of the pleura, obliteration of the pleural cavities.
Purulent exudate is rarely subjected to a complete resorption, more common encapsulation inflammatory exudates. The inflammatory process in empyema can progress to the interstitial tissue of the lung (interstitial purulent pneumonia).
There are cases of spontaneous breaking of purulent exudate as the external environment due to melting of the tissues of the chest and in the bronchi of the lungs, often in the peritoneal cavity, the pericardium and mediastinum.

Fig. 2. Pleural spike, tightening the surface of the lung.

Chronic pleurisy. Often chronic pleurisy occurs when the empyema. In these cases, the exudate is fading, falling apart, turns into a brand Carovigno mass or gruel with the presence of cholesterol crystals; microorganisms may disappear. Pleural sheets are sharply thickened, dense, sometimes with a focal pacificasia and even ossification. Significant deposits of limestone masses is especially characteristic for tuberculous empyema. Empyema may lead to purulent-resorptive fever, sepsis, depletion and amyloidosis internal organs. Sometimes long-lasting, chronic observed in sero-fibrinous and fibrinous pleural effusion (Fig. 3).
In acute and chronic P. significant accumulation of fluid in the pleural cavity causes atelectasis corresponding light, mediastinal shift in the opposite direction and aperture protrudes into the peritoneal cavity. Obliteration pleural cavities may be accompanied sdavlennoy diaphragmatic, the vagus nerve, a large thoracic duct, and also nearby vessels. In cases where the overgrowing of the pleural cavity occurs in conditions stavshego or sklerozirovanie light, there may be a shift of the mediastinum towards obliteriruushih cavity. Cm. Also Pleura.

Fig. 3. Chronic pleurisy. Visceral pleura sharply thickened, with a large number of vessels and the effects of chronic inflammation. Pleural plaques fibrinous overlay.