Pleurisy: causes and pathogenesis

Depending on the etiology, all pleurisy can be divided into two large groups: infectious and non-infectious (aseptic). In infectious pleurisy, the inflammatory process in the pleura is caused by the action of infectious agents, with non-infectious pleurisy, pleural inflammation occurs without the involvement of pathogenic microorganisms.

Infectious pleurisy caused by the following pathogens:

• bacteria (pneumococcus, streptococcus, staphylococcus, hemophilic rod, Klebsiella, Pseudomonas aeruginosa, typhoid bacillus, brucella, etc.);
• mycobacteria of tuberculosis;
• rickettsia;
• the simplest (amoeba);
• fungi;
• parasites (echinococcus, etc.);
• viruses.

It should be noted that the most common infectious pleurisy is observed in pneumonia of different etiology (para- and metapneumonic pleurisy) and tuberculosis, less often - with lung abscess, festering bronchiectasis, sub-psiaphragmatic abscess.

Non-infectious (aseptic) pleurisy are observed in the following diseases:

• Malignant tumors (pleural carcinomatosis is the cause of pleurisy in 40% of cases). It can be a primary pleural tumor ( mesothelioma ); metastasis of a malignant tumor into the pleura, in particular, in ovarian cancer (Meigs syndrome - pleurisy and ascites in ovarian carcinoma); lymphogranulomatosis, lymphosarcoma, hemoblastosis and other malignant tumors;
• systemic connective tissue diseases (systemic lupus erythematosus, dermatomyositis, scleroderma, rheumatoid arthritis);
• systemic vasculitis;
• trauma of the chest, fractures of the ribs and surgical interventions (traumatic pleurisy);
• pulmonary infarction due to pulmonary embolism;
• acute pancreatitis (enzymes of the pancreas penetrate into the pleural cavity and develop "enzymatic" pleurisy);
• myocardial infarction (postressfarction syndrome Dressler);
• hemorrhagic diathesis;
• chronic renal failure (uraemic pleurisy);
• periodic disease.

Among all these reasons for pleurisy, pneumonia, tuberculosis, malignant tumors, systemic connective tissue diseases are the most frequent.

[1], [2], [3], [4], [5], [6], [7], [8]

Pathogenesis of infectious pleurisy

The most important condition for the development of infectious pleurisy is the penetration of the pathogen into the pleural cavity by one of the following ways:

• direct infection from infectious foci located in the lung tissue (pneumonia, abscess, festering cysts, tuberculosis lesions of the lungs and radical lymph nodes);
• lymphogenous infection of the pleural cavity;
• hematogenous pathway of infection;
• direct infection of the pleura from the external environment with chest injuries and operations; with a breach of the integrity of the pleural cavity.

Entered into the cavity of the pleura, infectious agents directly cause the development of the inflammatory process in the pleura. This is facilitated by a violation of the function of local bronchopulmonary protection and the immunity system as a whole. In a number of cases, the previous sensitization of the body with an infectious agent (for example, in case of tuberculosis) is of great importance. In this situation, the influx of even a small number of pathogens into the pleural cavity causes the development of pleurisy.

In the first day of pleurisy, lymphatic capillaries expand, vascular permeability increase, pleural edema, cellular infiltration of the subpleural layer, moderate effusion into the pleural cavity. With a small amount of effusion and well functioning lymphatic "hatches", the fluid part of the effusion is absorbed and fibrin, left from the exudate, is left on the surface of the pleural sheets - this is how fibrinous (dry) pleurisy is formed. However, with a high intensity of the inflammatory process, all conditions are created for the development of exudative pleurisy:

• a sharp increase in the permeability of the blood capillaries of the visceral and parietal pleura and the formation of a large number of inflammatory exudates;
• increased oncotic pressure in the pleural cavity due to the presence of protein in the inflammatory exudate;
• compression of lymphatic capillaries of both pleural sheets and lymphatic "hatches" of the parietal pleura and their closing with a film of precipitated fibrin;
• Excess of exudation speed over the rate of suction of effusion.

Under the influence of the above factors, exudate accumulates in the pleural cavity, exudative pleurisy develops.

In the case of infectious exudative pleurisy, various types of exudates are observed. The most common is serous-fibrinous exudate. When an exudate is infected with a pyogenic microflora, it becomes serous-purulent, and then purulent (empyema of the pleura).

In the future, with the reverse development of the pathological process, the rate of resorption begins to gradually prevail over the rate of exudation and the liquid part of the exudate resolves. Fibrinous depositions on the pleura undergo scarring, moorings are formed, which can cause more or less significant obliteration of the pleural cavity.

It should be emphasized that the purulent exudate is never resorbed, it can be evacuated only if the pleural empyema breaks through the bronchus outward or can be removed by puncturing or draining the pleural cavity.

In a number of cases, it is possible to consolidate the pleural sheets according to the border of the effusion, as a result of which a formed pleurisy is formed.

Pathogenesis of non-infectious pleurisy

In the pathogenesis of carcinomatous pleurisy and the formation of effusion, the influence on the pleura of the products of metabolism of the tumor itself, as well as the disturbance of lymph circulation due to blockage of its outflow (pleural "hatches", lymph nodes) by neoplasm or its metastases play a significant role. The pathogenesis of pleurisies developing under hemoblastoses is similar.

In the development of pleurisy with systemic diseases of connective tissue and systemic vasculitis, periodic disease, autoimmune mechanisms, generalized vascular lesions, and immunocomplex pathology are important.

Aseptic traumatic pleurisy is caused by the pleural reaction to the spilled blood, as well as by its direct damage (for example, with fracture of the ribs).

The development of pleurisy in chronic renal failure is due to irritation of the pleura with secreted uremic toxins - interstitial products of nitrogen metabolism.

Enzymatic pleurisy is caused by the damaging effect on the pleura of pancreatic enzymes entering the pleural cavity through the lymphatic vessels through the diaphragm.

In the development of pleurisy with myocardial infarction (Post-wrinkle syndrome Dressler), the leading role is played by the autoimmune mechanism.

Pleurisy with a lung infarction (due to pulmonary embolism) is caused by a direct transition of the aseptic inflammatory process from the infarcted lung to the pleura.

Classification of pleurisy

[9], [10], [11], [12]

The reason for pleurisy

1. Infectious pleurisy
2. Aseptic pleurisy

The nature of the pathological process

1. Dry (fibrinous) pleurisy
2. Exudative pleurisy

The nature of effusion in exudative pleurisy

1. Serous
2. Serous-fibrinous
3. Purulent
4. Putrefactive
5. Hemorrhagic
6. Eosinophilic
7. Cholesterol
8. Hilious
9. Mixed

The course of pleurisy

1. Acute pleurisy
2. Subacute pleurisy
3. Chronic pleurisy

Localization of pleurisy

1. Diffuse
2. Isolated (delimited)
   1. Apical (apical)
   2. Parietal (paracostal)
   3. Bony-diaphragmatic
   4. Diaphragmatic (basal)
   5. The paramediastinal
   6. Inter-lobe (interoblacial)