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, while in non-infectious pleurisy, inflammation of the pleura occurs without the participation of pathogenic microorganisms.

Infectious pleurisy is caused by the following pathogens:

• bacteria (pneumococcus, streptococcus, staphylococcus, Haemophilus influenzae, Klebsiella, Pseudomonas aeruginosa, typhoid bacillus, brucella, etc.);
• Mycobacterium tuberculosis;
• rickettsia;
• protozoa (amoebas);
• mushrooms;
• parasites (echinococcus, etc.);
• viruses.

It should be taken into account that infectious pleurisy is most often observed in pneumonia of various etiologies (para- and metapneumonic pleurisy) and tuberculosis, less often - in lung abscess, suppurating bronchiectasis, subdiaphragmatic abscess.

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

• malignant tumors (pleural carcinomatosis is the cause of pleurisy in 40% of cases). These may be primary pleural tumor ( mesothelioma ); metastases of a malignant tumor to the pleura, in particular, in ovarian cancer (Meigs syndrome - pleurisy and ascites in ovarian carcinoma); lymphogranulomatosis, lymphosarcoma, hemoblastoses and other malignant tumors;
• systemic connective tissue diseases (systemic lupus erythematosus, dermatomyositis, scleroderma, rheumatoid arthritis);
• systemic vasculitis;
• chest injuries, rib fractures and surgical interventions (traumatic pleurisy);
• pulmonary infarction due to pulmonary embolism;
• acute pancreatitis (pancreatic enzymes penetrate into the pleural cavity and “enzymatic” pleurisy develops);
• myocardial infarction (post-infarction Dressler syndrome);
• hemorrhagic diathesis;
• chronic renal failure ("uremic pleurisy");
• periodic disease.

Among all the listed causes of pleurisy, the most common are pneumonia, tuberculosis, malignant tumors, and systemic connective tissue diseases.

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Pathogenesis of infectious pleurisy

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

• direct transfer of infection from infectious foci located in the lung tissue (pneumonia, abscess, suppurating cysts, tuberculous lesions of the lungs and hilar lymph nodes);
• lymphogenous infection of the pleural cavity;
• hematogenous route of infection;
• direct infection of the pleura from the external environment during chest wounds and operations; in this case, the integrity of the pleural cavity is compromised.

Infectious agents that have penetrated the pleural cavity directly cause the development of an inflammatory process in the pleura. This is facilitated by a disruption of the function of the local bronchopulmonary defense and the immune system as a whole. In some cases, previous sensitization of the body by an infectious agent (for example, in tuberculosis) is of great importance. In such a situation, the entry of even a small amount of the pathogen into the pleural cavity causes the development of pleurisy.

During the first day of pleurisy development, the lymphatic capillaries expand, the vessels become more permeable, the pleura swells, the subpleural layer becomes cellularly infiltrated, and moderate effusion into the pleural cavity is observed. With a small amount of effusion and well-functioning lymphatic "hatches", the liquid part of the effusion is absorbed and fibrin that has fallen out of the exudate remains 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 the conditions for the development of exudative pleurisy are created:

• a sharp increase in the permeability of the blood capillaries of the visceral and parietal pleura and the formation of a large amount of inflammatory exudate;
• an increase in oncotic pressure in the pleural cavity due to the presence of protein in the inflammatory exudate;
• compression of the lymphatic capillaries of both pleural layers and the lymphatic “hatches” of the parietal pleura and their closure by a film of precipitated fibrin;
• excess of the rate of exudation over the rate of absorption of effusion.

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

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

Later, as the pathological process reverses, the rate of resorption gradually begins to prevail over the rate of exudation and the liquid part of the exudate is absorbed. Fibrinous deposits on the pleura undergo scarring, adhesions are formed, which can cause more or less significant obliteration of the pleural cavity.

It should be emphasized that purulent exudate is never resorbed; it can only be evacuated when the pleural empyema breaks through the bronchus to the outside or can be removed by puncture or drainage of the pleural cavity.

In some cases, fusion of the pleural sheets is possible according to the border of the effusion, resulting in the formation of encapsulated pleurisy.

Pathogenesis of non-infectious pleurisy

In the pathogenesis of carcinomatous pleurisy and the formation of effusion, a significant role is played by the effect of the pleura on the products of the tumor's metabolism, as well as by the disruption of lymph circulation due to the blockage of its outflow (pleural "hatches", lymph nodes) by the neoplasm or its metastases. The pathogenesis of pleurisy developing in hemoblastoses is similar.

In the development of pleurisy in systemic diseases of connective tissue and systemic vasculitis, periodic disease, autoimmune mechanisms, generalized vascular damage, and immune complex pathology are important.

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

The development of pleurisy in chronic renal failure is caused by irritation of the pleura by secreted uremic toxins - intermediate 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 during myocardial infarction (post-infarction Dressler syndrome), the autoimmune mechanism plays a leading role.

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

Classification of pleurisy

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Cause of pleurisy

1. Infectious pleurisy
2. Aseptic pleurisy

The nature of the pathological process

1. Dry (fibrinous) pleurisy
2. Exudative pleurisy

The nature of the effusion in exudative pleurisy

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

Course of pleurisy

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

Localization of pleurisy

1. Diffuse
2. Encapsulated (bounded)
   1. Apical
   2. Parietal (paracostal)
   3. Osteodiaphragmatic
   4. Diaphragmatic (basal)
   5. Paramediastinal
   6. Interlobar