POLYSEROSITIS

From Big Medical Encyclopedia

POLYSEROSITIS (polyserositis; grech, poly is a lot of + armor. [tunica] of serosa a serous cover + - itis) — a consecutive inflammation of several serous covers, simultaneous or close on time (pleurae, a pericardium, a peritoneum). Meets in the form of bilateral more often pleurisy (see) and pericardis (see) or pericardis, perihepatitis (see) and (or) episplenitis (see); other combinations are less often observed.

Items not an independent disease, but a syndrome of various diseases (infectious and noninfectious), during to-rykh are noted system reactions. The exception is made casuistic by seldom found Konkato's disease — a hyalinosis of serous covers of an unknown etiology.

Frequency of emergence and feature of a current of P. are connected with a basic disease. E.g., simultaneous defeat of pleural covers and a pericardium occurs at a half of patients with a system lupus erythematosus, thus, P.'s syndrome can have a certain diagnostic value.

Etiology and Pathogeny

Aetiology. Diseases, at to-rykh P. is observed, are numerous. Most often P. develops at a system lupus erythematosus, rheumatism, a pseudorheumatism, tuberculosis, septic diseases, a periodic disease, and also at uraemia, Dressler's syndrome, a postkomissurotomny syndrome. Due to the progress of antibacterial therapy extremely redkikhm primary and infectious P. Patogenez

became connected with development of allergic, infektsionnoallergichesky or immunopathological reaction. In rare instances of infectious P. its pathogeny matches the general patterns of development infectious inflammations (see) and its private features connected with an etiology (e.g., at grumous tubercular P.'s development). The community of reactions of serous covers of various localization is caused by their uniform mesodermal origin, close anatomic relationship, same gistol, a structure and similarity of functions. The inflammation of serous covers is followed by their hyperemia, increase in permeability plentiful submesothat-lialnoy a capillary network and an exit of plasma dialyzate in serous cavities, negative pressure in to-rykh facilitates this process. In the subsequent the exudate containing various cellular elements, protein (30 g/l and more), fibrin, proteolytic enzymes and other components of blood serum is formed. The composition of exudate depends on an etiology and a pathogeny of a basic disease therefore with the diagnostic purpose use determination of the content in it a complement and its components, glucose, immunoglobulins of various classes, including a lupoid factor and anti-immunoglobulins (such as rhematoid factors and agglutinators), and also make mikrobiol, researches.

Pathological anatomy

In morfol, P.'s relation divide on acute and chronic. Acute P. more often happens exudative and depending on character of exudate can be serous, fibrinous, is more rare hemorrhagic. Chronic P. develops, as a rule, in acute P.'s outcome and is shown hron, a productive inflammation with formation of commissures, is more rare an obliteration of serous cavities. Features morfol, P.'s manifestations depend on the nature of the main disease.

At rheumatism and similar diseases (a pseudorheumatism, a system lupus erythematosus) in serous cavities find serous, serofibrinous or fibrinous exudate. Quite often pleurisy and a pericardis are combined with peritonitis (see); at the same time in a serous cover, especially in an epicardium, note the expressed histiocytic reaction, sometimes define rheumatic granulomas. The organization of exudate with adhesive P.'s development leads to an union of serous leaves and an obliteration of serous cavities.

The similar pathoanatomical picture is observed in some cases P. developing as paraspecific process at tuberculosis. Actually tubercular P. can arise gematogenno and as a result of distribution of process on limf, to vessels during formation of primary complex. In such cases in cavities find serous or serofibrinous exudate; on a pleura, a pericardium and a peritoneum — tubercular hillocks which can be exposed to a necrosis with the subsequent organization and adjournment in the necrotic mass of salts of calcium. Tubercular hillocks on a peritoneum sometimes have the large sizes that macroscopically can simulate a picture of a carcinomatosis of a peritoneum. A peculiar P. with a characteristic morfol, a picture arises at uraemia.

In acute P.'s outcome a liquid part of exudate is soaked up, on a surface of serous covers the young granulyatsionny fabric growing into the mass of the dropped-out fibrin expands. It is resulted by a thickening of serous leaves, they take a whitish form, friable or more dense commissures are formed. In other cases process can have chronic productive character. A sharp focal or diffusion thickening of a serous cover with transformation it in a dense whitish translucent armor of various thickness call, according to Kurshmann's proposal (H. Curschmann, 1884), glaze. Together with a thickening of serous covers there is nek-paradise a deformation of the bodies covered by them. At microscopic examination on site of a serous cover note growth of the hyalinized fibrous fabric with scanty limfogistiotsitarny infiltrates between bunches of collagenic fibers. Tyazhi of fibrous fabric is found in superficial departments of a parenchyma of the struck bodies (a liver, a spleen, etc. as, e.g., at a perikarditichesky pseudocirrhosis of Peak).

The clinical picture

the Inflammation of several serous covers seldom arises in one step; usually in the beginning the pleura is surprised, then the pericardis or on the contrary (e.g. joins, at acute rheumatism) and respectively there are characteristic symptoms (see. Pericardis , Pleurisy ).

Most often patients complain of pains in a thorax of different intensity and localization (in a side, behind a breast), pains in an upper half of a stomach or on all stomach, amplifying at breath. Especially expressed pains happen at a periodic disease, acute rheumatism at children, diaphragmatites at a system lupus erythematosus. At a pseudorheumatism of P. can proceed asymptomatically and quite often it is found only at rentgenol. a research or is established at autopsy.

At P.'s development body temperature usually increases. During the first hours and days the pleural rub, a pericardium, a peritoneum is listened (over the surfaces of a liver or spleen). In process of accumulation of exudate the friction murmur and pains at breath is smart yp and yut sya or disappear; at considerable exudates short wind develops. Bystry and considerable accumulation of exudate leads to the expressed asthma, disturbances of blood circulation and emergence of symptoms of a prelum or shift exudate close located to it morfol, educations (bodies, vessels, etc.).

In case of infectious P. the condition of the patient can be extremely heavy because of the expressed intoxication, high fever, accumulation in serous cavities of a significant amount of exudate.

The item usually joins already to available a wedge, to symptoms of the main disease. At the same time find changes in separate serous cavities, characteristic of dry or vypotny P. However children and teenagers at acute rheumatism, a juvenile pseudorheumatism and nek-ry other diseases of P. can have the first a wedge, display of a disease.

P.'s emergence usually demonstrates active development of a basic disease and is followed by a leukocytosis (a leukopenia at a system lupus erythematosus), a neutrocytosis, considerable acceleration of ROE (more than 40 — 50 mm/hour).

The item proceeds from several weeks to one month both more and quite often comes to an end with formation of the commissures (plevrodiafragmalny, plevroperikardialny) leading to incomplete disclosure of costal and phrenic sine, decrease in an excursion of a diaphragm, its high standing; on limited sites the friction murmur of the struck serous cover is constantly listened. At a periodic disease of P. it is inclined to recuring, however permanent commissural process does not develop. The adhesive (squeezing) P. most often arises at tuberculosis and rheumatism and is characterized by slowly progressing obliteration of serous cavities fibroziruyushchy periviscerites with disturbance of functioning of bodies. Recurrent P. at a system lupus erythematosus leads to considerable disturbance of ventilating function of lungs because of high standing of a diaphragm and considerable reduction of lung volume.

Treatment

Treatment is carried out taking into account an etiology of the Item. At rheumatism, a pseudorheumatism, a system lupus erythematosus P.'s emergence serves as the indication for active antiinflammatory therapy, including glucocorticosteroid hormones in average doses (30 — 40 mg of Prednisolonum a day). Items at a periodic disease stop colchicine 1 mg 2 — 3 times a day with the subsequent transition to a maintenance dose on 1 mg a day; glucocorticosteroid hormones in this case are inefficient. At adhesive P. the dose of Prednisolonum shall be smaller — 15 — 20 mg a day; the respiratory gymnastics is shown. At infectious P. appoint antibiotics (inside and intracavitary and at tuberculosis carry out active specific antitubercular therapy in a combination to average and small doses of Prednisolonum.

At bystry accumulation of exudate irrespective of P.'s etiology make a puncture of a serous cavity with removal of exudate and the subsequent introduction to a cavity of a hydrocortisone in a dose of 50 — 100 mg, if necessary apply antibiotics. At the squeezing pericardis the pericardectomy is shown.

Prevention consists in early and adequate treatment of a basic disease.



Bibliography: Vinogradova O. M. Periodic disease, M., 1973; Nasonova V. A. System lupus erythematosus, M., 1972; Nesterov A. I. Rheumatism, M., 1973; Oleneva T. N. and Prokhorov E. P. Therapy by antibacterial drugs and corticosteroid hormones of patients with tubercular pleurisy, pneumopleuritis and polyserosites, Probl, tube., No. 7, page 24, 1960; With t r at to about in A. I. and Fluently r I am A. G N. Pathological anatomy and pathogeny of collagenic diseases, M., 1963; With t r at to about in A. I. and With ER about in V. V. Pathological anatomy, M., 1979; Tareev E. M. Collagenoses, M., 1965.


V. A. Nasonova; M. N. Lantsman (stalemate. An.).

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