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Purulent pleurisy or empyema of a pleura call accumulation of a purulent exudate in a pleural cavity.
Most often causative agents of purulent pleurisy are staphylococcus, streptococci, a pyocyanic stick, colibacillus. Quite often in crops of pleural contents a pneumococcus, proteas, the klebsiyella and barmy fungi meet. At many patients sow two and more activators. In recent years at purulent pleurisy even more often find anaerobic bacteria which found, mainly, at the putrefactive empyemas complicating the course of gangrene of a lung earlier.
1. Increase of permeability of a visceral pleura in connection with an inflammation.
2. Disturbance of a drainage through a parietal pleura.
3. Blocking of outflow tracts of a lymph from lungs metastasises or a chronic inflammation-> the retrograde movement of a lymph towards a visceral pleura.
4. A role of immunological reactions mainly 3 and 4 types in a zone of pleural leaves with release of biokativny substances and disturbance of microcirculation.
Accumulation of liquid is promoted:
1. Na delay + and decrease in protein, for example at a nephrotic syndrome, heart failure.
2. Increase of the ABP in pulmonary arteries, it at insufficiency of a left ventricle, fibrinferment of pulmonary veins, increase of pressure in pulmonary capillaries.
The pathogeny of dry pleurisy only differs in formation of commissures as fibrin drops out. Pain pathogeny: inflammatory hypostasis of a parietal pleura which is extremely sensitive to pain and a visceral pleura does not possess painful sensitivity-> interlobar pleurisy without pain.
Pathogeny and classification
Purulent pleurisy, as a rule, is the secondary disease complicating the course of pneumonia, including influenzal, abscesses of a lung and tuberculosis. The empyema of a pleura can arise after the getting wounds of a thorax, traumatic damages of bodies of a chest cavity, including iatrogenic, and at purulent processes of various localization.
Most often meet couple - and metapneumonic purulent pleurisy between which difference consists in time of development of suppuration in a pleura in relation to the pneumonia which caused it – in a heat or at the end of a disease. Their division in the retrospective analysis sometimes happens very difficult. At break the empyema with destruction of pulmonary fabric develops in a pleural cavity of one or several subplevralno the located abscesses of a lung. If in a pleural cavity the intra pulmonary abscess which is reported with bronchial tubes breaks there is a pyopneumothorax supported by the bronchopleural fistulas which are formed at the same time. Less often the infection gets into a pleural cavity in the lymphogenous way. In this case suppuration of a pleural exudate can not be followed by emergence of the centers of disintegration in a pulmonary parenchyma. Such empyema without destruction of pulmonary fabric is called "a simple empyema". Infection of a pleura can happen also in the hematogenous way from sources of an infection of extra pulmonary localization. The empyema at the same time has character of metastatic. At purulent pancreatitis, paranephrites and subphrenic abscesses when the diaphragm and the diaphragmal pleura adjoining to it is involved in inflammatory process, the empyema develops so-called sympathetic (or consensual).
Allocate 3 stages of purulent pleurisy which are passing one into another and having various duration at different patients. At the first stage as a result of a pleura inflammation in her cavity serous exudate appears. At correctly picked up antibacterial therapy accumulation of exudate can stop and liquid will undergo a spontaneous resorption. If therapy is inadequate and bacteria in one way or another get into pleural exudate and breed in it, there is the second stage of a disease – fibrinopurulent. In liquid the quantity of bacteria, polymorphonuclear leukocytes and a detritis increases. Transparent serous exudate grows turbid and quickly gains purulent character. Under the influence of fibroblasts on a surface of parietal and, especially, visceral pleura fibrinous films are formed, and between leaves of a pleura there are unions – at first friable, and then more and more dense. Commissures limit distribution of pus on a pleural cavity and promote emergence of intrapleural encystments. The purulent exudate which is contained in them becomes dense and cannot independently resolve. The third stage, a stage of the fibrous organization, is characterized by education dense shvart, covering a kollabirovany lung. The last becomes motionless and ceases to function, and further is exposed to fibrous changes. There is so-called pleurogenic cirrhosis of a lung.
Precisely it is possible to define the beginning of purulent pleurisy not always as its symptoms are, as a rule, veiled by symptomatology of the disease which caused pleurisy: the abscessing pneumonia, acute pancreatitis, subphrenic abscess, etc., and it is frequent and are similar to it. Patients complain of the accruing short wind, cough, fever, oznoba. Pleurisy can begin with emergence of the stitches amplifying at breath, and sometimes is followed by abdominal pains and paresis of intestines. At development of a metapneumonic empyema these symptoms appear and amplify after subsiding of symptoms of an inflammation of a lung, 3–5 days later after crisis as the second wave of an infection. Strengthening of intoxication and respiratory insufficiency at the height of pneumonia forces to suspect development of a parapneumonic empyema or pyopneumothorax. Emergence of the last can be followed by clinic of pleural shock – the sharpest stitch, an asthma, cold then, sometimes a kollaptoidny state. However the erased clinical forms of complication are more often observed: pains are absent or are expressed slightly. There are no acute disorders of breath. Gradually intoxication symptoms amplify, cough accrues, the quantity of a phlegm increases. The patient adopts the forced provision on a sick side, and at vertical position is bent in the sick party. Occasionally sacculated purulent exudate breaks through the burst abscess wall in rather large bronchial tube. In this case sudden emergence of the plentiful purulent phlegm with an unpleasant smell expectorated by "a full mouth" will be the leading symptom.
Sometimes pus from inadequately trained intrapleural abscess can get into fabrics of a chest wall and into hypodermic cellulose. The clinical picture in the developed phase of purulent pleurisy is defined by symptoms is purulent - resorptive fever which cornerstone three factors are: suppuration, absorption (resorption) of decomposition products of fabrics and activity of microbes and loss of an organism, inevitable at a purulent inflammation. Degree of manifestation of these symptoms and weight of a condition of the patient can be various – from moderately expressed to the hardest, and not always strictly correlate with sizes of a cavity of an empyema and amount of pus in it. Against strengthening of intoxication there are functional disturbances from cardiovascular system, a liver and kidneys which in process of progressing of an illness at inadequate treatment can be replaced by the organic changes of internals characteristic of a septic state. The expressed losses of protein and electrolytes in an acute phase of an inflammation at their insufficient compensation lead to volemichesky and water and electrolytic frustration, reduction of muscle bulk and weight loss. On this background pastosity of the person, the struck half of a thorax is often noted, there can be hypostases of the lower extremities. In process of progressing of a disease it is purulent - resorptive fever gradually passes into exhaustion. As a rule, it is observed at patients with a pleura empyema with extensive destruction of a lung. Against the progressing hypoproteinemia patients take a form is long starving. Integuments become dry. The fever which had earlier remittiruyushchy or intermittent character is replaced by subfebrile condition or normalized that is predictively the adverse sign testimonial of sharp decrease in reactivity of an organism. Dystrophic changes of a myocardium, liver, kidneys, adrenal glands lead to the expressed disturbances of their function. Patients become sluggish and apathetic. Hypo - and a disproteinemia, caused by disturbances of belkovoobrazuyushchy function of a liver, activate coagulant system of blood that sharply increases danger of a thrombogenesis and an embolism from which patients quite often also perish. To bring the patient out of a state it is purulent - resorptive exhaustion extremely difficult, and the forecast at the same time bad.