Purulent pleurisy. Symptoms and treatment of purulent pleurisy of the lungs

The most common causative agents of purulent pleurisy are staphylococci, streptococci, Pseudomonas aeruginosa, and Escherichia coli. Often in cultures of pleural contents there are pneumococcus, proteus, klebsiella and yeast fungi (G.I. Lukomsky, 1976). In many patients, two or more pathogens are cultured (J. Bartlett et al., 1974). In recent years, with purulent pleurisy Anaerobic bacteria are increasingly being discovered which were previously found mainly in putrefactive empyemas, which complicated the course of lung gangrene.

Purulent pleurisy is usually secondary disease, complicating course of pneumonia, including influenza, lung abscesses and tuberculosis . Pleural empyema can occur after penetrating wounds of the chest, traumatic injuries to the organs of the chest cavity, including iatrogenic ones, and during purulent processes various localizations.

The most common pairs are And metapneumonic* * purulent pleurisy, the difference between them lies in the time of development of suppuration in the pleura in relation to the pneumonia that caused it - at the height or at the end of the disease. Their separation in retrospective analysis can sometimes be very difficult. Upon a breakthrough in pleural cavity one or more subpleurally located lung abscesses develops empyema with destruction lung tissue. If an intrapulmonary abscess breaks into the pleural cavity, communicating with the bronchi, a pyopneumothorax , supported by the resulting bronchopleural fistulas. Less commonly, the infection penetrates the pleural cavity through the lymphogenous route. In this case, suppuration of the pleural effusion may not be accompanied by the appearance of foci of decay in the pulmonary parenchyma. Such empyema without destruction of lung tissue is called “simple empyema.” Infection of the pleura can also occur hematogenously from sources of infection of extrapulmonary localization. Empyema is characterized by metastatic . With purulent pancreatitis, paranephritis and subphrenic abscesses, when the diaphragm and the adjacent diaphragmatic pleura are involved in the inflammatory process, the so-called sympathetic (or concomitant) empyema.

Highlight 3 stages of purulent pleurisy (N. Andrews et al., 1962), transforming into one another and having different durations in different patients. At the first stage as a result of inflammation of the pleura in its cavity serous exudate appears . With properly selected antibacterial therapy, the accumulation of exudate can stop and the fluid will undergo spontaneous resorption. If therapy is inadequate and bacteria penetrate into the pleural exudate in one way or another and multiply in it, the second stage of the disease is fibrinous-purulent. The number of bacteria, polymorphonuclear leukocytes and detritus increases in the liquid. The transparent serous exudate becomes cloudy and quickly becomes purulent. Under the influence of fibroblasts, fibrinous films are formed on the surface of the parietal and, especially, visceral pleura, and adhesions occur between the layers of the pleura - first loose, and then more and more dense. Adhesions limit the spread of pus throughout the pleural cavity and contribute to the occurrence of intrapleural encysts. The purulent exudate they contain becomes thick and cannot resolve on its own. Third stage stage of fibrous organization, characterized by the formation of dense moorings, covering the collapsed lung. The latter becomes immobile and ceases to function, and is subsequently subjected to fibrotic changes. There is a so-called pleurogenic cirrhosis of the lung.

Many authors of past years (S.I. Spasokukotsky, 1938; V.I. Kolesov, 1955; B.E. Linberg, 1960, etc.) distinguished acute and chronic pleural empyema, basing their division on the time factor. However The timing of the transition of acute empyema to chronic was determined by them very arbitrarily and ranged from 1 to 4-6 months. According to G.I. Lukomsky (1976), it is advisable to separate acute and chronic empyema on the basis of morphological changes in the visceral pleura, which determine the ability of the lung to re-expand and, consequently, the choice of treatment tactics. “How rigid or pliable the visceral pleura is, how strong the connective tissue formations that hold the lung are - these are the boundaries of the transition from an acute process to a chronic one... and, consequently, the transition to chronic inflammation cannot be limited by any calendar dates.” *

It is not always possible to accurately determine the onset of purulent pleurisy, since its symptoms are usually veiled by the symptoms of the disease that caused pleurisy: abscess pneumonia, acute pancreatitis, subphrenic abscess, etc., and are often similar to it. Patients complain of increasing shortness of breath, cough, fever, chills. Pleurisy may begin with the appearance pain in the side, aggravated by breathing, and sometimes accompanied by abdominal pain and intestinal paresis. With the development of metapneumonic empyema, these symptoms appear and intensify after the symptoms of pneumonia have subsided, 3-5 days after the crisis, as a second wave of infection. Increased intoxication and respiratory failure at the height of pneumonia makes one suspect the development of parapneumonic empyema or pyopneumothorax. The occurrence of the latter may be accompanied by clinical pleural shock - severe pain in the side, shortness of breath, cold sweat, sometimes a collapsing state. However, more often, subtle clinical forms of the complication are observed: pain is absent or mildly expressed. There are no acute respiratory problems. The symptoms of intoxication gradually intensify, the cough increases, and the amount of sputum increases. The patient takes a forced position on the painful side, and when in an upright position, bends towards the painful side. Occasionally, an encysted purulent effusion breaks through the bursting wall of the abscess into a fairly large bronchus. In this case, the leading symptom will be the sudden appearance of profuse purulent sputum with an unpleasant odor, expectorated “with a mouthful.”

Sometimes pus from an inadequately drained intrapleural abscess can penetrate into the tissue of the chest wall and into the subcutaneous tissue. In this case, it develops empyema necessitatis. ** Its occurrence is preceded by the appearance of a flat, limited and painful swelling on the corresponding side of the chest. This swelling may increase with coughing and deep breaths. Over time, an area of ​​hyperemia appears on it, the skin becomes thinner, becomes tense, and eventually pus can break out.

The clinical picture in the advanced phase of purulent pleurisy is determined by the symptoms of purulent-resorptive fever, which is based on three factors: suppuration, absorption (resorption) of tissue decay products and microbial activity, and loss of the body, inevitable with purulent inflammation. The severity of these symptoms and the severity of the patient’s condition can vary - from moderate to severe, and do not always strictly correlate with the size of the empyema cavity and the amount of pus in it. Against the background of increased intoxication, functional disorders of the cardiovascular system, liver and kidneys, which, as the disease progresses and with inadequate treatment, can be replaced by organic changes in the internal organs characteristic of a septic condition. Marked losses of protein and electrolytes V acute phase inflammation with insufficient compensation lead to volemic and water-electrolyte disorders, decreased muscle mass and losing weight. Against this background, pastiness of the face and the affected half of the chest is often noted, and swelling may occur lower limbs. As the disease progresses, purulent-resorptive fever gradually turns into exhaustion. As a rule, this is observed in patients with pleural empyema with extensive destruction of the lung. Against the background of progressive hypoproteinemia, patients take on the appearance of long-term starvation. The skin becomes dry and pellagroid. Fever, which previously had a remitting or intermittent nature, gives way to low-grade fever or normalizes, which is a prognostically unfavorable sign, indicating a sharp decrease in the body's reactivity. Dystrophic changes in the myocardium, liver, kidneys, and adrenal glands lead to severe disturbances in their function. Patients become lethargic and apathetic. Hypo- and dysproteinemia, caused by disturbances in the protein-forming function of the liver, activate the blood coagulation system, which sharply increases danger of thrombosis and embolism, from which patients often die. It is extremely difficult to remove a patient from a state of purulent-resorptive exhaustion, and the prognosis is poor.

In typical cases, the presence of fluid in the pleural cavity can be detected through a physical examination. However, with pronounced inflammatory infiltration in the lung, the appearance of a relatively small amount of exudate may go unnoticed even with careful percussion and auscultation. That's why In the diagnosis of pleural effusion, the main role belongs to x-ray examination.

In most cases, with the development of purulent pleurisy, the effusion first accumulates in the supradiaphragmatic space, in its lowest located parts - the sinuses. In this regard, the first radiological signs of the presence of fluid in the pleural cavity are the smoothness of the costophrenic sinus on radiographs in direct and, especially, lateral projections and the apparent high position of the dome of the diaphragm (L.D. Lindenbraten, 1961; L.S. Rosenshtrauch and M.G. Winner, 1968). Massive inflammatory infiltration of the lower lobe of the lung may make it difficult to identify these symptoms. In this case, it is recommended to do X-ray with the patient lying on the affected side . In this case, the liquid is distributed along the chest wall and becomes clearly visible. This allows not only to confirm the presence of effusion in the pleural cavity, but also approximately determine its volume . If the thickness of the liquid strip is more than 10 mm, the amount of the latter is more than 200 ml and during pleural puncture it can be aspirated with a syringe (R. Light, 1986). However, this technique only works when the pleural cavity is free from adhesions, as does the appearance of an oblique upper border of opacification, known as the Ellis-Damoiso line, which occurs as the volume of effusion increases. Further accumulation of exudate leads to increasing darkening of the hemithorax and displacement of the mediastinum to the opposite side. The latter symptom, however, is noted only in cases where the lung, due to inflammatory infiltration, loses its elasticity and does not collapse under the pressure of the surrounding fluid, or with a very large volume of effusion.

In the presence of bronchopleural fistula an accumulation of air can be seen in the pleural cavity. The upper limit of the effusion becomes clearly visible in the form of a horizontal level. Against the background of air, as a rule, a compressed lung becomes visible, which makes it possible to evaluate the degree of its collapse . To collapse of the first degree G.I. Lukomsky (1976) classifies those cases of empyema, in which the lung is compressed within the anatomical boundaries of the cloak, as II degree collapse - within the trunk, and III degree collapse - within the core. The degree of collapse determines the magnitude of the functional decrease in lung volume and is directly proportional to the severity of respiratory failure, which in cases of valvular (tension) pyopneumothorax is pronounced and threatens the patient’s life.

By prevalence and location allocate total empyema, involving the entire pleural cavity from the dome to the diaphragm, common, in which the empyema is limited to two or three anatomical walls of the pleural cavity (for example, costal and diaphragmatic, or mediastinal, diaphragmatic and costal) and limited, in the formation of which one pleural wall takes part. According to localization, such empyemas are parietal, apical and basal.

The presence of adhesions significantly changes the x-ray picture, often complicating the diagnosis of empyema. Sometimes it can be very difficult to determine where the purulent cavity is located - in the lung or in the pleura , especially if there are several of these cavities. Are they foci of parenchymal destruction or limited intrapleural abscesses? At the same time, I.A. Sanpeter and G.I. Lukomsky (1976) give preference multi-axis fluoroscopy with persistent attempts to bring the outer edge of the cavity perpendicular to the axis of transmission. If it is possible to see the shadow of the visceral pleura or the edge of the lung, the presence of empyema can be largely excluded. spherical or slightly oval shape the cavity also indicates a lung abscess, elongated in the caudal-cranial direction - empyema. With empyema, the diameter of the cavity at its lower pole always exceeds that at the upper one. The walls of the abscess cavity are approximately equal in thickness, while the medial wall of the empyema cavity, formed by the visceral pleura, is usually thinner than the lateral one. The internal contours of the abscess wall are more lumpy and uneven.

If purulent pleurisy is accompanied by significant destruction of the lung, then the internal border of the encysted cavity of the empyema may not be the visceral pleura, but the destroyed and deformed lung parenchyma. A similar picture can also arise in cases where purulent fusion is subjected to outer wall extensive solitary subpleurally located lung abscess. Characteristic radiological sign such an “abscess-empyema” is an uneven, pitted and thickened medial wall of the cavity. It is possible to most accurately determine the presence of fluid in the pleural cavity and localize intrapleural encystation CT scan. The introduction of contrast agent into the cavity - pleurofistulography.

Ultrasonic echolocation is very informative for encysted empyema. In the presence of pleural exudate, the proximal echo from the skin, intercostal muscles and parietal pleura is separated from the distal echo of the visceral pleura by an echo-free space. Ultrasound can detect even small amounts of pleural fluid, it is successfully used to determine the location of pleural puncture.

Pleural empyema does not have a characteristic bronchoscopic picture. Only with significant collapse of the lung can one notice the convergence of the segmental bronchi, loss of their tone, sometimes swelling of the mucosa and an increase in its folding - the mucosa in the form of “washerwoman’s hands” (G.I. Lukomsky et al., 1982). However, bronchoscopy is very important to exclude intrabronchial pathology, which may cause the development of pneumonia and purulent pleurisy complicating it. First of all, this applies to central lung cancer, bronchial foreign bodies and other, more rare diseases bronchial system. In addition, bronchoscopy allows us to identify the presence and form of endobronchitis and determine indications for sanitation of the tracheobronchial tree.

X-ray and ultrasound examinations make it possible to determine the presence of fluid in the pleural cavity, its location and approximate volume. However To study the effusion itself and confirm its purulent nature, pleural puncture is necessary. The pleura is punctured using a long and fairly thick needle connected to a syringe with a silicone rubber tube. When emptying the syringe, the tube is clamped to prevent air from entering the pleural cavity. The puncture is performed under local anesthesia. The optimal puncture site is the point in the 6-7th intercostal space along the posterior axillary line with the patient in a sitting position. With encysted empyema, the puncture site is determined by fluoroscopy or ultrasound.

If the effusion is purulent, bacteriological examination to determine microflora and its sensitivity to antibiotics. If the resulting liquid is clear or slightly cloudy, then in addition to inoculation, it is recommended to centrifuge it and Examine the sediment under a microscope. The presence of a large number of neutrophils indicates the onset of purulent pleurisy, and the growth of pathogenic microflora in the culture confirms this diagnosis. A number of additional studies of pleural fluid help clarify the diagnosis. It is typical for purulent effusion low glucose (less than 40 mg per 100 ml), decrease in pH (less than 7.0), and in case of empyema caused by esophageal perforation or pancreatic necrosis, a high amylase content is determined in the exudate (R.W. Light, W.C. Ball, 1973). Cytological examination of exudate, especially with its purulent-hemorrhagic nature, it is necessary to diagnose primary or secondary tumor lesions of the pleura, as evidenced by atypical cells found in smears.

The main task of local treatment of pleural empyema is the effective emptying of its cavity from purulent contents. For this purpose, various methods of drainage and lavage of the pleural cavity by introducing silicone rubber drainages into it. The most effective is the combination of active aspiration of purulent effusion with drip injection into the cavity of antiseptic solutions (furacillin, furagin K, dioxidin) with the addition of proteolytic enzymes and fibrinolytic drugs (Ya.N. Shoikhet et al., 1996). In the presence of pleural encystations, it is sometimes necessary to drain each cavity separately. Multiple and wide bronchopleural fistulas make it difficult to adequately lavage the empyematous cavity. In these cases, temporary blockade of the bronchial tubes carrying fistulas using various obturators introduced during bronchoscopy. Such a blockade lasting from several days to 2-3 weeks prevents lavage fluid from entering the bronchial tree, promotes more effective washing of the pleura and straightening of adjacent parts of the lung with subsequent obliteration of the pleural cavity. For re-expansion of a collapsed lung in the stage of fibrinous-purulent inflammation, in recent years it has been successfully performed therapeutic videopleuroscopy (thoracoscopy) , during which loose adhesions are destroyed and fibrin deposits are removed from the surface of the visceral pleura (H. Striffeler et al., 1994; V.A. Porkhanov, 1996; O.O. Yasnogorodsky et al., 1997), and ultrasound or plasma sanitation of the pleural cavity (I.I. Kotov, 1997). As empyema becomes chronic and progresses to the stage of fibrous organization tight moorings become an obstacle to the expansion of the lung and require surgical treatment. At this stage they perform decortication of the lung, surgically removing thickened and rigid visceral pleura from its surface, and, if necessary, combining this operation with resection of destroyed parts of the lung. With encysted empyema The ideal surgical option is to remove the entire empyema sac - empyemectomy. Correction of volemic disorders

By creating a complete outflow of purulent contents from the pleural cavity through drainage and, if necessary, carrying out bronchoscopic sanitation of the tracheobronchial tree, the resorption factor is eliminated and thereby reduces the intoxication of the body. However, the loss factor remains, because along with the flowing pus and sputum, a large amount of protein and electrolytes is lost. Their loss and imbalance lead to pronounced volemic disorders, the phases of which objectively reflect transition of purulent-resorptive fever to purulent-resorptive exhaustion (G.I. Lukomsky, M.E. Alekseeva, 1988). The total protein losses in patients with pleural empyema, especially with massive destruction of the lungs, are, according to G.I. Lukomsky and M.E. Alekseeva, from 7 to 20 g of nitrogen per day, which is equivalent to the loss of 44-125 g of protein or 300-500 g of muscle tissue. Such losses must be made up partial parenteral nutrition, simultaneously pursuing the goal of correcting volemic disorders that occur in almost all patients with purulent pleurisy. For this, amino acid mixtures, protein hydrolysates (aminopeptide, casein hydrolysate, L-103 hydrolysate), as well as protein, plasma and red blood cells are used at the rate of 1-2 g of protein per 1 kg of body weight, depending on the phase of volemic disorders. Despite the fact that plasma and blood proteins begin to participate in metabolism a long time after their administration, plasma and red blood cells help eliminate anemia, hypoproteinemia and hypoalbuminemia. Their role is also great in maintaining the oncotic pressure of circulating blood.

To utilize the administered proteins, it is necessary to supply a sufficient amount of non-protein energy resources at the rate of 15-25 kcal per 1 kg of body weight per day, depending on the stage of the disease. Such caloric intake can be provided by fat emulsions, concentrated (50%) glucose solutions 600-1000 ml per day with the obligatory addition of insulin, or a combination of 10-14% glucose solution (1.5-2 g per 1 kg of body weight per day) with ethyl alcohol(1-1.5 g per 1 kg of body weight per day). Without the introduction of energy carriers, most of the introduced nitrogen goes to replenish energy costs. Mixtures based on fat emulsions and glucose solutions with a concentration of no higher than 10% can be injected into peripheral veins, while infusion of a 50% glucose solution is possible only by catheterizing the central veins and inserting a catheter into the superior vena cava to avoid the development of phlebitis. The absorption of injected nitrogen increases with the combined use of anabolic hormones and vitamins. Protein synthesis will be incomplete if the infused solutions do not contain extracellular cations (at least 3 mEq of potassium per 1 g of nitrogen) and the content of magnesium and phosphorus is inadequate. This is the only way to achieve replenishment of water-binding structures that play an active role in volemic disorders.

The role of antibiotics very important at the beginning of the development of the purulent process in the pleura, decreases as a dense pyogenic capsule forms, surrounding the purulent cavity, and as inflammation transitions from the stage of purulent-resorptive fever to the stage of purulent-resorptive exhaustion. The selection of antibiotics is carried out on the basis of the sensitivity to them of the microflora of the pleural cavity, sputum or blood (if the results of their cultures are positive). As first-line drugs prescribed before obtaining bacteriological examination data, we can recommend cephalosporin antibiotics, especially II and III generation: cefuroxime, cefoxitin, cefotaxime, cefoperazone, ceftriaxone, active against both gram-positive and gram-negative flora. The exception is for patients in whom cephalosporins have already been used previously to treat pneumonia or another source of infection complicated by purulent pleurisy, and therefore are ineffective. In such patients it is better to immediately prescribe aminoglycosides (gentamicin, tobramycin) or modern drugs monobactams, carbapenems. Antibiotics are best administered intravenously in combination with metronidazole.

When choosing rational antibiotic therapy, one must take into account the fact that as the microbial background transforms, even the most modern, newly synthesized drugs quite soon cease to be effective against antibiotic-resistant generations of microorganisms and require replacement.

In complex therapy of purulent pleurisy good effect observed from the use of ultraviolet irradiation of blood, hemosorption, plasmapheresis and plasmacytopheresis, which help normalize homeostasis, reduce intoxication of the body and increase its immune-resistant capabilities. In the acute phase of the disease, it is recommended to correct proteolytic and inhibitory imbalances and regulate phagocyte function (E.A. Tseymakh, 1996; Ya.N. Shoikhet et al., 1996). In recent years, good results have been obtained using extracorporeally stimulated monocytes, immunostimulating and immunomodulating drugs.

The prognosis for pleurisy depends on the cause of this disease, as well as on the stage of the disease ( at the time of diagnosis and initiation of therapeutic procedures). Availability inflammatory reaction in the pleural cavity accompanying any pathological processes in the lungs is an unfavorable sign and indicates the need for intensive treatment.

Since pleurisy is a disease that can be caused by a fairly large number of pathogenic factors, there is no one treatment regimen indicated in all cases. In the vast majority of cases, the goal of therapy is the initial ailment, after which the inflammation of the pleura is eliminated. However, in order to stabilize the patient and improve his condition, they often resort to the use of anti-inflammatory drugs, as well as surgical treatment ( puncture and extraction of excess fluid).

Interesting Facts

• pleurisy is one of the most common pathologies in therapy and occurs in almost every tenth patient;
• it is believed that the cause of death of the French queen Catherine de Medici, who lived in the 14th century, was pleurisy;
• drummer of the Beatles ( The Beatles) Ringo Starr suffered from chronic pleurisy at the age of 13, which caused him to miss two years of school and never finish school;
• first description of pleural empyema ( accumulation of pus in the pleural cavity) was given by an ancient Egyptian physician and dates back to the third millennium BC.

Pleura and its damage

Damage to the pleura with the formation of an inflammatory process and the formation of an excess amount of pleural fluid can occur under the influence of infections ( directly affecting the pleura or involving nearby lung tissue), injuries, pathologies of the mediastinum ( cavity located between the lungs and containing the heart and important vessels, trachea and main bronchi, esophagus and some others anatomical structures ), against the background of systemic diseases, as well as due to metabolic disorders of a number of substances. In the development of pleurisy and other lung diseases, the place of residence and type of activity of a person is important, since these factors determine some aspects of the negative impact of a number of toxic and harmful substances on the respiratory system.

It should be noted that one of the main signs of pleurisy is pleural effusion - excessive accumulation of fluid in the pleural cavity. This condition is not necessary for inflammation of the pleural layers, but occurs in most cases. In some situations, pleural effusion occurs without the presence of an inflammatory process in the pleural cavity. As a rule, such a disease is considered precisely as pleural effusion, but in some cases it can be classified as pleurisy.

Causes of pleurisy

Some authors also classify cases of pleural effusion without an obvious inflammatory response as pleurisy. This situation is not entirely correct, since pleurisy is a disease that involves an obligatory inflammatory component.

The following causes of pleurisy are distinguished:

• infectious lesion of the pleura;
• allergic inflammatory reaction;
• autoimmune and systemic diseases;
• exposure to chemicals;
• chest injury;
• exposure to ionizing radiation;
• exposure to pancreatic enzymes;
• primary and metastatic pleural tumors.

Infectious lesion of the pleura

Pleural infection is a serious illness that in many cases can be life-threatening. Adequate diagnosis and treatment this state requires coordinated actions of pulmonologists, therapists, radiologists, microbiologists and, often, thoracic surgeons. The therapeutic approach depends on the nature of the pathogen, its aggressiveness and sensitivity to antimicrobial drugs, as well as the stage of the disease and the type of infectious-inflammatory focus.

Pleurisy of an infectious nature affects patients of all age categories, but they are most common among the elderly and children. Men get sick almost twice as often as women.

The following concomitant pathologies are risk factors for the development of infectious lesions of the pleura:

• Diabetes. Diabetes mellitus develops as a result of a violation of the endocrine function of the pancreas, which produces insufficient amounts of insulin. Insulin is a hormone that is necessary for the normal metabolism of glucose and other sugars. In diabetes mellitus, many internal organs are affected, and a slight decrease in immunity occurs. In addition, excessive concentrations of glucose in the blood create favorable conditions for the development of many bacterial agents.
• Alcoholism . With chronic alcoholism, many internal organs suffer, including the liver, which is responsible for the production of protein components of antibodies, the lack of which leads to a decrease in the body's protective potential. Chronic alcohol abuse leads to disruption of the metabolism of a number of nutrients, as well as a decrease in the number and quality of immune cells. Additionally, people with alcoholism are more prone to chest injuries as well as respiratory tract infections. This occurs due to hypothermia combined with decreased sensitivity and behavioral disturbances, as well as suppression of protective reflexes, which increases the risk of inhaling infected materials or one’s own vomit.
• Rheumatoid arthritis. Rheumatoid arthritis is an autoimmune disease that can independently cause damage to the pleura. However, this disease is also a serious risk factor for the development of infectious lesions of the pleura. This is due to the fact that drugs that reduce immunity are often used to treat this disease.
• Chronic diseases lungs. Many chronic lung diseases, such as chronic bronchitis, chronic obstructive pulmonary disease, emphysema, asthma and some other pathologies create the preconditions for infectious damage to the pleura. This happens for two reasons. Firstly, many chronic lung diseases are characterized by sluggish infectious and inflammatory processes that can progress over time and cover new tissues and areas of the lungs. Secondly, with these pathologies, the normal functioning of the respiratory apparatus is disrupted, which inevitably leads to a decrease in its protective potential.
• Pathologies gastrointestinal tract. Diseases of the dental apparatus can cause the accumulation of infectious agents in the oral cavity, which, after a deep breath ( for example, during sleep) can end up in the lungs and cause pneumonia with subsequent damage to the pleura. Gastroesophageal reflux ( backflow of food from the stomach into the esophagus) promotes respiratory tract infection by increasing the risk of inhaling gastric contents that may be infected and which reduces local immunity ( due to the irritating effect of hydrochloric acid).

Infectious agents can enter the pleural cavity in the following ways:

• Contact with an infectious focus in the lungs. When the infectious-inflammatory focus is located in close proximity to the pleura, direct transfer of pathogens with the development of pleurisy is possible.
• With lymph flow. The penetration of microorganisms along with the lymph flow is due to the fact that the lymphatic vessels of the peripheral areas of the lungs drain into the pleural cavity. This creates the preconditions for the penetration of infectious agents from areas that do not come into direct contact with the serous membrane.
• With blood flow. Some bacteria and viruses are capable of penetrating into the bloodstream at a certain stage of their development, and at the same time into various organs and fabrics.
• Direct contact with the external environment ( injuries). Any penetrating trauma to the chest cavity is considered potentially infected and, accordingly, as a possible source of pleural infection. Openings and incisions in the chest wall made for therapeutic purposes, but under inappropriate conditions or lack of proper care, can also act as a source of pathogenic microorganisms.

Under the influence of these microorganisms, an inflammatory process develops, which is a special protective reaction aimed at eliminating infectious agents and limiting their spread. Inflammation is based on a complex chain of interactions between microorganisms, immune cells, biologically active substances, blood and lymphatic vessels and tissues of the pleura and lungs.

In the development of pleurisy, the following successive stages are distinguished:

• Exudation phase. Under the influence of biologically active substances that are secreted by immune cells activated as a result of contact with infectious agents, blood vessels dilate and their permeability increases. This leads to increased production of pleural fluid. At this stage, the lymphatic vessels cope with their function and adequately drain the pleural cavity - excess accumulation no liquid occurs.
• The phase of formation of purulent exudate. As the inflammatory reaction progresses, deposits of fibrin, a “sticky” plasma protein, begin to form on the pleura. This occurs under the influence of a number of biologically active substances that reduce the fibrinolytic activity of pleural cells ( their ability to destroy fibrin threads). This leads to significantly increased friction between the pleural layers, and in some cases, adhesions occur ( areas of “gluing” of serous membranes). This course of the disease contributes to the formation of separated areas in the pleural cavity ( so-called “pockets” or “bags”), which significantly complicates the outflow of pathological contents. After some time, pus begins to form in the pleural cavity - a mixture of dead bacteria, absorbed immune cells, plasma and a number of proteins. The accumulation of pus is facilitated by progressive swelling of mesothelial cells and tissues located close to the inflammatory focus. This leads to the fact that the outflow through the lymphatic vessels decreases and an excess volume of pathological fluid begins to accumulate in the pleural cavity.
• Recovery stage. At the recovery stage, either resorption occurs ( resorption) pathological foci, or, if it is impossible to independently eliminate the pathogenic agent, connective tissue ( fibrous) formations that limit the infectious-inflammatory process with the further transition of the disease into a chronic form. Foci of fibrosis adversely affect lung function, as they significantly reduce their mobility, and in addition, increase the thickness of the pleura and reduce its ability to reabsorb fluid. In some cases, either separate adhesions are formed between the parietal and visceral layers of the pleura ( moorings), or complete overgrowth with fibrous fibers ( fibrothorax).

Tuberculosis

Tuberculous pleurisy occurs as a result of penetration of Mycobacterium tuberculosis, also known as Koch's bacillus, into the pleural cavity. This disease is considered the most common form of extrapulmonary infection, which can occur when the primary foci are located both in the lungs and in other internal organs. It can develop against the background of primary tuberculosis, which occurs upon first contact with the pathogen ( typical for children and adolescents), or secondary, which develops as a result of repeated contact with a pathogenic agent.

Penetration of mycobacteria into the pleura is possible in three ways - lymphogenous and contact when the primary focus is located in the lungs or spine ( rarely), and hematogenous, if the primary infectious focus is located in other organs ( gastrointestinal tract, lymph nodes, bones, genitals, etc.).

The development of tuberculous pleurisy is based on an inflammatory reaction supported by the interaction between immune cells ( neutrophils during the first few days and lymphocytes thereafter) and mycobacteria. During this reaction, biologically active substances are released that affect the tissues of the lung and serous membranes, and which maintain the intensity of inflammation. Against the background of dilated blood vessels within the infectious focus and reduced lymph outflow from the pleural cavity, pleural effusion is formed, which, unlike infections of other nature, is characterized by an increased content of lymphocytes ( more than 85%).

It should be noted that for the development of tuberculosis infection a certain unfavorable combination of circumstances is necessary. Most people do not become infected by simple contact with the Koch bacillus. Moreover, it is believed that in many people, Mycobacterium tuberculosis can live in the tissues of the lungs without causing disease or any symptoms.

The following factors contribute to the development of tuberculosis:

• High density of infectious agents. The likelihood of developing an infection increases as the number of bacilli inhaled increases. This means that the higher the concentration of mycobacteria in environment, the higher the chances of infection. This development of events is facilitated by staying in the same room with tuberculosis patients ( at the stage of releasing pathogenic agents), as well as the lack of adequate ventilation and small volume of the room.
• Long contact time. Prolonged contact with infected people or long stay in a room where mycobacteria are in the air, is one of the main factors contributing to the development of infection.
• Low immunity. Under normal conditions, with periodic vaccinations, the human immune system copes with tuberculosis pathogens and prevents the development of the disease. However, in the presence of any pathological condition in which there is a decrease in local or general immunity, the penetration of even a small infectious dose can cause infection.
• High aggressiveness of infection. Some mycobacteria have greater virulence, that is, an increased ability to infect people. The penetration of such strains into the human body can cause infection even with a small number of bacilli.

Decreased immunity is a condition that can develop against the background of many pathological conditions, as well as with the use of certain medications.

The following factors contribute to decreased immunity:

• chronic diseases of the respiratory system ( infectious and non-infectious nature);
• diabetes;
• chronic alcoholism;
• treatment with drugs that suppress the immune system ( glucocorticoids, cytostatics);
• HIV infection ( especially at the stage of AIDS).

Allergic inflammatory reaction

Pleurisy can develop with the following types of allergic reactions:

• Exogenous allergic alveolitis. Exogenous allergic alveolitis is a pathological inflammatory reaction that develops under the influence of external foreign particles - allergens. In this case, damage to the lung tissue directly adjacent to the pleura often occurs. The most common allergens are fungal spores, plant pollen, house dust, some medicinal substances.
• Drug allergy. Drug allergies are common in modern world. Quite a large number of people are allergic to certain antibiotics, local anesthetics and other pharmacological drugs. A pathological response develops within minutes or hours after drug administration ( depending on the type of allergic reaction).
• Other types of allergies . Some other types of allergies that do not directly affect lung tissue can cause activation of pleural immune cells with the release of biologically active substances and the development of edema and exudation. After eliminating the effect of the allergen, the scale of inflammation decreases, reverse suction excess fluid from the pleural cavity.

It is necessary to understand that the inflammatory reaction underlying allergies differs slightly from the inflammatory reaction that develops during an infectious process. Moreover, in most cases, microorganisms provoke an allergic reaction in the pleura, which contributes to the development of pleurisy and the formation of exudate.

Autoimmune and systemic diseases

Autoimmune diseases are pathologies in which the immune system begins to attack its own tissues ( usually connective tissue fibers). As a result, a chronic inflammatory reaction develops, which affects many organs and tissues ( mainly – joints, skin, lungs).

Pleurisy can develop with the following systemic pathologies:

• rheumatoid arthritis;
• systemic lupus erythematosus;
• dermatomyositis;
• Wegener's granulomatosis;
• Churg-Strauss syndrome;
• sarcoidosis

Exposure to chemicals

Chemicals can enter the pleural cavity in the following ways:

• With open trauma. With an open chest injury, various chemically active substances - acids, alkalis, etc. - can enter the pleural cavity.
• For closed chest injuries. Closed chest injuries can cause rupture of the esophagus with subsequent entry of food or gastric contents into the mediastinum and onto the parietal layers of the pleura.
• Inhalation of chemicals. Inhalation of certain hazardous chemicals can cause burns to the upper and lower respiratory tract, as well as an inflammatory process in the lung tissues.
• Injections of chemicals. When substances not intended for such use are administered intravenously, they can enter the tissues of the lungs and pleura and cause serious impairment of their function.

Chest trauma

If the pleural layers are damaged as a result of exposure to a mechanical factor ( with closed and open injuries ) an inflammatory response occurs, which, as described above, leads to increased production of pleural fluid. In addition, traumatic exposure disrupts lymph circulation in the damaged area, which significantly reduces the outflow of pathological fluid and contributes to the development of pleural effusion. The penetration of pathogenic infectious agents is another additional factor that increases the risk of developing post-traumatic pleurisy.

Damage to the esophagus, which can occur with a strong blow to the chest cavity, is accompanied by the release of food and gastric contents into the mediastinal cavity. Due to the frequent combination of a rupture of the esophagus with a violation of the integrity of the pleural layers, these substances can enter the pleural cavity and cause an inflammatory reaction.

Exposure to ionizing radiation

Effects of pancreatic enzymes

Pleurisy develops due to the destructive effect of pancreatic enzymes on the serous membranes, which, when inflamed, enter the blood ( normally they are transported directly to the duodenum). These enzymes partially destroy blood vessels, the connective tissue basis of the pleura, and activate immune cells. As a result, exudate accumulates in the pleural cavity, which consists of leukocytes, blood plasma and destroyed red blood cells. Amylase concentration ( pancreatic enzyme) in pleural effusion can be several times higher than the concentration in the blood.

Pleural effusion in pancreatitis is a sign of severe damage to the pancreas and, according to a number of studies, occurs more often with pancreatic necrosis ( death of a significant part of the organ cells).

Primary and metastatic pleural tumors

Pleurisy can develop with the following types of tumors:

• Primary pleural tumors . A primary pleural tumor is a neoplasm that has developed from cells and tissues that make up the normal structure of this organ. In most cases, such tumors are formed by mesothelial cells and are called mesotheliomas. They occur in only 5–10% of cases of pleural tumors.
• Metastatic foci in the pleura. Pleural metastases are tumor fragments that have separated from the primary focus located in any organ and which have migrated to the pleura, where they continued to develop. In most cases, the tumor process in the pleura is of a metastatic nature.

Pleural effusion, which is the most common manifestation of tumor pleurisy, develops as a result of the interaction of several pathological mechanisms on the pleura. Firstly, a tumor focus that occupies a certain volume in the pleural cavity reduces the area of ​​effectively functioning pleura and reduces its ability to reabsorb fluid. Secondly, under the influence of products produced in tumor tissues, the concentration of proteins in the pleural cavity increases, which leads to an increase in oncotic pressure ( proteins are able to “attract” water – a phenomenon called oncotic pressure). And thirdly, the inflammatory reaction that develops against the background of primary or metastatic neoplasms increases the secretion of pleural fluid.

Types of pleurisy

• dry ( fibrinous) pleurisy;
• exudative pleurisy;
• purulent pleurisy;
• tuberculous pleurisy.

Dry ( fibrinous) pleurisy

In dry pleurisy, due to increased vascular permeability under the influence of pro-inflammatory substances, the liquid component of the plasma and some proteins begin to leak into the pleural cavity, among which fibrin is of greatest importance. Under the influence of the environment in the inflammatory focus, fibrin molecules begin to unite and form strong and adhesive threads that are deposited on the surface of the serous membrane.

Since with dry pleurisy the amount of effusion is minimal ( the outflow of fluid through the lymphatic vessels is slightly impaired), fibrin threads significantly increase friction between the layers of the pleura. Since the pleura contains a large number of nerve endings, increased friction causes significant pain.

The inflammatory process in fibrinous pleurisy affects not only the serous membrane itself, but also the cough nerve receptors located in its thickness. Thanks to this, their sensitivity threshold is reduced, and a cough reflex occurs.

Exudative ( effusion) pleurisy

Since the fluid accumulated in the pleural cavity reduces to some extent the friction between the layers of the pleura, at this stage the irritation of the serous membranes and, accordingly, the intensity of the pain is somewhat reduced.

Purulent pleurisy

Purulent pleurisy can form both when the pleura is directly damaged by infectious agents, and when an abscess opens on its own ( or other collection of pus) lung into the pleural cavity.

Empyema usually develops in debilitated patients who have serious damage to other organs or systems, as well as in people with reduced immunity.

Tuberculous pleurisy

Symptoms of pleurisy

• cause of pleurisy;
• intensity of the inflammatory reaction in the pleural cavity;
• stage of the disease;
• type of pleurisy;
• volume of exudate;
• nature of the exudate.

The following symptoms are characteristic of pleurisy:

• increased body temperature;
• tracheal displacement.

Dyspnea

Shortness of breath appears as a feeling of lack of air. This symptom can occur during physical activity of varying intensity, and in the case of severe disease or massive pleural effusion - at rest. With pleurisy, shortness of breath may be accompanied by a subjective feeling of insufficient expansion or filling of the lungs.

Typically, shortness of breath caused by isolated pleural damage develops gradually. It is often preceded by other symptoms ( chest pain, cough).

Dyspnea that persists after treatment of pleurisy and drainage of pleural effusion indicates a decrease in the elasticity of the lung tissue or that adhesions have formed between the layers of the pleura ( moorings), which significantly reduce mobility and, accordingly, the functional volume of the lungs.

It should be borne in mind that shortness of breath can also develop with other pathologies of the respiratory system that are not associated with pleurisy, as well as with impaired cardiac function.

Cough

The appearance of sputum ( purulent or mucous) or bloody discharge during cough indicates the presence of an infectious ( more often) lung damage.

Chest pain

Increased body temperature

With pleurisy, the following variants of elevated body temperature are possible:

• Temperature up to 38 degrees. Body temperature up to 38 degrees is typical for small infectious and inflammatory foci, as well as for some pathogenic agents with low virulence. Sometimes this temperature is observed at some stages of systemic diseases, tumor processes, as well as pathologies of other organs.
• The temperature is within 38 - 39 degrees. An increase in body temperature to 38 - 39 degrees is observed with pneumonia of a bacterial and viral nature, as well as with most infections that can affect the pleura.
• Temperature above 39 degrees . A temperature above 39 degrees develops with severe disease, with the accumulation of pus in any cavity, as well as with the penetration of pathogens into the blood and with the development of a systemic inflammatory response.

In addition to the body temperature itself, the nature of its increase and decrease is important. In most cases, during an acute infectious process, the temperature rises quickly during the first few hours from the onset of the disease, which is accompanied by a feeling of chills ( reflects the process of activation of mechanisms aimed at preserving heat). A decrease in temperature is observed when the scale of the inflammatory process decreases, after the eradication of infectious agents, as well as when the accumulation of pus is eliminated.

Separate mention should be made of fever due to tuberculosis. This infection is characterized by low-grade fever ( within 37 – 37.5), which are accompanied by a feeling of chills, night sweats, a productive cough with sputum, and weight loss.

Tracheal displacement

With pleurisy, some other symptoms may be present, which depend on the pathology underlying the inflammation of the pleura. These manifestations are of great diagnostic importance, as they allow us to establish the cause of the disease and begin adequate treatment.

Diagnosis of pleurisy

The following examinations are used to diagnose pleurisy:

• examination and interview of the patient;
• clinical examination of the patient;
• X-ray examination;
• blood analysis;
• pleural effusion analysis;
• microbiological research.

Examination and interview of the patient

During the examination, the doctor visually assesses the general condition of the patient and determines existing deviations from the norm.

Upon examination, the following pathological signs may be revealed:

• deviation of the trachea to the healthy side;
• blue discoloration of the skin ( indicates severe respiratory distress);
• signs of closed or open chest trauma;
• bulging in the intercostal spaces on the affected side ( due to the large volume of accumulated liquid);
• body tilt to the affected side ( reduces lung movement and, accordingly, irritation of the pleura during breathing);
• bulging neck veins ( due to increased intrathoracic pressure);
• lag of the affected half of the chest during breathing.

Clinical examination of the patient

• Auscultation . Auscultation is an examination method in which the doctor listens to sounds arising in the human body using a stethoscope ( before its invention - directly by the ear). When auscultating patients with pleurisy, a pleural friction noise can be detected, which occurs when the pleural sheets covered with fibrin threads rub against each other. This sound is heard during respiratory movements, does not change after coughing, and persists when breathing is imitated ( performing several breathing movements with the nose and mouth closed). With effusion and purulent pleurisy in the area of ​​fluid accumulation, there is a weakening of respiratory sounds, which sometimes may not be heard at all.
• Percussion. Percussion is a method of clinical examination of patients, in which the doctor uses his own hands or special devices ( hammer and small plate - plessimeter) taps organs or formations of varying density in the patient’s cavities. The percussion method can be used to determine the accumulation of fluid in one of the lungs, since percussion above the fluid produces a higher-pitched, dull sound, different from the sound that occurs above healthy lung tissue. When tapping the boundaries of this percussion dullness, it is determined that the fluid in the pleural cavity forms not a horizontal, but a somewhat oblique level, which is explained by uneven compression and displacement of the lung tissue.
• Palpation. Using the palpation method, that is, by “feeling” the patient, areas of the spread of painful sensations can be identified, as well as some others Clinical signs. With dry pleurisy, pain is observed when pressing between the legs of the sternocleidomastoid muscle, as well as in the area of ​​​​the cartilage of the tenth rib. When applying the palms to symmetrical points of the chest, a slight lag of the affected half in the act of breathing is noted. In the presence of pleural effusion, a weakening of vocal tremors is felt.

X-ray examination

With dry pleurisy, the following signs are determined on x-ray:

• on the affected side, the dome of the diaphragm is higher than normal;
• decreased transparency of the lung tissue against the background of inflammation of the serous membrane.

• smoothing of the aperture angle ( due to fluid accumulation);
• uniform darkening of the lower region of the pulmonary field with an oblique border;
• shift of the mediastinum towards the healthy lung.

Blood analysis

A biochemical blood test can reveal changes in the ratio of proteins in the blood plasma due to an increase in the content of alpha globulins and C-reactive protein.

Pleural effusion analysis

Laboratory analysis of pleural effusion allows you to determine the following indicators:

• quantity and type of proteins;
• glucose concentration;
• lactic acid concentration;
• number and type of cellular elements;
• presence of bacteria.

Microbiological examination

Treatment of pleurisy

Treatment of pleurisy with medications

It should be borne in mind that the choice of pharmacological drugs is based on previously obtained diagnostic data. Antibiotics are selected taking into account the sensitivity of pathogenic microorganisms ( determined by microbiological examination or identified by any other method). The dosage regimen of medications is set individually, depending on the severity of the patient’s condition.

Drugs used to treat pleurisy

When is puncture necessary for pleurisy?

Relative contraindications to pleural puncture are the following conditions:

• pathologies of the blood coagulation system;
• high blood pressure in the pulmonary artery system;
• chronic obstructive pulmonary disease in a severe stage;
• having only one functional lung.

With a significant volume of pleural effusion, puncture allows you to drain part of the pathological fluid, thereby reducing the degree of compression of the lung tissue and improving respiratory function. The therapeutic puncture is repeated as necessary, that is, as the effusion accumulates.

Is hospitalization necessary to treat pleurisy?

Is it possible to treat pleurisy at home?

Nutrition for pleurisy ( diet)

Salty, smoked, spicy and canned foods are contraindicated, as they provoke a feeling of thirst.

It is necessary to consume sufficient amounts of vitamins, as they are necessary for the normal functioning of the immune system. For this purpose, it is recommended to eat fresh vegetables and fruits.

Consequences of pleurisy

However, in many cases, pleurisy can cause partial or complete structural and functional restructuring of the pleural or lung tissue.

The consequences of pleurisy include:

• Adhesions between the layers of the pleura. Adhesions are connective tissue strands between the layers of the pleura. They are formed in the area of ​​inflammatory foci that have undergone organization, that is, sclerosis. Adhesions, called moorings in the pleural cavity, significantly limit the mobility of the lungs and reduce the functional tidal volume.
• Overgrowth of the pleural cavity. In some cases, massive pleural empyema can cause complete “overgrowth” of the pleural cavity with connective tissue fibers. This almost completely immobilizes the lung and can cause serious respiratory failure.

Purulent pleurisy- this is a purulent inflammation of the pleura with the accumulation of purulent exudate in its cavity. Purulent pleurisy is a septic manifestation of a common severe infection.

There are: acute, diffuse purulent pleurisy (pleural empyema); encysted purulent pleurisy, the spread of which is limited by the presence of adhesions and adhesions in the pleura; mantle-shaped, interlobar and mediastinal pleurisy.

Acute purulent pleurisy begins with an intermittent high temperature and increasing shortness of breath. The temperature may be low, but the general condition of the patient is serious. The position in bed is forced (half sitting). On examination, there is a lag in the act of breathing on the affected side of the chest, and there is pronounced smoothness of the intercostal spaces. The heartbeat is shifted to the healthy side. Voice tremors not determined.

On percussion - dullness spreading to the axillary region and to the anterior surface of the chest. The Sokolov-Damoiso line rarely retains its usual concavity. On the right, dullness merges with dullness of the liver. On the left there is no tympanitis in Traube space. Above dullness, a dull-tympanic percussion tone is determined, breathing with a bronchial hue is heard. General intoxication and respiratory failure increase.

With the accumulation of exudate, stagnation in the vena cava is observed. The pulse quickens, heart sounds become muffled. Breathing is shallow. As oxygen deprivation increases, breathing becomes Kussmaul-type. The liver enlarges due to toxic damage to the parenchyma; Renal function is impaired and albuminuria appears. In the future, dystrophy may develop with the manifestation of vitamin deficiency (dry and flaky skin, hemorrhages caused by capillary fragility). Functional disorders of the liver, autonomic and endocrine systems occur.

With pleural empyema radiologically determined total darkening. To more accurately identify the localization of pleural changes, tomography is necessary.
In the blood leukocytosis with shift leukocyte formula to the left and increased ESR.

For diagnostic purposes, a pleural puncture is performed, from which, as a rule, purulent exudate is obtained. Microscopically, a large number of leukocytes are detected in the liquid.

In the early childhood Rapidly developing purulent pleurisy gives a picture of a very serious illness. Cyanosis of the skin quickly gives way to pallor and sallow (hypoxia), sometimes with a yellowish tint (hemolysis). The amount of hemoglobin decreases, the amount of direct and indirect bilirubin increases. Often join purulent complications from the ears, pericardium, kidneys.
In children with reduced resistance, the development of purulent pleurisy occurs slowly. Usually the disease is preceded by fibrinous or fibrinous-purulent pleurisy with subsequent accumulation of pus in the pleural cavity.

Ensacculated purulent pleurisy occurs more often in the presence of previously formed adhesions after repeated pneumonia, less often purulent exudate is located between the layers of the pleura and encystes there. With this form there are no symptoms characteristic of diffuse pleurisy (dullness, lack of breathing, heart displacement, etc.). It is difficult to establish the presence of encysted pleurisy by objective examination. The diagnosis is confirmed by x-ray.

Plaque pleurisy characterized by the location of purulent exudate in a thin layer throughout the visceral pleura. The patient is bothered by sharp pain when breathing, and the symptoms of a general septic condition are increasing. Dullness of percussion tone is detected
all over the chest on the affected side. Auscultation - weakened breathing. The diagnosis is confirmed by x-ray.

Interlobar purulent pleurisy characterized by a protracted course. In this case, pain in the intercostal spaces and increased temperature are noted. The general condition of patients is not always severe. Percussion reveals dullness of sound from the corner of the scapula towards the anterior axillary line in the form of a narrow strip, breathing is weakened at the site of dullness. The decisive factor in clarifying the diagnosis is x-ray examination(typical wedge-shaped shadow with its base at the root of the lung).

Mediastinal purulent pleurisy starts sharply high fever, sharp pain in the chest, the appearance of a dull sound in the form of a strip located parallel to the sternum. There are symptoms of irritation and compression of the sympathetic nerve (constriction of the pupil and palpebral fissure). X-ray examination plays a decisive role in diagnosis (ribbon-shaped shadow, closely associated with the mediastinum).

TREATMENT

Applicable complex treatment , due to which in recent years the mortality rate has decreased by 2.5 times.

Main therapeutic measure is evacuation of pus from the pleural cavity. Suction of purulent exudate in children early age It is best to use a 20-gram syringe; in older children, use the Poten apparatus. After removing the purulent effusion, one of the antibiotics (penicillin, streptomycin, monomycin) is injected into the pleural cavity.

Subsequent treatment of empyema is carried out by repeated suction of pus and intrapleural administration of one of the antibiotics in the amount of 100-300 thousand units. However, when evacuating purulent exudate positive result is not always achieved. In such cases, surgery is recommended.

Great importance has a rational antibacterial therapy. It is necessary to first examine the purulent effusion of the pleural cavity for the sensitivity of the pathogen to antibiotics. In order to increase immunobiological reactivity, fractional transfusions of blood, plasma, concentrated albumin, etc. are used. Desensitizing agents include diphenhydramine, diprazine, and suprastin. Along with this, it is necessary to organize a balanced diet, careful care, and widely carry out aerotherapy. During the recovery period, physiotherapeutic measures (UHF therapy, quartz) and therapeutic exercises are used.

Forecast both purulent and serous pleurisy depends on the effectiveness of therapy for the underlying disease, complicated by pleurisy, on age, the form of pleurisy, the state of reactivity of the body, on the pathogen and its resistance to antibiotics.

The outcome of purulent pleurisy depends on early diagnosis and timely comprehensive treatment.

svetlana
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Acute purulent pleurisy is an acute purulent inflammation of the pleura. In the vast majority of cases, it is a secondary disease - a complication of purulent lesions of various organs.

Purulent pleurisy sometimes develops as a result of the spread of infection by the lymphogenous route during various purulent processes of the abdominal cavity, retroperitoneal space: purulent cholecystitis, appendicitis, pancreatitis, perforated gastric ulcer, subphrenic abscess, peritonitis, paranephritis, etc. The development of metastatic acute purulent pleurisy in sepsis is described, phlegmon, osteomyelitis and other purulent processes of various localizations. There are reports of pleurisy caused by a specific or mixed infection with scarlet fever, measles, typhus, etc.

The causative agents of the disease are various pyogenic microorganisms. During bacteriological examination of pus from the pleura, streptococcus is most often found (up to 90%), less often staphylococcus and pneumococcus. In children, pneumococcus is the most common (up to 70%). Mixed flora is often observed.

The pleura reacts to infection differently, which depends on the virulence of the latter and the reactivity of the organism.

With a weakly virulent infection, a small fibrinous effusion is formed, gluing the visceral and parietal pleura, which contributes to the formation of adhesions and adhesions around the source of infection - this is dry pleurisy. More virulent microbes cause the formation of abundant exudate - exudative pleurisy, which, with high virulence of the microflora, becomes purulent in nature.

There are several classifications of purulent pleurisy:

1) by pathogen - streptococcal, pneumococcal, staphylococcal, diplococcal, mixed, etc.;

2) according to the location of the pus: a) free - total, medium, small; b) encysted - multi-chamber and single-chamber (basal, parietal, paramediastinal, interlobar, apical);

3) according to pathological characteristics: a) acute purulent; b) putrefactive; c) purulent-putrefactive;

4) according to the severity of the clinical picture: a) septic; b) heavy; c) average; d) lungs.

Symptomatology and clinic. The clinical picture of acute purulent pleurisy is layered with the clinical manifestations of primary disease(pneumonia, lung abscess, etc.), of which it is a complication. The disease begins with severe stabbing pain in one side or another of the chest, sharply intensifying with breathing and coughing.

The temperature rises to 39-40°, the dry cough intensifies, the pulse becomes frequent and small. Increased stabbing pain when trying to deepen breathing leads to shallow, frequent breathing, which entails an increase in hypoxia. With an increase in the amount of exudate, the pleural layers move apart and the pain decreases somewhat, but compression of the lung by the exudate reduces the respiratory surface of the lungs, and shortness of breath appears.

When examining the patient, an increase in half of the chest on the side of the process, widening of the intercostal spaces, and a lag in breathing are noted. Vocal tremor on the affected side is weakened.

In the lower part of the pulmonary field - muffled percussion sound and weakened breathing, sometimes pleural friction noise, dry or moist rales are detected, lung excursions are limited.

With further progression of the disease, accumulation of pus in the pleura, the patient’s general condition worsens, the temperature remains high, sometimes fluctuations between morning and evening temperatures reach 2-2.5°, pain becomes less severe, a feeling of chest fullness appears, general weakness increases, appetite disappears.

On percussion, dullness is noted, its border is higher at the back, lower at the front (Demoiseau line), above and medially the dullness is a clear percussion sound in an area resembling a triangle in shape, which corresponds to the contour of the lung, pressed by the effusion to its gate.

The accumulation of pus leads to a displacement of the mediastinum to the healthy side, so at the bottom of the spine on the healthy side there is a triangular dullness above the displaced mediastinal organs. Cardiac dullness is shifted by exudate to the healthy side. With left-sided pleurisy with a large amount of effusion, the diaphragm lowers, and therefore Traube’s space disappears.

During auscultation in the area of ​​dullness there are completely no breath sounds, above the dullness, weakened breathing and pleural friction noise are detected. Blood changes are characterized by a decrease in the percentage of hemoglobin, an increase in the number of leukocytes, neutrophilia with a shift to the left, and an acceleration of ROE.

Often acute purulent pleurisy develops from the very beginning of the disease as encysted, which is explained by the presence of pleural adhesions and adhesions due to previous diseases. Localization, combination of cavities and their sizes can be very diverse.

Schematically, pleurisy can be divided into basal, parietal, paramediastinal, apical, interlobar, single and multiple.

General clinical manifestations with encysted pleurisy are almost the same as with free ones, but somewhat less pronounced. Poor general condition, localized chest pain, cough, high temperature, leukocytosis with neutrophilia, etc. are noted. Percussion and auscultation data can be obtained only with apical and parietal localization of the process.

Complications of purulent pleurisy. If the pleural cavity is not sufficiently cleared of pus, the latter finds its way into the muscle beds and subcutaneous tissue of the chest wall, most often along the mid-axillary line. With purulent inflammation of the visceral pleura, the process spreads along the lymphatic pathways, involving the cortical sections of the pulmonary parenchyma, and then the deeper sections of the lung with the lymph nodes of the root.

With long-term purulent pleurisy, the wall of the bronchus can melt with the formation of a bronchopleural fistula; when the lung collapses, irreversible sclerotic processes develop in it.

Diagnostics. Difficulties in diagnosing purulent pleurisy occur in cases where it develops against the background of unresolved pneumonia or a lung abscess. Of great importance for clarifying the diagnosis is an x-ray examination, which makes it possible to establish the presence of homogeneous darkening of the pleural cavity, the level of fluid in the pleura, the state of compressed lung tissue, the degree of displacement of the heart and blood vessels, the boundaries of pus and the airy lung tissue above it. If there is an inflammatory process in the compressed lung, then focal shadows are visible against the background of the lung tissue. On the affected side, the diaphragm is motionless. With free empyema, the costophrenic sinus is not visible. If clearing is noted in its area, this allows us to suspect the presence of encysted pleurisy. Dynamic radiological observation is especially important.

To clarify the diagnosis, a test puncture of the pleural cavity is crucial, which makes it possible to determine the nature of the effusion and bacteriologically examine it.

Acute purulent pleurisy must be differentiated from a lung abscess, suppurating cyst, subphrenic abscess, suppurating echinococcus, lung cancer with perifocal inflammation and effusion, interstitial pneumonia of the lower lobe, etc.

It is especially difficult to distinguish an abscess from encysted pleurisy. An important differential sign is a cough with large amounts of foul-smelling sputum, which is characteristic of an abscess. Auscultation with an abscess shows a rather motley picture: sometimes bronchial, sometimes weakened breathing, dry and moist wheezing. With pleurisy, breathing sounds are weakened or absent. Radiologically, with an abscess, a rounded shadow with a distinct lower border is observed; with pleurisy, the lower limit is not determined. Pleurisy is characterized by displacement of the mediastinum, filling of the costophrenic sinus, and changes in the fluid level when changing position.

With festering cysts, in contrast to pleurisy, the general condition of patients suffers less; there is a cough with copious sputum production; on X-ray examination, the cyst is characterized by rounded contours of the shadow and clearing in the costophrenic sinus.

A distinctive feature of the clinical picture of a subdiaphragmatic abscess is the significant severity of pain and muscle tension in the right hypochondrium, often an enlarged liver, and the appearance of jaundice. The history includes indications of influenza, pneumonia or some purulent disease. An X-ray examination reveals clearing of the costophrenic sinus; a gas bubble is sometimes visible above the fluid level.

The development of sympathetic pleurisy with serous effusion significantly complicates differential diagnosis. In these cases, a diagnostic puncture is of great help. The detection of pus during puncture through the diaphragm and serous fluid with a higher puncture of the pleura confirms the presence of a subdiaphragmatic abscess. The deep location of the encysted abscess with interlobar empyema makes diagnosis extremely difficult. X-ray examination allows us to establish the presence of triangular or fusiform tissue located along the interlobar fissure. However, it should be borne in mind that such a shadow can be caused by a lesion of the middle lobe on the right or the lingular segment on the left.

Apical empyemas are difficult to distinguish from apical lung cancer. With a basal location of the abscess, it is difficult to determine the supra- or subphrenic accumulation of pus. X-ray examination and test puncture are of decisive importance.

Treatment. Since acute purulent pleurisy is most often a secondary disease, its treatment can only be successful with simultaneous treatment of the primary disease.

All methods of treating purulent pleurisy are essentially aimed at reducing intoxication, increasing the immunobiological forces of the body, eliminating hypoxemia and improving the functioning of vital organs.

A). Conservative treatment of pleurisy: antibiotic therapy (parenterally and locally with repeated punctures). The punctures are repeated, the pus is removed and antibiotics are injected into the pleural cavity. wide range actions with preliminary determination of flora sensitivity. The puncture is performed in compliance with all rules of asepsis under local anesthesia. The point of greatest dullness is preliminarily determined. According to the instructions available in the literature and data from our clinic, purulent pleurisy is cured in 75% of patients by repeated punctures.

Much attention should be paid to detoxification and restorative therapy (blood transfusion, plasma, protein substitutes, glucose, administration of vitamins, high-calorie nutrition, etc.). Oxygen therapy, cardiac and sedatives are used according to indications.

b) Surgical treatment. Closed and open surgical methods are used. Both methods have the goal of creating unfavorable conditions for the development of infection by removing pus and creating favorable conditions for tissue regeneration.

1. When closed operative method drainage is inserted into the pleura through the intercostal space, the outer end of the drainage is connected to a device for constant active aspiration of pus (water-jet pump, three-flask suction device, etc.).

Drainage can be inserted into the pleura and through the bed of the resected rib. Wherein soft fabrics it is sutured around the drainage, fixed to the skin, and the outer end is attached to a device for active aspiration.

If there is no apparatus for active aspiration, then a valve made from the finger of a rubber glove is placed on the end of the drainage and lowered into a bottle of antiseptic liquid suspended below the patient.

2. With the open surgical method, the pleura is widely opened through the bed of the resected rib. A wide drainage is inserted into the pleural cavity without connecting it to the suction apparatus. This method is now rarely used.

Closed treatment methods have the advantage that after removal of pus, negative pressure is formed in the pleural cavity. This promotes rapid expansion of the lung, fusion of the visceral and parietal pleura and elimination of purulent inflammation.

At open methods the air entering the pleura prevents the expansion of the lung, fixes the collapsed lung with scars, adhesions, contributes to the development of pneumosclerosis, residual pleural cavity and chronic pleurisy. However, if there are large clots of fibrin, sequestration of lung tissue, etc. in the pleural cavity, open emptying of the cavity has advantages. After a wide thoracotomy, formations are less likely than with closed drainage. encysted pleurisy with multiple cavities.

The choice of method for evacuation of pus should be individual, taking into account the advantages and disadvantages of each of them.

c) Postoperative treatment. In the postoperative period, a constant outflow of pus from the cavity is ensured, infection is fought, measures are taken to increase the body's resistance and to quickly expand the lung.

Ensuring good emptying of the pleural cavity from pus requires constant monitoring of the condition of the drainage and regular x-ray monitoring of the amount of fluid in the pleural cavity. It is necessary to strive for complete evacuation of pus whenever possible. The exudate should be sucked out slowly, since rapid emptying can lead not only to hyperemia ex vasio, but also to a sharp displacement of the mediastinum, which will cause severe disturbances of cardiac and respiratory functions.

Antibiotic therapy is carried out taking into account the sensitivity of the microflora; on the first day after surgery, the doses of antibiotics should be large. They are administered both intramuscularly and locally using a puncture at the upper point of the purulent cavity.

To reduce intoxication and increase immunobiological strength, blood and plasma transfusions are performed, glucose and vitamins are administered, and high-calorie nutrition is provided. Therapeutic breathing exercises are of great importance for early expansion of the lung.

Guide to clinical surgery, 1967

According to statistics, purulent pleurisy is considered one of the most common lung diseases. Men and women are equally at risk. When the disease occurs, the outer lining of the lungs becomes inflamed and purulent exudate forms in its cavity.

Causes

Not considered in medical practice independent disease. Basically, this pathology appears as a result of the presence of diseases of other organs. The causes of the disease are divided into 2 groups:

• infectious;
• non-infectious.

Diseases that can provoke the development of infectious pleurisy include diabetes mellitus, alcoholism, diseases of the gastrointestinal tract and other chronic lung pathologies.

As for non-infectious causes of the disease, this group includes malignant formations outer lining of the lungs, connective tissue disorders such as arthritis or lupus.

The principles of pathology development vary depending on the etiology. Infectious bacteria affect the pleural cavity, entering it in all sorts of ways. Infectious pathogens enter the pleural cavity during pneumonia, abscess, cyst, bronchiectasis or tuberculosis. A direct hit is possible in case of wound or trauma to the thoracic region.

The causes of the development of a purulent form of pathology can be acute pancreatitis, tumor or vasculitis. With such diseases, the permeability of blood and lymphatic vessels increases, and the reactivity of the body decreases.

A slight accumulation of fluid that forms during inflammation can be absorbed into the lining of the lungs and at the same time form a fibrin layer. As a result, a dry form of pleurisy appears. If the fluid is not absorbed by the pleura, then an exudative type of pathology develops.

Forms

According to the degree of effusion and the manifestation of clinical symptoms in medical practice, several forms of the disease are distinguished: dry, exudative and purulent.

The dry form is considered the initial stage of the development of pathology. In medical practice, with the dry type, no infectious pathogens are observed in the pulmonary cavity. This type is characterized by active damage to blood vessels.

At this stage of development of the pathology, vascular permeability increases due to the action of pro-inflammatory components, and leakage of the liquid part of the plasma is observed. As a result, fibrous threads form on the surface of the lung.

When the outflow of exudate is impaired, fibrous threads increase friction between the layers of the pleura and thus cause severe pain.

If treatment is not started in a timely manner, dry pleurisy progresses to the next stage of pathology development. The exudative type is characterized by the spread of inflammation. At this stage, enzyme activity decreases significantly and a pocket is formed, in which pus can subsequently form. At exudative form The disease increases the volume of pleural fluid, which reduces the vital volume of the lung. In advanced stages, respiratory failure may develop. Due to the accumulated fluid in the pleural cavity, friction between the layers of the pleura is reduced and the pain syndrome becomes less intense.

The next stage of development is purulent pleurisy, or pleural empyema. Due to the accumulation of purulent exudate in the serous membrane, this form is considered extremely complex and is life-threatening. Without rendering adequate treatment signs of intoxication of the body can lead to death. Empyema formation usually occurs when serious illnesses other organs or in persons with a weak immune system.

Acute purulent pleurisy in patients is accompanied by fever and severe shortness of breath. The patient's general condition is considered extremely serious.

Symptoms

The main symptom of the disease is shortness of breath. It occurs when the lung tissue is damaged or the functional volume of the organ decreases. The patient may complain of lack of air. At the initial stages of development of the pathology, shortness of breath appears after physical exertion, and in advanced stages it can also occur at rest.

Associated symptoms of shortness of breath are chest pain and cough. Painful sensations arise as a result of irritation of the receptors of the outer lining of the lungs under the influence of inflammatory components. As a rule, the pain is acute. It gets worse when you cough or take a deep breath. Depending on the location of the source of inflammation, pain may be felt on the left or right side chest. Pain in advanced stages of pleurisy can spread to the abdomen or shoulder.

When the nerve roots located in the pleura are irritated, patients experience coughing attacks. Often the cough is dry. Attacks can worsen with a sudden change in body position or during a deep breath. If the cough is accompanied by sputum, this indicates purulent pleurisy.

With a slight inflammatory process, the patient’s body temperature can reach 38°C. As the focus of inflammation increases, the mark rises to 39-40°C. Clinical symptoms include severe headache, lethargy and muscle pain. In rare cases, fever may occur.

One of the symptoms of the pathology is displacement of the trachea, which occurs as a result of excess pressure in the lungs. Displacement of the trachea is typical with extensive pleural effusion. In this case, the fluid puts strong pressure on the organs, which leads to a displacement of the lung in the healthy direction.

Consequences

Without treatment, the consequences of the disease can be life-threatening. Purulent form pleurisy can lead to the formation of a lung abscess. When a purulent pocket breaks through, the infection enters the pleural cavity, which can trigger the development of pneumonia, lung gangrene or cyst formation.

When an abscess ruptures, the patient’s body temperature rises sharply, the pulse quickens and the cough intensifies. Breathing becomes frequent and painful. The consequences of rupture of the abscess lead to an increase in hypoxia.

In advanced stages of pleurisy, the patient's affected part of the chest increases significantly. As the pathology progresses, the patient's general condition worsens significantly. Accumulated pus leads to expansion of the intercostal spaces and respiratory arrest.

As a result of lack of treatment, the consequences of pleurisy can manifest themselves in the form of the formation of adhesions, limited mobility of the lung, or calcification of the pleura. In addition, pleurisy can lead to acute pulmonary heart failure, shock, liver or brain abscess, collapse or septicopyemia.

Treatment

If pleurisy is suspected, the patient is hospitalized, because the degree of danger is very high. The main goal of treatment is to stabilize the patient, normalize the breathing process, and eliminate the root cause that provoked the development of the disease.

Often pleurisy is infectious nature, therefore treatment is carried out with antibacterial and anti-inflammatory drugs.

The group of antibiotics includes Clindamycin, Ampicillin and Ceftriaxone. These agents prevent the proliferation of bacteria and thereby lead to their death. To restore water and electrolyte balance, doctors prescribe saline or glucose solution. Thanks to this, renal filtration is accelerated and toxic breakdown products are eliminated.

To remove water from the body and reduce the absorption of potassium and sodium, the patient is prescribed diuretics. In order to prevent the synthesis of pro-inflammatory components, doctors prescribe glucocorticosteroids. For severe pain, the patient is given non-steroidal anti-inflammatory drugs, for example Meloxicam or Diclofenac.

In the dry form of pleurisy, the patient is prescribed bed rest. Drug treatment involves taking antimicrobial, anti-inflammatory and painkillers. At the initial stage of development of pathology, pleurisy can be treated with folk remedies. Warm compresses, tight bandaging of the chest area and cupping are considered the most effective.

He is being treated in a hospital. Conservative treatment is carried out with antitumor and anti-infective agents. The patient is prescribed therapeutic diet, rich in proteins and vitamins. Salt is completely excluded from the diet, and liquid intake is also minimized.

If excess fluid accumulates in the pleural cavity, doctors perform a puncture. To carry out the procedure, the patient is given local anesthesia. The procedure consists of inserting a special needle into the patient’s pleural cavity on the side of the scapula. Puncture allows you to remove excess fluid, reduce pressure in the lung cavity and normalize breathing.

After removing excess fluid, the patient is prescribed physiotherapeutic procedures and therapeutic exercises.

Purulent pleurisy is treated exclusively in a hospital setting. Treatment of pathology at home can be dangerous to the health and life of the patient. The main task of doctors is to prevent tissue destruction. Punctures are performed daily. The patient is given cavity drainage and the cavity is regularly washed with an antiseptic.

For acute purulent pleurisy, drug treatment is ineffective, so doctors perform surgery. Depending on the degree of damage to the lung, during surgery doctors can remove dense scars of the pleura or the parietal layer of the pleura. In rare cases, part of the ribs may be removed.