Differential diagnosis of exudate and transudate

Pleural effusion is an accumulation of pathological fluid in the pleural cavity due to inflammatory processes in adjacent organs or pleural layers, or due to a disturbance in the relationship between the colloid osmotic pressure of blood plasma and the hydrostatic pressure in the capillaries.

Pleural fluid of inflammatory origin is an exudate. Fluid accumulated due to a violation of the relationship between the colloid-osmotic pressure of the blood plasma and the hydrostatic pressure in the capillaries is a transudate.

After obtaining the pleural fluid, it is necessary to determine whether the effusion is an exudate or a transudate, depending on the color, transparency, relative density, biochemical and cytological composition.

Differential diagnostic differences between pleural effusion and transudate

Signs	Exudate	Transudate
Onset of the disease	Spicy	Gradual
Presence of chest pain at the onset of the disease	Typical	Not typical
Increased body temperature	Typical	Not typical
The presence of general laboratory signs of inflammation (increased ESR, “biochemical inflammation syndrome”*)	Characteristic and very pronounced	Not typical, sometimes general laboratory signs of inflammation may be present, but, as a rule, they are weakly expressed
Appearance of liquid	Cloudy, not quite transparent, intense lemon-yellow color (serous and serous-fibrinous exudate), often hemorrhagic, may be purulent, putrid with an unpleasant odor	Transparent, slightly yellowish, sometimes colorless liquid, odorless
Change in appearance of pleural fluid after standing	It becomes cloudy, more or less abundant fibrin flakes fall out. Serous-purulent exudate is divided into two layers (upper - serous, lower - purulent). The effusion coagulates when standing	Remains transparent, sediment does not form or is very delicate (in the form of a cloud), there is no tendency to curdle
Protein content	> 30 g/l	< 20 g/l
LDG	> 200 U/l or > 1.6 g/l	< 200 U/l or < 1.6 g/l
Pleural fluid protein/plasma protein	> 0.5	< 0.5
Pleural fluid LDH/plasma LDH	> 0.6	< 0.6
Glucose level	< 3.33 mmol/l	> 3.33 mmol/L
Pleural fluid density	> 1.018 kg/l	< 1.015 kg/l
Effusion cholesterol/serum cholesterol	> 0.3	< 0.3
Rivalta test**	Positive	Negative
Pleural fluid white blood cell count	> 1000 in 1 mm 3	< 1000 in 1 mm 3
Red blood cell count in pleural fluid	Variable	< 5000 in 1 mm 3
Cytological examination of pleural fluid sediment	Neutrophilic leukocytosis predominates	A small amount of desquamated mesothelium

Notes:

* biochemical inflammation syndrome - increased levels of seromucoid, fibrin, haptoglobin, sialic acids in the blood - non-specific indicators of the inflammatory process;

** Rivalta test - a test for determining the presence of protein in pleural fluid: water in a glass cylinder is acidified with 2-3 drops of 80% acetic acid, then the pleural fluid being tested is dripped drop by drop into the resulting solution. If it is an exudate, then a cloud in the form of cigarette smoke is drawn after each drop in the water; with transudate, this trace is absent.

After determining the nature of the effusion (exudate or transudate), it is advisable to take into account the most common causes of exudate and transudate, which to a certain extent facilitates further differentiation of pleural effusions.

The nature of the exudate is determined not only by the variety of causes, but also by the ratio of accumulation and resorption of the effusion, the duration of its existence:

• moderate effusion and its good resorption - fibrinous pleurisy;
• exudation exceeds the absorption of exudate - serous or serous-fibrinous pleurisy;
• infection of exudate with purulent microflora - purulent pleurisy (pleural empyema);
• the rate of resorption exceeds the rate of exudation - formation of adhesions during resorption;
• carcinomatosis, pleural mesothelioma, pulmonary infarction and trauma, pancreatitis, hemorrhagic diathesis, overdose of anticoagulants - hemorrhagic effusion;
• predominance of allergic processes - eosinophilic exudate;
• trauma to the thoracic duct due to tumor or tuberculous lesions - chylous exudate;
• chronic long-term course of exudative pleurisy, in particular, in tuberculosis - cholesterol effusion.

Causes of pleural effusion (S. L. Malanichev, G. M. Shilkin, 1998, as amended)

Type of effusion	Main reasons	Less common causes
Transudate	Congestive heart failure	Nephrotic syndrome (glomerulonephritis, renal amyloidosis, etc.); liver cirrhosis; myxedema, peritoneal dialysis
Inflammatory infectious exudates	Parapneumonic effusion; tuberculosis; bacterial infections	Subphrenic abscess; Intrahepatic abscess; Viral infection; Fungal infections
Inflammatory non-infectious exudates	Pulmonary embolism	Systemic connective tissue diseases; pancreatitis (enzymatic pleurisy); drug reactions; asbestosis; post-infarction Dressler syndrome; yellow nail syndrome*; uremia
Tumor exudates	Cancer metastases; leukemia	Mesothelioma; Meigs syndrome"
Hemothorax	Trauma; cancer metastasis; pleural carcinomatosis	Spontaneous (due to hemostasis disorders); rupture of a vessel in pleural adhesions with spontaneous pneumothorax; rupture of an aortic aneurysm into the pleural cavity
Chylothorax	Lymphoma; thoracic duct injury; carcinoma	Lymphangioleiomyomatosis

Notes:

* "Yellow nails" syndrome is a congenital hypoplasia of the lymphatic system: characterized by thickened and curved yellow nails, primary lymphatic edema, and, less commonly, exudative pleurisy and bronchiectasis.

** Meigs syndrome - pleurisy and ascites in ovarian carcinoma.

Tuberculous pleurisy

Tuberculosis is a common cause of exudative pleurisy. Most often, tuberculous pleurisy develops against the background of some clinical form of pulmonary tuberculosis (disseminated, focal, infiltrative), bronchoadenitis or primary tuberculosis complex. In rare cases, tuberculous exudative pleurisy may be the only and primary form of pulmonary tuberculosis. According to A. G. Khomenko (1996), there are three main types of tuberculous pleurisy: allergic, perifocal and pleural tuberculosis.

Allergic pleurisy

It is hyperergic. It is characterized by the following clinical features:

• acute onset with chest pain, high body temperature, rapid accumulation of exudate, severe shortness of breath;
• rapid positive dynamics (exudate is absorbed within a month, rarely longer);
• increased sensitivity to tuberculin, which causes a positive tuberculin test;
• eosinophilia in the peripheral blood and a significant increase in ESR;
• the exudate is predominantly serous (in the early stages it can be serous-hemorrhagic), contains a large number of lymphocytes, sometimes eosinophils;
• often combined with other manifestations caused by hyperergic reactivity - polyarthritis, erythema nodosum;
• absence of Mycobacterium tuberculosis in pleural effusion.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ], [ 6 ], [ 7 ], [ 8 ], [ 9 ]

Perifocal pleurisy

An inflammatory process in the pleural sheets in the presence of pulmonary tuberculosis - focal, infiltrative, cavernous. Perifocal pleurisy occurs especially easily with a subpleural location of the pulmonary tuberculosis focus. The features of perifocal pleurisy are:

• long-term, often recurring course of exudative pleurisy;
• formation of a large number of pleural adhesions during the resorption phase;
• serous nature of the exudate with a large number of lymphocytes and a high content of lysozyme;
• absence of mycobacteria in exudate;
• the presence of one of the forms of tuberculous pulmonary lesions (focal, infiltrative, cavernous), which is diagnosed using an X-ray examination method after a preliminary pleural puncture and evacuation of exudate;
• strongly positive tuberculin tests.

Tuberculosis of the pleura

Direct pleural involvement by the tuberculous process may be the only manifestation of tuberculosis or be combined with other forms of pulmonary tuberculosis. Pleural tuberculosis is characterized by the appearance of multiple small foci on the pleural sheets, but large foci with caseous necrosis are possible. In addition, an exudative inflammatory reaction of the pleura develops with the accumulation of effusion in the pleural cavity.

Clinical features of pleural tuberculosis:

• long-term course of the disease with persistent accumulation of effusion;
• the exudate may be serous with a large number of lymphocytes and lysozyme (with the development of pleurisy due to seeding of the pleura and the formation of multiple foci) or neutrophils (with caseous necrosis of individual large foci). With widespread caseous pleural lesions, the exudate becomes serous-purulent or purulent (with very extensive lesions) with a large number of neutrophils;
• Mycobacterium tuberculosis is detected in pleural effusion, both by microscopy and by sowing the exudate.

With widespread caseous necrosis of the pleura, disintegration of large tuberculous foci on the pleura and blockade of the mechanisms of exudate resorption, purulent tuberculous pleurisy (tuberculous empyema) may develop. In this case, a very pronounced intoxication syndrome dominates in the clinical picture: body temperature rises to 39 C and above; severe sweating appears (especially characteristic are profuse sweats at night); patients lose weight. Shortness of breath, significant weakness, pain in the side, pronounced leukocytosis in the peripheral blood, increased ESR, often lymphopenia are characteristic. Pleural puncture reveals purulent exudate.

Tuberculous empyema of the pleura may be complicated by the formation of a bronchopleural or thoracic fistula.

When diagnosing tuberculous pleurisy, the following are of great importance: anamnesis data (the presence of pulmonary tuberculosis or other localization in the patient or close relatives), detection of Mycobacterium tuberculosis in the exudate, detection of extrapleural forms of tuberculosis, specific results of pleural biopsy and thoracoscopy data. Characteristic signs of pleural tuberculosis in thoracoscopy are millet-like tubercles on the parietal pleura, extensive areas of caseosis, and a pronounced tendency to form pleural adhesions.

Parapneumonic exudative pleurisy

Bacterial pneumonias are complicated by exudative pleurisy in 40% of patients, viral and mycoplasmal - in 20% of cases. Streptococcal and staphylococcal pneumonias are especially often complicated by the development of exudative pleurisy.

The main characteristic features of parapneumonic exudative pleurisy are:

• acute onset with severe chest pain (before the appearance of effusion), high body temperature;
• predominance of right-sided effusions;
• significantly higher frequency of bilateral effusions compared to tuberculous exudative pleurisy;
• development of exudative pleurisy against the background of diagnosed pneumonia and a radiologically determined pneumonic focus in the lung parenchyma;
• high frequency of purulent exudates with a large number of neutrophils, however, with early and adequate antibacterial therapy, the exudate may be predominantly lymphocytic. In some patients, hemorrhagic exudate is possible, in isolated cases - eosinophilic or cholesterol effusion;
• significant leukocytosis in the peripheral blood and an increase in ESR of more than 50 mm h (more often than with other etiologies of pleurisy);
• rapid onset of a positive effect under the influence of adequate antibacterial therapy;
• detection of the pathogen in the effusion (by sowing the exudate on certain nutrient media), the mycoplasma nature of exudative pleurisy is confirmed by an increase in the titers of antibodies to mycoplasma antigens in the blood.

Exudative pleurisy of fungal etiology

Fungal pleural effusions account for about 1% of all effusions. Fungal exudative pleurisy develops primarily in individuals with significant immune system impairment, as well as those receiving treatment with immunosuppressants, glucocorticoids, and in patients suffering from diabetes mellitus.

Exudative pleurisy is caused by the following types of fungi: aspergilli, blastomycetes, coccidioides, cryptococci, histoplasma, actinomycetes.

Fungal exudative pleurisy is similar to tuberculosis in its course. Usually, pleural effusion is combined with fungal infection of the lung parenchyma in the form of focal pneumonia, infiltrative changes; abscesses and even decay cavities.

Pleural effusion in fungal exudative pleurisy is usually serous (sero-fibrinous) with a marked predominance of lymphocytes and eosinophils. When a subcapsular abscess breaks through into the pleural cavity, the effusion becomes purulent.

The diagnosis of fungal exudative pleurisy is verified by repeated detection of fungal micelles in pleural fluid, in sputum, and also by repeated isolation of fungal culture during sowing of exudate, pleural biopsy, sputum, and pus from fistulas. According to the data of K. S. Tyukhtin and S. D. Poletaev, fungal culture is isolated from exudate in 100% of patients with blastomycosis, in 40-50% with cryptococcosis, in 20% of patients with coccidioidomycosis, and in almost all cases during sowing of pleural biopsy.

In addition, serological methods of studying blood serum and exudate are of great importance in the diagnosis of fungal exudative pleurisy - high titers of antibodies in the reaction of complement fixation, agglutination-precipitation with antigens of certain fungi. Antibodies can also be detected using immunofluorescence and radioimmunological methods. Positive skin tests with the introduction of allergens of the corresponding fungus can have a certain diagnostic value.

[ 10 ], [ 11 ]

Aspergillosis pleurisy

Aspergillosis exudative pleurisy most often develops in patients with therapeutic artificial pneumothorax (especially in the case of bronchopleural fistula formation) and in patients who have undergone lung resection. Pleural fluid may contain brown lumps in which aspergilli are found. The presence of calcium oxalate crystals in the effusion is also characteristic

The diagnosis is confirmed by identifying aspergilli in the culture of pleural fluid when seeded on special media, and by detecting antiaspergilli in pleural effusion using the radioimmunological method.

[ 12 ], [ 13 ]

Blastomycosis pleurisy

Blastomycotic exudative pleurisy resembles tuberculous pleurisy in its clinical picture. Infiltrative changes are often observed in the lung parenchyma. Lymphocytes predominate in the exudate. Microscopic analysis can detect typical yeast fungi Blastomyces dermatitidis, pleural fluid culture for blastomycosis is always positive. Non-caseous granulomas are detected in pleural biopsies.

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Coccidioidomycosis pleurisy

Exudative pleurisy in coccidioidomycosis in 50% of cases is accompanied by infiltrative changes in the lungs, nodular or multiform erythema, eosinophilia in the peripheral blood. Pleural effusion is an exudate, it contains many small lymphocytes and a high glucose level is determined, eosinophilia of the effusion is not characteristic.

Pleural biopsy reveals caseous and non-caseous granulomas. Pleural biopsy culture for coccidiosis is positive in 100% of cases, while effusion culture is positive in only 20% of cases. All patients have a positive skin test for Coccidioides immitis. Six weeks after the onset of the disease, antibodies are detected in a titer of 1:32 using the complement fixation reaction.

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Cryptococcotic pleurisy

Cryptococcus neotormans is ubiquitous and inhabits soil, especially if it is contaminated with pig excrement. Exudative pleurisy of cryptococcal genesis most often develops in patients suffering from hemoblastoses, and is usually unilateral. In most patients, along with pleural effusion, there is lung parenchyma damage in the form of interstitial infiltration or nodular formation. Pleural effusion is an exudate and contains many small lymphocytes. High levels of cryptococcal antigens are found in pleural fluid and blood serum. Cryptococcosis genesis of pleurisy is confirmed by a positive result of pleural fluid culture and pleural or lung biopsy for cryptococci.

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Histoplasmosis pleurisy

Histoplasma capsulatum is widespread in the soil and rarely causes pleural effusion. Typically, exudative pleurisy caused by histoplasma has a subacute course, with changes in the lungs in the form of infiltrates or subpleural nodules.

Pleural effusion is an exudate and contains many lymphocytes. A non-caseating granuloma is detected during pleural biopsy. The diagnosis is verified by obtaining a Histoplasma culture during pleural fluid, sputum, pleural biopsy, and by bacterioscopy of biopsy material. There may be high titers of antibodies to Histoplasma in the blood of patients, which is determined by immunoelectrophoresis.

Actinomycotic pleurisy

Actinomycetes are anaerobic or microaerophilic gram-positive bacteria that normally inhabit the oral cavity. Infection with actinomycetes usually occurs from infected gums, carious teeth, and tonsils of the patient himself. Actinomycosis is characterized by the formation of abscesses, the transition of the inflammatory process to the chest wall with the formation of pleurothoracic fistulas. The formation of peripheral skin, subcutaneous, and muscle abscesses is possible.

A characteristic feature of pleural exudate in actinomycosis is the presence of sulfur granules with a diameter of 1-2 mm - these are lumps of thin bacterial threads. The diagnosis of actinomycotic exudative pleurisy is established by identifying Actinomyces Israeli when sowing pleural fluid on special media. It is also possible to stain smears of exudate according to Gram and detect thin gram-positive threads with long branches, which is characteristic of actinomycosis.

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Pleurisy of parasitic etiology

Most often, exudative pleurisy is observed in amebiasis, echinococcosis, and paragonimiasis.

Amebic pleurisy

The causative agent of amebiasis is Entamoeba histolytica. Amebic exudative pleurisy usually occurs when an amoebic liver abscess breaks through the diaphragm into the pleural cavity. This is accompanied by sharp pain in the right hypochondrium and right half of the chest, shortness of breath, and a significant increase in body temperature, which is accompanied by chills. The patient develops purulent pleurisy. Pleural effusion is an exudate, has a characteristic appearance of "chocolate syrup" or "herring butter" and contains a large number of neutrophilic leukocytes, hepatocytes, and small solid insoluble particles of liver parenchyma. In 10% of patients, amoebas are found in the exudate. Using immunoradiological methods, high titers of antibodies to amoebas can be detected. Ultrasound and computed tomography of the liver can diagnose liver abscess.

[ 23 ], [ 24 ]

Echinococcal pleurisy

Echinococcal exudative pleurisy develops when an echinococcal cyst of the liver, lung or spleen breaks through into the pleural cavity. Very rarely, a cyst develops primarily in the pleural cavity itself. At the moment of breakthrough, a very sharp pain appears in the corresponding half of the chest, severe shortness of breath, and anaphylactic shock may develop in response to the entry of echinococcal antigens. When a suppurating echinococcal cyst breaks through into the pleural cavity, pleural empyema is formed.

Pleural effusion is an exudate and contains a large number of eosinophils (neutrophils in case of secondary infection of the fluid), as well as scolexes with hooks of echinococci, membranes of the echinococcal cyst. In the pleural biopsy, scolexes with hooks of the parasite are also detected.

The skin test with echinococcal antigen (Katsoni test) is positive in 75% of cases. Antibodies to echinococcal antigen are also detected in the blood using the complement fixation reaction (Weinberg test).

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Paragonimiasis pleurisy

Paragonimiasis develops when infected with the lung fluke Paragonimus westermani or miyazflkii. A person becomes infected when eating raw or undercooked crabs or crayfish containing parasite larvae. The larvae enter the human intestine, then penetrate the intestinal wall into the abdominal cavity, then migrate to the diaphragm, through it penetrate into the pleural cavity and then through the visceral pleura into the lungs. In the lungs, the larvae turn into adult lung flukes, which parasitize the lungs for many years and produce about 10,000 eggs daily.

The development of exudative pleurisy is extremely characteristic of paragonimiasis. At the same time, many patients show focal and infiltrative changes in the lungs. The characteristic features of paragonimiasis exudative pleurisy are:

• long-term course with the formation of pronounced pleural adhesions;
• low glucose content in pleural exudate and high levels of lactate dehydrogenase and IgE, with IgE content even higher than in the blood;
• marked eosinophilia of pleural fluid;
• detection of shell-coated eggs of the lung fluke in pleural fluid, sputum, and feces;
• positive skin test with lung fluke antigen;
• high titers of antibodies in the blood.

Endemic foci of infection are located in the Far East.

Pleurisy of tumor etiology

Among all pleural effusions, tumor effusions account for 15-20%. According to Light (1983), 75% of malignant pleural effusions are caused by lung cancer, breast cancer, and lymphoma. Lung cancer is the most common tumor causing pleural effusion. According to N. S. Tyukhtin and S. D. Poletaev (1989), lung cancer (usually central) is diagnosed in 72% of patients with tumor pleurisy.

The second most common cause of malignant exudative pleurisy is metastatic breast cancer, the third is malignant lymphoma, lymphogranulomatosis. In other cases, we are talking about pleural mesothelioma, ovarian and uterine cancer, cancer of various parts of the gastrointestinal tract and tumors of other localizations.

The main mechanisms of formation of pleural effusion in malignant tumors are (Light, 1983):

• tumor metastases to the pleura and a significant increase in the permeability of its vessels;
• obstruction of lymphatic vessels by metastases and a sharp decrease in fluid resorption from the pleural cavity;
• damage to the mediastinal lymph nodes and decreased lymph drainage from the pleura;
• obstruction of the thoracic lymphatic duct (development of chylothorax);
• development of hypoproteinemia due to cancer intoxication and disruption of the protein-forming function of the liver.

Pleural effusion of tumor origin has quite characteristic features:

• gradual development of effusion and other clinical symptoms (weakness, anorexia, weight loss, shortness of breath, cough with sputum, often with blood);
• detection of a sufficiently large amount of fluid in the pleural cavity and its rapid accumulation after thoracentesis;
• detection using computed tomography or radiography (after preliminary removal of exudate from the pleural cavity) of signs of bronchogenic cancer, enlarged mediastinal lymph nodes, and metastatic lung lesions;
• hemorrhagic nature of the effusion; in malignant lymphoma - chylothorax is often observed;
• compliance of pleural effusion with all the criteria of exudate and very often low glucose content (the lower the glucose level in the exudate, the worse the prognosis for the patient);
• detection of malignant cells in pleural effusion; it is advisable to analyze several samples of pleural fluid to obtain more reliable results;
• detection of carcinoembryonic antigen in pleural fluid.

In the absence of malignant cells in the pleural exudate and suspicion of a tumor process, thoracoscopy with pleural biopsy and subsequent histological examination should be performed.

Pleurisy in malignant mesothelioma

Malignant mesothelioma develops from the mesothelial cells lining the pleural cavity. People who have worked with asbestos for a long time are particularly susceptible to developing this tumor. The period between the development of the tumor and the time of contact with asbestos is from 20 to 40 years.

The age of patients ranges from 40 to 70 years. The main clinical symptoms of malignant mesothelioma are:

• gradually increasing pain of a constant nature in the chest without a clear connection with breathing movements;
• paroxysmal dry cough, constantly increasing shortness of breath, weight loss;
• Pleural effusion is the most common and early-appearing sign of malignant mesothelioma;
• superior vena cava compression syndrome by a growing tumor (swelling of the neck and face, dilation of the veins in the neck and upper chest, shortness of breath); tumor growth into the pericardium and the walls of the heart cavities leads to the development of exudative pericarditis, heart failure, and cardiac arrhythmias;
• characteristic data in computed tomography of the lungs - thickening of the pleura with an uneven nodular internal border, especially at the base of the lung, in some cases tumor nodules are detected in the lungs;
• Features of pleural fluid: yellowish or serous-bloody color; has all the signs of exudate; decreased glucose content and pH value; high content of hyaluronic acid and associated high viscosity of the fluid; large number of lymphocytes and mesothelial cells in the exudate sediment; detection of malignant cells in multiple studies of exudate in 20-30% of patients.

For final verification of the diagnosis, multiple biopsies of the parietal pleura, thoracoscopy with biopsy, and even diagnostic thoracotomy should be performed.

Pleurisy in Meigs syndrome

Meigs syndrome is ascites and pleural effusion in malignant tumors of the pelvic organs (ovarian cancer, uterine cancer). In tumors of this localization, significant ascites develops due to peritoneal carcinomatosis and ascitic fluid leaks through the diaphragm into the pleural cavity. Most often, pleural effusion is observed on the right, but bilateral localization is also possible. Pleural effusion can also be caused by tumor metastases to the pleura.

Pleural effusion in Meigs syndrome is an exudate, and malignant cells can be found in it.

Pleurisy in systemic diseases of connective tissue

Most often, exudative pleurisy develops in systemic lupus erythematosus. Pleural damage in this disease is observed in 40-50% of patients. Exudative pleurisy is usually bilateral, the exudate is serous, contains a large number of lymphocytes, lupus cells, antinuclear antibodies are found in it. A characteristic feature of exudative pleurisy in systemic lupus erythematosus is the high efficiency of glucocorticoid therapy. Pleural biopsy reveals chronic inflammation and fibrosis.

In rheumatism, exudative pleurisy is observed in 2-3% of patients, the effusion is a serous exudate, contains many lymphocytes. Usually, pleurisy develops against the background of other clinical manifestations of rheumatism, primarily rheumatic carditis, and responds well to treatment with non-steroidal anti-inflammatory drugs. Puncture biopsy reveals a picture of chronic inflammation of the pleura and its fibrosis.

Exudative pleurisy in rheumatoid arthritis is characterized by a chronic relapsing course, the exudate is serous lymphocytic, contains rheumatoid factor in high titers (< 1:320), low glucose levels, a high level of LDH is noted, and cholesterol crystals are detected.

Exudative pleurisy can also develop with other systemic diseases of connective tissue - scleroderma, dermatomyositis. To establish an etiological diagnosis of exudative pleurisy, diagnostic criteria of these diseases are used and other causes of pleural effusion are excluded.

Pleurisy in acute pancreatitis

Pleural effusion in acute pancreatitis or severe exacerbation of chronic pancreatitis is observed in 20-30% of cases. The pathogenesis of this effusion is the penetration of pancreatic enzymes into the pleural cavity through the lymphatic vessels through the diaphragm.

Pleural effusion corresponds to the signs of exudate, serous or serous-hemorrhagic, rich in neutrophils and contains a large amount of amylase (more than in the blood serum). Pancreatogenic effusion is more often localized on the left and has a tendency to chronic course.

Pleurisy with uremia

Exudative uremic pleurisy is usually combined with fibrinous or exudative pericarditis. The exudate is serous-fibrinous, can be hemorrhagic, contains few cells, usually monocytes. The creatinine level in the pleural fluid is elevated, but it is lower than in the blood.

Drug-induced pleurisy

Pleural effusion may occur with treatment with hydralazine, novocainamide, isoniazid, chlorpromazine, phenytoin, and sometimes with bromocriptine. Long-term treatment with these drugs leads to effusion. Drug-induced lung injury is also common.

Empyema of the pleura

Empyema of the pleura (purulent pleurisy) is an accumulation of pus in the pleural cavity. Empyema of the pleura can complicate the course of pneumonia (especially streptococcal), spontaneous pneumothorax penetrating chest wounds, pulmonary tuberculosis, and can also develop due to the transition of the purulent process from neighboring organs (in particular, with a rupture of a lung abscess)

Pleural empyema is characterized by the following clinical and laboratory features:

• intense chest pain and shortness of breath appear;
• body temperature rises to 39-40°C, severe chills and profuse sweating appear;
• swelling of the chest tissue on the affected side occurs;
• pronounced symptoms of intoxication are noted: severe pain, general weakness, anorexia, myalgia, arthralgia;
• peripheral blood analysis is characterized by significant leukocytosis, a shift in the leukocyte formula to the left, a sharp increase in ESR, and toxic granularity of neutrophils;
• characterized by a tendency to encapsulation;
• the exudate is purulent, the cellular composition is characterized by a large number of neutrophilic leukocytes (more than 85% of all cells, absolute neutrophil count> 100,000 in 1 mm), low glucose levels (less than 1.6 mmol/l), absence of fibrinogen (a clot is not formed), high levels of total LDH (more than 5.5 mmol/l/h), low LDH1 (less than 20%) and high levels of LDH5 (more than 30%); pH<7.2;
• From the exudate it is possible to isolate a culture of streptococcus, pathogenic staphylococcus and other pathogens, especially anaerobic bacteria.

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Pleural effusions in pulmonary embolism

Pleural effusions are observed in pulmonary embolism in 30-50% of cases. Their appearance is caused mainly by increased permeability of the visceral pleura in the projection of the pulmonary infarction. In 20% of cases, pleural effusion in pulmonary embolism is a transudate; in other cases, these are exudates, sometimes hemorrhagic.

Chylothorax

Chylothorax is a chylous pleural effusion, i.e. accumulation of lymph in the pleural cavity. The main causes of chylothorax are damage to the thoracic lymphatic duct (during operations on the esophagus, aorta and trauma), as well as blockage of the lymphatic system and mediastinal veins by a tumor (most often lymphosarcoma). The development of chylothorax is also extremely characteristic of lymphangioleiomyomatosis.

Often, the cause of chylothorax cannot be determined. Such chylothorax is called idiopathic. According to Light (1983), idiopathic chylothorax in adults is most often a consequence of minor trauma to the thoracic lymphatic duct (during coughing, hiccups), which occurs after eating fatty foods. In rare cases, chylothorax develops with liver cirrhosis, heart failure.

The clinical manifestations of chylothorax are completely consistent with the symptoms of pleural effusion: patients complain of progressive dyspnea and heaviness in the corresponding half of the chest. Acute onset of the disease is characteristic. Unlike pleural effusions of other origins, chylothorax is usually not accompanied by chest pain and fever, since the lymph does not irritate the pleura.

During an objective examination of the patient, signs of pleural effusion are detected, which is confirmed by X-ray examination.

The diagnosis of chylothorax is verified by pleural puncture. The following properties of pleural fluid are characteristic of chylothorax:

• the color is milky white, the liquid is not transparent, cloudy, has no smell;
• contains a large amount of neutral fat (triglycerides) and fatty acids, as well as chylomicrons. It is generally accepted that chylothorax is characterized by a triglyceride content of more than 100 mg%. If the triglyceride level is less than 50 mg%, the patient does not have chylothorax. If the triglyceride content is between 50 and 110 mg%, it is necessary to determine the lipoproteins in the pleural fluid using the disk electrophoresis method in polyacrylamide gel. If chylomicrons are found in the pleural fluid, then this is chylothorax.

Chylothorax is also characterized by the detection of a large number of drops of neutral fat (triglycerides) during microscopy of smears of chylous fluid after staining with Sudan.

With prolonged existence of chylothorax, especially with accumulation of large amount of lymph in the pleural cavity, it is necessary to perform frequent pleural punctures due to compression of the lung and displacement of the mediastinum. This leads to loss of large amount of lymph and exhaustion of the patient. This is due to the fact that about 2500-2700 ml of fluid containing large amount of protein, fats, electrolytes and lymphocytes enters daily through the thoracic lymphatic duct. Naturally, frequent removal of lymph from the pleural cavity leads to weight loss of the patient and disruption of the immunological status.

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Pseudochylous pleural effusion

Pseudochylous pleural effusion (pseudochylothorax) is the accumulation of turbid or milky fluid containing large amounts of cholesterol in the pleural cavity, without damage to the thoracic duct.

As a rule, patients with pseudochylothorax have thickening and often calcification of the pleura as a result of the long presence of effusion in the pleural cavity. The duration of pleural effusion can vary from 3 to 5 years, sometimes even longer. It is assumed that cholesterol is formed in the pleural fluid as a result of degenerative changes in erythrocytes and leukocytes. Pathological changes in the pleura itself disrupt the transport of cholesterol, which leads to its accumulation in the pleural fluid.

It is generally accepted that chyle-like pleural effusion is observed in patients with long-standing pleural effusion. This is most often observed in tuberculosis and rheumatoid arthritis.

The clinical picture of pseudochylothorax is characterized by the presence of the above-described physical and radiographic symptoms of pleural effusion. The final diagnosis is established by pleural puncture and analysis of the obtained pleural fluid. It is necessary to conduct differential diagnostics between chylous and pseudochylous effusion.

Example of diagnosis formulation

Right-sided lower lobe pneumonia, severe form. Right-sided pneumococcal serous-fibrinous pleurisy, acute course. Respiratory failure stage II.

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