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Pleural effusion

 
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Last reviewed: 12.07.2025
 
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Pleural effusion is an accumulation of fluid in the pleural space. Effusions can have a variety of causes, so they are usually classified as transudates or exudates. They are identified by physical examination and chest radiography; thoracentesis followed by examination of the pleural fluid can often identify the cause of the effusion. Asymptomatic transudates do not require treatment. In contrast, symptomatic transudates and almost all exudates require thoracentesis, drainage, pleurodesis, and/or pleurectomy.

Normally, 10 to 20 ml of pleural fluid, similar in composition to blood plasma but with a lower protein content (< 1.5 g/dl), are thinly distributed between the visceral and parietal pleura. This is necessary to facilitate movements between the lung and the chest wall. The fluid enters the pleural cavity from the blood capillaries of the parietal pleura and is removed into the pleural lymphatic vessels. Accumulation of pleural fluid occurs when it enters the pleural cavity significantly or is removed from there too slowly.

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Epidemiology

According to several studies, pleural effusion is diagnosed in more than 20% of patients in the intensive care unit. Pleural effusion is rarely an independent reason for hospitalization of patients in the intensive care unit (except for cases of massive pleural effusion with severe dyspnea); this condition develops as a complication of various diseases. Thus, pleural effusion is recorded in 40-60% of cases with pneumonia, in 40% with pulmonary embolism, and in 50% with congestive heart failure. Pleural effusion is also found in 7-27% of HIV-infected patients hospitalized in hospital.

Pleural effusion may result from several mechanisms, including increased pleural permeability, increased pulmonary capillary pressure, decreased negative intrapleural pressure, decreased plasma oncotic pressure, and obstruction of lymphatic drainage pathways.

Normally, the pleural cavity contains no more than 30 ml of fluid, and the total fluid production is about 0.3 ml/kg per day. The appearance of pleural effusion indicates the presence of serious extrapulmonary pathology or lung pathology. Under normal conditions, the drainage system of the pleural cavities can cope with a more than 20-fold increase (approximately 700 ml) influx of fluid into the pleural cavity. Since differential diagnostics includes a wide range of diseases, the physician must ensure a systematic approach to examining such a patient to establish the correct diagnosis in the shortest possible time, performing a minimum number of invasive studies.

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What causes pleural effusion?

Pleural effusions have many causes and are usually classified as transudates or exudates based on their laboratory findings. A transudate can usually be treated without further investigation, whereas the cause of an exudate requires clarification. Bilateral effusions usually have similar characteristics.

Causes of pleural effusion

Reasons Comments
Heart failure Bilateral (81%), right-sided (12%), left-sided (7%). Left ventricular failure increases interstitial pressure, leading to fluid transudation and pleural effusion.
Liver cirrhosis with ascites (hepatic hydrothorax) Right-sided (70%); left-sided (15%); bilateral (15%). Ascitic fluid migrates into the pleural cavity through diaphragmatic defects; occurs in approximately 5% of patients with clinically evident ascites
Nephrosis Uncommon. Bilateral in >90% of cases; decreased intravascular oncotic pressure causes transudation into the pleural cavity; associated with edema or anasarca in other areas
Hydronephrosis Usually bilateral, often subpulmonary; decreased intravascular oncotic pressure combined with hypervolemia leads to transudation into the pleural cavity
Superior vena cava syndrome Urine spreads retroperitoneally into the pleural cavity, resulting in urinothorax.
Constrictive pericarditis Malignant neoplasms or thrombosed central catheters block the intrathoracic lymphatic duct
Atelectasis Increased hydrostatic pressure in veins; in some cases accompanied by massive anasarca; mechanism similar to hepatic hydrothorax
Peritoneal dialysis Increases negative intrapleural pressure Mechanism similar to hepatic hydrothorax; pleural fluid has characteristics similar to dialysate
Armored lung The formation of a fibrous capsule leads to an even greater decrease in intrapleural pressure
Systemic capillary leak syndrome Rarely occurs in combination with anasarca and pericardial effusion
Myxedema Occurs in approximately 5%; transudate if pericardial effusion is also present; however, isolated pleural effusion may have both exudate and transudate
Pneumonia (parapneumonic exudate) May be uncomplicated, fragmented and/or purulent (empyema); pleural puncture is necessary for differential diagnosis
Malignant neoplasms Most commonly lung cancer, pleural mesothelioma and breast cancer, but effusion may occur with any tumor that metastasizes to the pleura; chest pain, usually dull and constant
Pulmonary embolism Occurs in approximately 30% of cases; almost always - exudate; hemorrhagic - less than 50%; suspicion of thromboembolism occurs when dyspnea is disproportionate to the volume of effusion
Viral infection Effusion, usually small, with or without parenchymal infiltrate; systemic symptoms predominate rather than pulmonary manifestations
Coronary artery bypass grafting Left-sided or more on the left (73%); bilateral, equal in volume (20%); right-sided or more on the right (7%). In 10% of cases, more than 25% of the chest volume is filled within 30 days after surgery; hemorrhagic effusions are associated with postoperative bleeding and resolve; nonhemorrhagic effusions recur, their cause often remains unknown
Tuberculosis Effusion, usually unilateral or from the side of the parenchymatous infiltrate; caused by a hypersensitivity reaction to the protein of Mycobacterium tuberculosis; the pathogen is isolated by cultivation in less than 20% of cases.
Sarcoidosis Effusion occurs in 1-2% of cases; patients have extensive parenchymal involvement and often extrathoracic involvement; lymphocytes predominate in pleural fluid
Uremia Effusion occurs in approximately 3% of cases; more than 50% of patients have clinical manifestations, usually fever (50%), chest pain (30%), cough (35%), and dyspnea (20%); diagnosis is made by exclusion of other possible causes
Subphrenic abscess Causes sympathetic subpulmonary effusion; pleural fluid is dominated by neutrophils, but pH and glucose concentration are normal
HIV infection There are several possible causes: parapneumonic, tuberculous, Kaposi's sarcoma of the lung, pneumonia caused by Pneumocystis jiroveci (previously called P. carinii) and other opportunistic infections
Rheumatological diseases Typical patient is an elderly person with rheumatoid nodules and deforming arthritis; must be differentiated from parapneumonic effusion
Systemic lupus erythematosus May be the first manifestation of SLE; often seen in drug-induced SLE; diagnosis is based on serologic testing of blood but not pleural fluid
Side effect of drug therapy Many drugs can cause pleural effusion, most commonly bromocriptine, dantrolene, nitrofurantoin, interleukin-2 (used to treat renal cell carcinoma and melanoma), and methysergide. Also seen in drug-induced lupus
Ovarian hyperstimulation syndrome Complicates ovulation induction with human chorionic gonadotropin (hCG) and, sometimes, clomiphene; effusion develops 7-14 days after hCG administration; right-sided effusion is observed in 52% of cases, and bilateral effusion is observed in 27% of cases
Pancreatitis Acute: occurs in approximately 50% of cases; bilateral (77%); left-sided (16%); right-sided (8%). It is the result of transdiaphragmatic spread of inflammatory exudate and inflammation of the diaphragm. Chronic: caused by penetration of the contents of the pancreatic pseudocyst through the diaphragm into the pleural cavity; clinical manifestations from the chest, not the abdominal cavity, predominate, patients visually give the impression of cancer patients
Esophageal rupture The patient is in an extremely serious condition; emergency condition; development of complications and mortality are caused by infection of the mediastinum and pleural cavity
Simple asbestosis Occurs more than 30 years after initial exposure; often asymptomatic, tends to increase and disappear; mesothelioma must be excluded
Ovarian tumors (Meig's disease) The mechanism is similar to hepatic hydrothorax; not all patients with ovarian tumors with ascites and pleural effusion are inoperable
Yellow nail syndrome Triad of pleural effusion, lymphedema, and yellow nails; individual elements of the syndrome may appear separately over several decades; pleural fluid has a relatively high protein content but low LDH concentration; effusion tends to recur, no pleuritic chest pain

Transudate is formed by a combination of increased hydrostatic pressure and decreased oncotic pressure in the pulmonary or systemic circulation. The most common cause of this condition is heart failure, less often it is caused by liver cirrhosis with ascites and hypoalbuminemia, usually resulting from nephrotic syndrome.

Exudate is caused by local processes that increase capillary permeability, resulting in the leakage of fluid, protein, cells, and other components of blood plasma through their walls. Causes are numerous, the most common being pneumonia, malignant neoplasms, pulmonary embolism, viral infections, and tuberculosis. Yellow nail syndrome is a rare disorder that causes chronic exudative pleural effusions, lymphedema, and dystrophic changes in the nails, where they become yellow; all manifestations are considered to be the result of impaired drainage function of the lymphatic vessels.

Chylous effusion (chylothorax) is a milky-white effusion with a high content of triglycerides caused by traumatic or tumor (most often, lymphomatosis) damage to the thoracic duct.

Lymphoid (cholesterol or pseudochylous) effusion resembles chylous effusion but has low triglyceride and high cholesterol content. Lymphoid effusions probably develop due to cholesterol release from lysed red blood cells and neutrophils in long-standing effusions when effusion absorption is impaired due to pleural thickening.

Hemothorax is the presence of hemorrhagic fluid (the hematocrit of the pleural fluid is more than 50% of that of the peripheral blood) in the pleural cavity, resulting from trauma or, rarely, from coagulopathy or rupture of large blood vessels (eg, the aorta or pulmonary artery).

Empyema is the presence of pus in the pleural cavity. It can be a complication of pneumonia, thoracotomy, abscess (lung, liver or subdiaphragmatic), and penetrating trauma. Subsequently, the spread of pus into the soft tissues develops, leading to infection of the chest wall and external drainage of the purulent focus.

Armored lung is a lung enclosed in a fibrous shell (armor) due to empyema or tumor. Since the lung cannot expand, the pressure in the pleural cavity is further reduced, which increases the transudation of fluid from the parietal pleural capillaries. The characteristics of the fluid are on the border between transudate and exudate, including biochemical parameters - within 15% of the diagnostic values of Light's criteria.
Iatrogenic effusions can be caused by migration or displacement of a feeding or central venous catheter, which leads to the entry of food or intravenous solutions into the pleural cavity.

Effusions without an obvious cause (idiopathic) are often due to silent pulmonary emboli, tuberculosis, or malignancies. The etiology is not established in approximately 15% of cases, even after careful investigation; many of these effusions are thought to be due to viral infections.

Symptoms of pleural effusion

Some pleural effusions are asymptomatic and are discovered incidentally on physical examination or chest radiography. Many cause dyspnea and/or pleuritic chest pain. Pleuritic pain, a vague discomfort or sharp pain in the chest that worsens with inspiration, suggests inflammation of the parietal pleura. Pain is usually felt in the area of inflammation, but the posterior and peripheral portions of the diaphragmatic pleura are innervated by more than six lower intercostal nerves, and irritation in these areas may cause lower chest or abdominal pain, sometimes mimicking abdominal disease. Irritation of the central portion of the diaphragmatic pleura, innervated by the phrenic nerves, causes pain radiating to the neck and shoulder.

Physical examination reveals absence of vocal fremitus, dullness to percussion, and decreased breath sounds on the side of the effusion. These findings may also result from pleural thickening. With large effusions, respirations are usually rapid and shallow. A pleural friction rub, although uncommon, is a classic physical sign. Its severity may vary from a small number of intermittent crackling sounds to an intense, widespread, harsh friction, creaking, or skin-crumpling sound that coincides with breathing and is heard on inspiration and expiration. Friction heard in the precordial area (pleuropericardial rub) may vary with cardiac contractions and may be mistaken for a pericardial friction rub. The latter is best heard at the left sternal border in the third and fourth intercostal spaces as a characteristic biphasic sound synchronous with the heartbeat and largely independent of respiration. The sensitivity and specificity of physical examination for detecting effusion are low.

Parapneumonic effusion and pleural empyema

About 55% of all cases of pneumonia requiring hospitalization of patients are accompanied by the formation of effusion in the pleural cavity. The severity of parapneumonic pleural effusions varies significantly - from uncomplicated effusion to the development of pleural empyema. Some forms of parapneumonic effusion do not require special therapy, except for the prescription of antibacterial drugs, while in complicated pleurisy, surgical intervention is often performed. Conventionally, in the process of formation of parapneumonic effusion, three stages are distinguished: uncomplicated parapneumonic effusion, complicated parapneumonic effusion, pleural empyema.

Uncomplicated parapneumonic effusion is a sterile exudate of a neutrophilic nature (the number of neutrophils usually exceeds 10x103 cells /ml), which does not require special procedures or treatment, and resolution occurs as pneumonia regresses.

The development of complicated parapneumonic effusion (also neutrophilic exudate) is associated with the penetration of infectious agents into the pleural cavity. Bacteria cause the reorganization of glucose metabolism to the anaerobic pathway, which results in a decrease in glucose concentration and the development of pleural fluid acidosis, and as a result of leukocyte lysis, an increase in the LDH activity of the effusion is determined. Bacteria are cleared from the pleural cavity fairly quickly, patients are prescribed antibacterial treatment, therefore complicated parapneumonic effusion is usually sterile. Persistent inflammation causes fibrin deposition on the visceral and parietal pleural layers and leads to the development of adhesions and encapsulation of the effusion.

Pleural empyema is defined as the presence of pus in the pleural cavity. This stage of parapneumonic effusion is characterized by a large number of bacteria (detected by Gram staining) and leukocytes (more than 25x103 / ml, their presence determines the macroscopic picture of purulent effusion). When purulent effusion is formed, fibrin clots and membranes are almost always formed on the pleural sheets, as well as encapsulation of the effusion, in addition, at later stages (2-3 weeks), migration of fibroblasts into fibrin deposits is noted, which leads to the organization of the pleural cavity. When empyema develops, drainage of the pleural cavity and, often, surgical decortication of the pleura are mandatory.

The occurrence of complicated pleural effusions and empyema is most often caused by the presence of such background diseases as diabetes mellitus, alcoholism, COPD, bronchiectasis, rheumatoid arthritis. In men, these forms of pleurisy are diagnosed approximately twice as often.

Microbiology of parapneumonic effusions reflects the spectrum of causative factors of pneumonia. As studies have shown, in recent years there have been significant changes in the properties of microorganisms causing parapneumonic pleurisy (this fact is associated with the use of antimicrobial drugs for the treatment of pneumonia). Currently, the main cause of complicated parapneumonic effusions is considered to be the penetration of gram-positive (Streptococcus pneumoniae, Streptococcus pyogenes, Staphylococcus aureus) and gram-negative (Escherichia coli, Haemophilus influenzae, Klebsiella spp., Pseudomonas spp.) aerobic bacteria into the pleural cavity. Anaerobic microorganisms (usually together with aerobic bacteria) lead to the formation of 36-76% of all empyemas, however, approximately 15% of parapneumonic effusions occur exclusively as a result of anaerobic infections Prevotella spp, Fusobacterium nucleatum, Streptococcus intermedius, Bacteroides spp are anaerobic microorganisms that most often lead to the formation of complicated parapneumonic effusions.

Pleural effusion in pulmonary embolism

Small pleural effusion is found in 40% of patients admitted to hospital with pulmonary embolism. Of these, 80% of effusions are exudates, 20% are transudates, and as a rule, the pleural fluid contains blood (in 80% of cases). If a large number of red blood cells are detected in the pleural fluid (more than 100,000 cells/mm3 ), it is necessary to exclude a malignant neoplasm, pulmonary infarction, or trauma. A smaller number of red blood cells has no diagnostic value. Effusions caused by pulmonary embolism do not have specific features. Therefore, the diagnosis is established based on clinical data that allow one to suspect pulmonary embolism with a high probability.

Tuberculous pleurisy

Acid-fast bacilli are detected in smears in only 10-20% of patients with tuberculous pleurisy, and pleural fluid culture allows to identify Mycobacterium tuberculosis in only 25-50% of cases. Histological examination and culture of pleural biopsy improves the diagnosis of tuberculosis up to 90%. In tuberculosis, unlike exudates of other etiologies, an increase in the activity of adenosine deaminase occurs in the pleural fluid. However, an increase in this indicator is also recorded in empyema, rheumatoid pleurisy and malignant diseases, which leads to a decrease in the diagnostic value of adenosine deaminase analysis in countries with a low incidence of tuberculosis. An increase in adenosine deaminase activity does not occur in patients with HIV infection suffering from tuberculosis.

Pleural effusion in HIV infection

Pleural effusion is diagnosed in 7-27% of HIV-infected patients hospitalized in hospital Kaposi's sarcoma, parapneumonic effusions and tuberculosis are the main causes of pleural damage in such patients. A prospective study involved 58 people suffering from HIV infection. All subjects had radiographic signs of pleural effusion. As the study showed, the cause of pleural effusion in a third of patients was Kaposi's sarcoma, in 28% of patients - parapneumonic effusion, and tuberculosis and pneumonia caused by Pneumocystis jiroveci - in 14% and 10%, respectively. Lymphoma was diagnosed in 7% of patients participating in the study.

Chylothorax and pseudochylothorax

True chyloid effusion occurs when the thoracic duct or its branches rupture, allowing lymph to enter the pleural cavity. In approximately 50% of such cases, patients have malignant neoplasms (mainly lymphomas). The presence of trauma (especially during surgical interventions) also causes the formation of true chyloid effusion (25% of cases). Sometimes this condition is caused by diseases such as tuberculosis, sarcoidosis or amyloidosis.

Chylothorax should be distinguished from pseudochylothorax, or "cholesterol pleurisy," which is formed as a result of the accumulation of cholesterol crystals in a long-standing pleural effusion. In this case, as a rule, significant thickening of the pleura and its fibrosis are detected. The main causes of pseudochylothorax are considered to be tuberculosis and rheumatoid arthritis. The diagnosis of chylothorax and pseudochylothorax is established on the basis of an analysis of the lipid content of the pleural fluid.

In rare cases, milky effusion similar to chylothorax is observed with empyema. These conditions are distinguished by centrifugation. After it, with pleural empyema, a transparent supernatant is formed, and the cellular mass settles. Chylous fluid retains a milky appearance after centrifugation.

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Diagnosis of pleural effusion

Diagnostic tests are ordered to document the presence of pleural fluid and determine its cause.

Chest radiography is the first test performed to confirm the presence of pleural fluid. If pleural effusion is suspected, a lateral chest radiograph should be performed with the patient upright. In this case, 75 ml of fluid is localized in the posterior costophrenic angle. Large pleural effusions are visualized as opacities in part of the chest; effusions larger than 4 L may cause complete opacification and even mediastinal displacement.

Localized (encapsulated) effusions are accumulations of fluid located between pleural adhesions or within the interlobar fissure. If the nature of the opacity is unclear, as well as whether the suspected effusion is encapsulated or free, a lateral chest radiograph, chest CT, or chest ultrasound should be performed. These studies are more sensitive than upright radiographs and can detect fluid volumes less than 10 ml. Encapsulated fluid, especially in a horizontal or oblique interlobar fissure, may be mistaken for a solid lung mass (false tumor). This mass may change shape and size with changes in the patient's position and the amount of pleural effusion.

CT is not routinely performed but is useful for assessing adjacent lung parenchyma for infiltrates or tumors when the lung is obscured by effusion and in the differential diagnosis of encapsulated fluid collections from solid lesions.

Thoracentesis should be performed in almost all patients with a new, unexplained pleural effusion that is more than 10 mm thick on a lateral decubitus radiograph or on ultrasound. Despite common practice, chest radiography should not be repeated after this procedure unless the patient develops symptoms suggestive of pneumothorax (shortness of breath or chest pain) or air may have entered the pleural space during the procedure. Thoracentesis and subsequent pleural effusion testing are also often unnecessary for chronic pleural effusions that have a known cause and are asymptomatic.

Ultrasonography is useful for localizing pleural fluid prior to puncture when blind thoracentesis has failed.

Pleural fluid examination is performed to diagnose the cause of the pleural effusion. It begins with a visual inspection that differentiates hemorrhagic and chylous (or chylous-like) effusions from other effusions; it can also identify purulent effusions suggesting empyema and the viscous fluid characteristic of some mesotheliomas. In all cases, total protein, lactate dehydrogenase, cell count and composition, microscopy after Gram stain, and aerobic and anaerobic culture are performed. Other tests ( glucose concentration, cytology, fluid markers for tuberculosis (adenosine deaminase or interferon gamma), amylase, mycobacteria, and microscopy after fungal stain and culture) are used in appropriate clinical situations.

Fluid chemistry can differentiate transudates from exudates; there are many criteria, none of which is universally applicable. When using Light's criteria, blood should be drawn as close to the time of thoracentesis as possible to determine serum LDH and total protein concentrations for comparison with those of pleural fluid. Light's criteria correctly identify almost all exudates but falsely identify approximately 20% of transudates as exudates. If a transudate is suspected (eg, in heart failure or cirrhosis) and no biochemical parameter is more than 15% above the Light criteria cutoff, the difference in serum and pleural fluid total protein concentrations is tested. If the difference is more than 3.1 g/dL, a transudate is likely.

If the diagnosis remains unclear after pleural fluid analysis, spiral CT is performed to detect pulmonary emboli, pulmonary infiltrates, or mediastinal lesions. Detection of a pulmonary embolus indicates the need for long-term anticoagulant therapy; parenchymal infiltrate requires bronchoscopy; mediastinal mass lesions require transthoracic aspiration biopsy or mediastinoscopy. However, spiral CT requires holding the breath for more than 24 s, which is not possible for all patients. If spiral CT is not informative, the best option for further examination is observation, unless the patient has a history of malignancy, weight loss, persistent fever, or other changes that raise suspicion of malignancy or tuberculosis; in the latter situation, thoracoscopy may be performed. Puncture biopsy of the pleura may be performed if thoracoscopy is impossible. If thoracoscopy is uninformative, thoracotomy should be performed in some cases. Most patients with exudative effusion should also undergo a tuberculin test with control.

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How is pleural effusion treated?

The underlying disorder is treated; the effusion itself does not require treatment if it is asymptomatic, as many of them resolve spontaneously, especially those resulting from uncomplicated pneumonia, pulmonary embolism, and surgery. Pleuritic pain is usually relieved by oral analgesics, although a short course of oral opioids is occasionally required.

Pleural puncture with evacuation of exudate is sufficient treatment for many symptomatic effusions and may be repeated if fluid reaccumulates. Removal of more than 1.5 L of pleural fluid at one time is unacceptable, as this may lead to pulmonary edema due to rapid expansion of alveoli previously compressed by fluid.

Chronic, recurrent effusions that are symptomatic may be treated with periodic thoracentesis or permanent pleural drainage. Effusions due to pneumonia and malignancy may require additional specific treatment.

Drug treatment

Transudates usually do not require mechanical removal of fluid from the pleural cavity, except in cases of massive pleural effusions causing severe dyspnea. As a rule, the main method of treating transudates is considered to be treatment of the underlying disease, for example, improving myocardial contractility and correcting fluid metabolism in congestive heart failure. The administration of diuretics and albumin solution has a fairly good effect in the treatment of patients with transudates against the background of hypoproteinemia. Correction of severe hypoproteinemia should be carried out gradually to prevent a rapid increase in the volume of intravascular fluid. It is preferable to perform long-term infusions of furosemide (simultaneously correcting the loss of potassium and magnesium), rather than administering it as a bolus. In severe hypoproteinemic conditions, spironolactone is recommended. The management of patients with parapneumonic pleural effusion and pleural empyema is a particular problem.

The treatment of parapneumonic pleural effusion depends primarily on its stage and the risk of an unfavorable outcome. In 2000, at a meeting of the American College of Chest Physicians, the ABC classification of parapneumonic pleural effusions was proposed, developed taking into account the anatomical characteristics of the pleural effusion (A), pleural fluid bacteriology (B), and pleural fluid biochemical analysis data (C). Based on this classification, four prognostic categories are distinguished in the parapneumonic effusion group, determining the indications for the installation of a drainage tube (necessary for patients in risk category III and IV).

In uncomplicated parapneumonic pleural effusion, the patient is monitored and antimicrobial therapy is prescribed. Second- or third-generation cephalosporins or inhibitor-protected penicillins are recommended for the treatment of patients with community-acquired pneumonia.

If contamination with anaerobic flora is suspected, combination therapy with metronidazole or clindamycin, inhibitor-protected penicillins or carbapenems is prescribed. Antibiotics that penetrate well into the pleural cavity include penicillins, metronidazole, ceftriaxone, clindamycin, vancomycin. Aminoglycosides practically do not penetrate into the pleural cavity. There is currently no evidence of the effectiveness of direct instillation of antibacterial drugs into the pleural cavity.

Antibacterial drug regimens used for initial therapy of pleural effusions with negative pleural fluid cultures

Community-acquired infection

Cefuroxime at a dose of 1.5 g (3 times a day intravenously) in combination with 400 mg metronidazole (3 times a day orally) or with 500 mg metronidazole (3 times a day intravenously)

Amoxicillin/clavulanate 825/125 mg (3 times daily)

Amoxicillin/clavulanate 1.2 g (3 times daily intravenously) in combination with 400 mg ciprofloxacin (2 times daily intravenously)

Amoxicillin 1 g (3 times daily) in combination with 400 mg metronidazole (3 times daily)

Meropenem at a dose of 1 g (3 times a day intravenously) in combination with 400 mg metronidazole (3 times a day orally) or with 500 mg metronidazole (3 times a day intravenously)

Clindamycin at a dose of 300 mg (4 times a day)

Hospital acquired infection

Piperacillin/tazobactam 4.5 g (3 times daily intravenously)

They don't use it

Ceftazidime at a dose of 2 g (3 times a day intravenously)

Meropenem at a dose of 1 g (3 times a day intravenously) is sometimes combined with 400 mg metronidazole (3 times a day orally) or with 500 mg metronidazole (3 times a day intravenously)

In complicated pleural effusion, a drainage tube is installed or thoracocentesis is performed (as repeated punctures). In empyema, drainage of the pleural cavity is considered the method of choice. The drainage tube is usually installed under the control of X-ray examination, ultrasound or CT. In the presence of several encapsulated cavities, several drainage tubes are used. It is preferable to use large-diameter tubes (24-36 P), especially if there is viscous exudate in the pleural cavity. Usually, negative pressure (10-20 cm H2O) is set during the manipulation. With the correct positioning of the tube, rapid evacuation of fluid and straightening of the lung occurs. When the pleural discharge decreases (up to 50 ml per day), the drainage tube is removed.

In the presence of adhesions in the pleural cavity or if encapsulated cavities are detected, adequate drainage of the pleural cavity can be achieved by introducing fibrinolytics into it, which dissolve fibrin clots and membranes. Most often, streptokinase (at a dose of 250,000 units) or urokinase (at a dose of 100,000 units) are used; the drugs are introduced into 100 ml of physiological solution and the drainage tube is blocked for 2-4 hours, then the pleural fluid is removed. Depending on the clinical response, fibrinolytic instillations are repeated for 3-14 days. Intrapleural administration of fibrinolytics does not cause systemic fibrinolysis. The effectiveness of fibrolytic drugs in the treatment of encapsulated pleural effusions is 70-90%.

Contraindications to the use of fibrinolytic drugs

  • Absolute contraindications
    • Previous allergic reactions
    • Presence of bronchopleural fistula
    • Trauma or surgery (within the previous two days)
  • Relative contraindications
    • Major surgeries performed in the last two weeks
    • History of hemorrhagic stroke
    • Head injury or surgery (within the previous two weeks)
    • Coagulation system disorders
    • Prior thrombolysis with streptokinase (contraindication for streptokinase only)
    • Pre-existing streptococcal infections (contraindicated for streptokinase only)

Thoracoscopy is an alternative fibrinolytic method of therapy for encapsulated pleural effusions. The effectiveness of thoracoscopy in draining pleural empyema reaches 90%. If there is no effect from pleural cavity drainage, fibrinolytic therapy and thoracoscopy, surgical drainage is used - open thoracotomy and decortication of the lung.

Surgical treatment

Surgical methods are highly effective (up to 95%), but their implementation is associated with a certain operational risk.

Parapneumonic effusion

In the presence of unfavorable prognostic factors (pH < 7.20; glucose concentration < 60 mg/dL; lactate dehydrogenase content > 1000 IU/L; detection of microorganisms on microscopy after Gram staining or by culture on a nutrient medium; pleural empyema), it is necessary to completely remove the fluid by pleural drainage or puncture. If complete drainage is impossible, intrapleural fibrinolytic agents are administered (eg, urokinase at a dose of 100,000 U per 100 ml of saline). If this treatment is ineffective, thoracoscopy is performed to destroy adhesions and ensure drainage of the lesion. If this is ineffective, thoracotomy and decortication of the lung (with removal of adhesions, clots, or fibrous capsule surrounding the lung) are performed.

Pleural effusion in malignant tumors

If dyspnea due to malignant pleural effusion improves after thoracentesis but fluid continues to accumulate, a permanent pleural drain or pleurodesis is placed; asymptomatic effusions and effusions resistant to thoracentesis do not require additional treatment.

Permanent drainage is the preferred treatment for outpatients because it can be performed on an outpatient basis and pleural fluid is evacuated directly into vacuum bottles. Shunting of pleural fluid into the peritoneal cavity (pleuroperitoneal shunt) is used in patients with malignant effusions when pleurodesis fails or when a shell lung develops.

Pleurodesis is performed by introducing a sclerosing agent into the pleural cavity to induce fusion of the visceral and parietal pleural layers and obliteration of the pleural cavity. The most effective and commonly used sclerosing agents are talc, doxycycline, and bleomycin, administered through a chest tube or during thoracoscopy. Pleurodesis is contraindicated in cases of mediastinal shift toward the effusion and failure to re-expand the lung after placement of a chest tube.

What is the prognosis for pleural effusion?

The prognosis of pleural effusions depends mainly on their nature. However, it can be assumed that the formation of pleural effusion worsens the prognosis of the underlying disease. Pleural effusion is one of the independent prognostic factors of community-acquired pneumonia, which is part of some prognostic indices. As studies have shown, pleural effusion is an unfavorable prognostic sign, especially for patients with pneumonia caused by legionella and for patients with HIV infection.

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