The pleural cavity is a potential space located between the lungs and the chest wall. Under normal circumstances, there is a thin layer of fluid on the surfaces of the visceral pleura and the parietal pleura, which plays a lubricating role during respiratory movements. In each respiratory cycle, the shape and pressure of the pleural cavity change greatly, allowing the continuous filtration and reabsorption of fluid in the pleural cavity and maintaining a dynamic balance. Any factor that causes too quick production of fluid in the pleural cavity and/or too slow reabsorption results in pleural effusion.
Pathogenesis
Pleural effusion is common in clinical practice and can be caused by pulmonary, pleural, and extrapulmonary diseases. The common etiologies and pathogenesis are as follows.
Increased hydrostatic pressure in the systemic circulation and/or pulmonary circulation is present. The former increases the amount of fluid filtered into the pleural cavity, and the latter reduces the reabsorption of fluid in the pleural cavity. Large amounts of fluid are filtered from the parietal pleural capillaries, exceeding the reabsorption capacity, thereby resulting in pleural effusion. Clinically, common conditions such as congestive heart failure, constrictive pericarditis, increased blood volume, and obstruction of the superior vena cava or azygos vein can produce pleural transudate.
When plasma albumin decreases and plasma colloid osmotic pressure decreases, the colloid osmotic pressure of the parietal pleural capillaries decreases, the filtration of the parietal pleural capillaries increases, and the colloid osmotic pressure of the visceral pleural capillaries decreases. The colloid osmotic pressure of the pleural capillaries decreases, reducing the reabsorption of pleural fluid and increasing the amount of pleural effusion. Clinically, common conditions such as hypoproteinemia, cirrhosis, nephrotic syndrome, acute glomerulonephritis, and myxedema can produce pleural transudate.
When there is inflammation of the pleural cavity and its adjacent organ tissues or pleural tumors, due to direct involvement of the pleura or the release of various enzymes, complements, and bioactive substances such as histamine by damaged cells, the permeability of the pleural capillary increases, and large amounts of fluid containing proteins and cells enter the pleural cavity. The protein content in the pleural fluid increases, and the colloid osmotic pressure increases, further promoting the accumulation of pleural fluid. Clinically, common conditions such as pleural inflammation (pulmonary tuberculosis, parapneumonic pleural effusion), connective tissue diseases (systemic lupus erythematosus, rheumatoid arthritis), pleural tumors (metastasis of malignant tumors, pleural mesothelioma), pulmonary infarction, and subdiaphragmatic inflammation (subdiaphragmatic abscess, liver abscess, acute pancreatitis) can produce pleural exudate.
The fluid and protein in the pleural fluid return to the circulatory system through the lymphatic system. Therefore, cancerous lymphatic obstruction, congenital dysplasia causing abnormal lymphatic drainage and trauma causing lymphatic reflux disorder can produce pleural effusion with high protein content.
Rupture of aortic aneurysms, rupture of the esophagus, and rupture of the thoracic duct can produce hemothorax, empyema, and chylothorax.
Drugs, radiotherapy, digestive endoscopy examination and treatment, bronchial artery embolization, ovarian hyperstimulation syndrome, fluid overload, coronary artery bypass graft surgery, bone marrow transplantation, central venous perforation in catheterization, and peritoneal dialysis can cause exudative or transudative pleural effusion.
Clinical manifestations
Symptoms are related to the amount of effusion. When the amount of effusion is less than 0.3 - 0.5 L, symptoms are often not obvious. In case of massive effusion, dyspnea is the most common symptom, often accompanied by thoracodynia and cough. As the amount of pleural effusion increases, thoracodynia may be relieved, but chest tightness and tachypnea exacerbate.
Symptoms vary depending on the primary disease. For example, tuberculous pleurisy is more common in young adults, often accompanied by fever, dry cough, and thoracodynia; pleural effusion caused by heart failure has manifestations of cardiac insufficiency; right-sided pleural effusion associated with liver abscess can be caused by reactive pleurisy or empyema, with fever and pain in the liver.
Signs are related to the amount of effusion. In case of small amounts of effusion, there are not significant signs, but pleural friction sensation can be felt and pleural friction rub can be heard. In case of moderate to large amounts of effusion, the affected side of the chest is full, tactile fremitus is weakened, local percussion shows dullness, and respiratory sounds are decreased or absent. Displacement of the trachea and mediastinum to the healthy side may be accompanied. Pleural effusion caused by extrapulmonary diseases such as rheumatoid arthritis and Sjogren syndrome often has signs of the primary disease.
Laboratory and other examinations
Imaging examination
Chest x-ray changes are related to the amount of effusion and whether there is encapsulation or adhesion. Lateral chest x-ray films are particularly important for diagnosing small amounts of pleural effusion. In case of small amounts of free pleural effusion, the frontal chest x-ray film may show blunting or absence of the costophrenic angle. When the amount of effusion increases, there is an effusion opacity with an arcuate upper edge outward and upward. When there are large amounts of effusion, the affected side of the chest shows dense opacity, and the trachea and mediastinum are pushed to the healthy side. In recumbent position, the effusion spreads out, and the lucency of the entire lung field decreases. There is an air-fluid level in hydropneumothorax. Encapsulated effusion does not change with body position, has a smooth and full edge, and is mostly confined between the lobes or between the lung and the diaphragm. Pleural effusion at the base of the lung may only have elevation or shape changes of the diaphragm.
Figure 1 Left pleural effusion on chest x-ray
Chest CT can show small amounts of pleural effusion and distinguish encapsulated effusion and its location. Chest CT can show lesions in the lungs, pleura, diaphragm, hilum, and mediastinum, is helpful for etiological diagnosis, and can also assess the amount of effusion.
Figure 2 Left pleural effusion on CT
Ultrasound has high sensitivity in detecting pleural effusion, can estimate the depth and amount of pleural effusion, assist in the positioning of pleural puncture, and can determine whether there is encapsulation or separation of the effusion. Ultrasound-guided pleural puncture can reduce the operational risk.
MRI has a high resolution for soft tissues and can assist in differentiating benign and malignant pleural effusion, especially suitable for patients allergic to contrast agents for contrast-enhanced CT.
PET-CT is a functional imaging technique widely used in oncology and based on the difference in glucose metabolism levels in normal and abnormal tissues and accelerated uptake of fludeoxyglucose (18F) in tumor cells. It has certain value in assisting in differentiating benign and malignant pleural effusion, and can also assist in tumor staging and finding the primary lesion.
Laboratory examination
General examination
Transudate is mostly light yellow, transparent, and clear, does not coagulate when standing still, and the specific gravity is < 1.016 - 1.018. Exudate is slightly turbid and prone to clotting, and the specific gravity is > 1.018. Hemorrhagic pleural effusion is like blood in the water or venous blood, more common in tumors, tuberculosis, and pulmonary embolism. Chylous pleural effusion is mostly chylothorax, mostly caused by tumors, parasites, trauma (thoracic surgery, chest trauma), or tuberculosis leading to compression or rupture of the thoracic duct. Chocolate-colored pleural effusion suggests the possibility of rupture of amoebic liver abscess into the pleural cavity. Black pleural effusion may be due to aspergillus infection. Yellowish green pleural effusion is more common in rheumatoid arthritis.
Pleural effusion with anaerobic bacterial infection often has a foul smell, suggesting the possibility of empyema. If the effusion has a urine smell, it may indicate urinothorax, and the creatinine level in the pleural effusion is often higher than in serum.
Cell count and classification
Various inflammatory cells and proliferated and degenerated mesothelial cells can be seen in pleural effusion. The count of cells in transudate is less than 100×106/L; the count of nucleated cells in exudate often exceeds 500×106/L, and in empyema, the count of nucleated cells is more than 10×109/L. However, there is no definite boundary in cell count between transudate and exudate, and comprehensive analysis is required.
An increase in neutrophils is common in acute inflammation. Lymphocyte-predominant pleural effusion is more common in tuberculosis, congestive heart failure, and malignancy. Eosinophils accounting for ≥ 10% in pleural effusion can be seen in parasitic infections, eosinophilia, asbestosis, drugs, and tumors.
Biochemical examination
The pH of normal pleural effusion is close to 7.6. Decreased pH can be seen in empyema, esophageal rupture, and rheumatoid arthritis, as well as tuberculosis and malignant pleural effusion. pH < 7.0 is only seen in empyema and pleural effusion caused by esophageal rupture.
The glucose level in normal pleural effusion is close to that in peripheral blood, and the glucose content in transudate and most exudate is normal. Glucose in pleural effusion of tuberculosis pleurisy, malignancy, and lupus pleurisy can be lower than blood glucose. Complicated parapneumonic pleural effusion, empyema, and rheumatoid arthritis are the most common causes of significantly decreased glucose levels (< 3.3 mmol/L) in pleural effusion.
The protein content of exudate is higher (> 30 g/L), and the ratio of pleural effusion/serum protein is > 0.5; the protein content of transudate is lower (< 30 g/L), mainly albumin, and Rivalta test is negative.
The lactate dehydrogenase (LDH) content in exudate increases, and the ratio of pleural effusion/serum LDH is > 0.6. LDH > 500 IU/L often suggests malignancy or thoracic infection.
Adenosine deaminase (ADA) is an enzyme present in various cells, especially in activated T lymphocytes, and plays an important role in the differentiation of lymphocytes. The ADA level in tuberculous pleurisy is mostly more than 45 IU/L, and its sensitivity for diagnosing tuberculous pleurisy is high. In AIDS patients with concurrent tuberculous pleurisy, the ADA level in pleural effusion is often lower than 40 IU/L. Elevated ADA is also seen in pleural effusion caused by empyema, rheumatoid arthritis, systemic lupus erythematosus, and malignant pleural effusion. There are two isoenzymes of ADA, ADA1 and ADA2, which can be used to distinguish between tuberculous and non-tuberculous diseases.
Increased amylase can be seen in acute pancreatitis, esophageal rupture, and malignancy. About 10% of patients with acute pancreatitis can be complicated with pleural effusion. Amylase escapes into the pleural effusion and is even higher than the serum amylase level.
Chylous pleural effusion contains more triglycerides (> 1.24 mmol/L), and its composition changes are related to diet. Pleural effusion is red in Sudan III staining, while the cholesterol content is normal. In pseudochylous pleural effusion, the cholesterol content is high (> 5.18 mmol/L), mainly due to cholesterol accumulation, but there are no chylomicrons, the triglyceride in the effusion is normal, and Sudan III staining is negative, mainly in old tuberculous pleural effusion and rheumatoid arthritis-related pleural effusion.
Carcinoembryonic antigen (CEA) is a marker associated with various tumors. Pleural effusion CEA > 10μg/L or effusion/serum CEA > 1 often suggests malignant pleural effusion, with high specificity and low sensitivity. CEA has higher diagnostic value for pleural effusion caused by adenocarcinoma, especially CEA-secreting lung adenocarcinoma, gastrointestinal tumors, and breast cancer. Other tumor markers include cancer antigen CA125, cytokeratin 19 fragment (CYFRA 21-1), and neuron-specific enolase, which can be used for diagnosis.
The levels of γ-interferon and IL-27 increase in pleural effusion of tuberculous pleurisy, with high sensitivity and specificity. Interferon-gamma release assays (IGRAs) detect the IFN-γ level produced by T cells stimulated by specific antigens of Mycobacterium tuberculosis. The sensitivity and specificity of IGRAs in the diagnosis of tuberculous pleurisy in pleural effusion are not high.
The complement components (C3, C4) decrease and the content of immune complexes increases in pleural effusion caused by systemic lupus erythematosus and rheumatoid arthritis. The antinuclear antibody (ANA) titer in pleural effusion of systemic lupus erythematosus can reach more than 1:160. The rheumatoid factor in pleural effusion of rheumatoid arthritis is > 1:320.
The positive rate of smear examination for acid-fast staining of pleural effusion specimens is less than 10%. The positive rate of culture of Mycobacterium tuberculosis in pleural effusion is related to the culture medium. Compared with solid medium, liquid medium can improve the positive rate and shorten the culture time. Nucleic acid amplification tests of Mycobacterium tuberculosis in pleural effusion specimens have a specificity of more than 90% in the diagnosis of tuberculous pleurisy, but the sensitivity is low. Xpert MTB/RIF assay in pleural effusion has a high specificity (99%) in the diagnosis of tuberculous pleurisy, but the sensitivity is only 37% - 51%.
Bacterial smear, culture, and nucleic acid amplification tests of pleural effusion are helpful for the identification of pathogens of thoracic infections. Injection of pleural effusion into blood culture bottles for culture can improve the detection rate. Metagenomic next-generation sequencing (mNGS) can rapidly detect various pathogenic microorganisms and can detect pathogens that are difficult to be identified by other traditional methods, including Nocardia, Pneumocystis, Mycobacterium tuberculosis, Enterobacter, Streptococcus, Fusobacterium nucleatum, and Porphyromonas gingivalis. Compared with traditional microbial detection and culture of pleural effusion, mNGS is more sensitive but less specific, and comprehensive determination in combination with clinical information is required.
Malignant cells can be detected in about 40% - 87% of patients with malignant pleural effusion, and the diagnostic performance is related to the type and site of the primary tumor and the collection of specimens. Repeated examinations help to improve the detection rate.
Pleural biopsy
Percutaneous pleural biopsy is of great significance for the etiological diagnosis of pleural effusion and can detect tumors, tuberculosis, and other pleural granulomatous lesions. When tuberculous pleurisy is suspected, in addition to pathological examination, biopsy tissue specimens can also be used for Mycobacterium tuberculosis DNA detection and acid-fast staining, and Mycobacterium tuberculosis culture can also be conducted if necessary. Pleural puncture biopsy has the advantages of simplicity, feasibility, and less invasiveness. CT or ultrasound-guided pleural biopsy can improve the success rate.
Thoracoscopy or thoracotomy biopsy
If the above examinations are still inconclusive, biopsy under direct vision through thoracoscopy or thoracotomy can be performed if necessary. The sensitivity of thoracoscopy biopsy in diagnosing malignant pleural effusion is 92% - 97%, and the specificity is 99% - 100%. Through thoracoscopy, the pleural cavity can be comprehensively examined, the morphological characteristics, distribution, and involvement of adjacent organs can be observed, and multiple biopsies can be performed under direct vision. The etiology of pleural effusion in few patients is still difficult to determine after the above examinations, and if there are no special contraindications, exploratory thoracotomy can be considered.
Bronchoscopy
In patients with hemoptysis or suspected airway obstruction, especially with suspected lung cancer, bronchoscopy can be performed to assist in the diagnosis. If there are no such abnormalities in patients, the diagnostic yield is low.
Diagnosis and differential diagnosis
The diagnosis and differential diagnosis of pleural effusion are divided into 3 steps.
Determination of presence or absence of pleural effusion
The diagnosis of moderate or severe pleural effusion is not difficult, and the symptoms and signs are often evident. Small amounts of pleural effusion only show blunting of the costophrenic angle, and are sometimes easily confused with pleural adhesion. Chest x-ray in lateral decubitus position can be performed, and the fluid can spread to the outer zone of the lung. Examinations such as ultrasound and CT can determine whether there is pleural effusion.
Differentiation of transudate and exudate
Diagnostic thoracentesis can distinguish the nature of the effusion. Transudate is clear, transparent, colorless, or light yellow, and does not coagulate. Exudate is transparent or turbid, brownish yellow or bloody, and can coagulate spontaneously. Differentiation can be based on specific gravity (with 1.018 as the cutoff), protein content (with 30g/L as the cutoff), and cell count (with 500 × 106/L as the cutoff). Below these values indicates transudate, and vice versa is exudate. However, the sensitivity and specificity are limited.
Table 1 Differentiation between exudate and transudate (Light criteria)
Light criteria are usually used to distinguish transudate from exudate, mainly measuring the protein content and lactate dehydrogenase (LDH) in pleural effusion. According to Light criteria, if at least one of the criteria is met, the effusion is exudate, and if none is met, the effusion is transudate. Light criteria have low specificity for the judgment of exudate. According to these criteria, about 25% of transudate is misclassified as exudate.
Etiological diagnosis
The main causes of transudate include:
- Congestive heart failure, often bilateral, mostly right side (Intense diuresis can cause pseudo-exudate. N-terminal pro-B-type natriuretic peptide (NT-proBNP) > 1,500 pg/ml in pleural effusion has a good diagnostic value for pleural effusion caused by heart failure)
- Nephrotic syndrome, often bilateral, improved with the correction of protein loss
- Cirrhosis, mostly accompanied by ascites, mainly in the right pleural cavity
- Others, such as acute glomerulonephritis, constrictive pericarditis, peritoneal dialysis, myxedema, drug allergies, and radiation reactions.
There are various causes of exudate, and the common causes include: parapneumonic effusion, tuberculosis, and malignancy.
Parapneumonic effusion, also known as parapneumonic pleural effusion, is pleural effusion caused by infections such as pneumonia, lung abscess, and bronchiectasis. Parapneumonic effusion can be divided into simple parapneumonic effusion and complicated parapneumonic effusion according to the pathogenesis. Simple parapneumonic effusion is caused by the reactive exudation of the pleura and is reabsorbed as pneumonia improves. When bacteria invade the pleural cavity, they can lead to complicated parapneumonic effusion. Patients often have symptoms such as fever, cough, expectoration, and thoracodynia. The white blood cell count is increased, neutrophils are increased, and there is left shift. X-ray or CT shows infiltration of the lung parenchyma, or manifestations of lung abscess and bronchiectasis, followed by pleural effusion. The amount of effusion is generally not large. Complicated parapneumonic effusion is mostly yellow and turbid, the nucleated cell count is significantly increased, mainly neutrophils, glucose and pH are decreased, and LDH is increased.
Table 2 Characteristics of parapneumonic pleural effusion and empyema
Empyema is the accumulation of pus caused by pathogenic bacteria infection in the thoracic cavity, mostly related to the failure to effectively control pulmonary infection and the direct invasion and penetration of pathogenic bacteria into the thoracic cavity. Acute empyema presents with high fever and thoracodynia. Chronic empyema has pleural thickening, chest collapse, chronic wasting, and clubbed fingers (toes). The pleural effusion is purulent and viscous, and the bacterial culture of the pus may be positive.
Thoracic infection is composed of complicated parapneumonic effusion and empyema. Most community-acquired thoracic infections are caused by Gram-positive aerobic bacteria, including Streptococcus and Staphylococcus aureus. Gram-negative bacteria are less common. Hospital-acquired thoracic infections are mainly caused by drug-resistant Gram-positive bacteria (including MRSA) and Gram-negative bacteria, such as Enterobacter and Pseudomonas. Anaerobic bacteria are often involved in thoracic infections. Thoracic infections caused by fungi, actinomycetes, and Nocardia are less common.
Tuberculous pleurisy can occur at any age and often coexists with pulmonary tuberculosis or tuberculosis in other parts of the body. The manifestations are thoracodynia and tachypnea, and may be accompanied by tuberculosis symptoms such as fever, diaphoresis, and emaciation. The tuberculin test is positive or strongly positive. Older patients may have no fever, and the tuberculin test is often negative, which should be noted. The pleural effusion is mostly yellow, but also bloody. The main cells are lymphocytes, and mesothelial cells < 5%. The levels of ADA, γ-interferon, and IL-27 are elevated. The positive rate of acid-fast staining of the sediment smear of pleural effusion is less than 10%, and the positive rate of Mycobacterium tuberculosis culture of the effusion is 18% - 40%. Nucleic acid amplification and Xpert MTB/RIF assays detecting MTB DNA and rifampicin resistance genes can be used for the diagnosis of tuberculous pleurisy, but have low sensitivity and high specificity.
Pleural puncture biopsy, especially CT or color Doppler ultrasound-guided pleural puncture biopsy, is of great significance for the diagnosis of tuberculous pleurisy. Granuloma can be seen in pathology, and Mycobacterium tuberculosis DNA detection and acid-fast staining can also be conducted. The sensitivity is 60% - 80%. Culture of Mycobacterium tuberculosis in the biopsy tissue can further increase the sensitivity. Thoracoscopic pleural biopsy (pathology, DNA detection, culture) has a higher sensitivity in the diagnosis of tuberculous pleurisy.
Malignant pleural effusion is pleural effusion caused by primary malignant tumors of the pleura or metastasis of malignant tumors from other parts to the pleura, including lung cancer, breast cancer, hematological tumors, gastrointestinal tumors, gynecological malignancies, and malignant pleural mesothelioma. Malignant pleural effusion is a common complication of advanced tumors, usually grows rapidly and persists, has poor treatment response and poor prognosis, and is more common in middle-aged and older adults. The main clinical manifestations include dyspnea, thoracodynia, bloody expectoration, and emaciation. The pleural effusion is mostly bloody, large in volume, and growing rapidly. CEA or other tumor markers increase, and LDH is mostly greater than 500 IU/L. Chest imaging examinations can provide diagnostic clues. The diagnosis of malignant pleural effusion is based on the presence of malignant tumor cells confirmed by pathology in the pleural effusion sample or pleural biopsy tissue. Cytology, pleural puncture biopsy, bronchoscopy, and thoracoscopy are helpful for further diagnosis and differentiation. Suspected tumors from other organs require corresponding examinations.
Treatment
Pleural effusion is part of thoracic or systemic diseases. Etiological treatment is particularly important. Transudate can often be reabsorbed after correcting the cause, and the treatment of exudate varies according to different etiologies.
Parapneumonic effusion
Simple parapneumonic effusion generally has small amounts of effusion and can be reabsorbed after antibiotic treatment. The treatment principles of thoracic infection (complicated parapneumonic effusion, empyema) are to control infection, drain pleural effusion, and provide nutritional support. The choice of antibiotics should be based on whether the infection is community-acquired or hospital-acquired, local microbial prevalence and resistance, and individual factors. The course of treatment is generally 2 - 6 weeks.
Whether to drain the pleural effusion should be comprehensively judged based on biochemical tests of the pleural effusion (pH, LDH, glucose) and imaging features (ultrasound, CT). Measures to drain the effusion include thoracentesis and thoracic catheter drainage. In patients with recurrent or chronic thoracic infections, especially those with atelectasis and inoperable patients, thoracic catheter drainage should be considered.
Chronic empyema may require improved drainage of the empyema cavity. Surgical treatment strategies such as pleurectomy and thoracoplasty often need to be considered. In addition, general supportive treatment is also quite important. High-energy, high-protein, and vitamin-rich foods should be given, electrolyte disturbances should be corrected, and acid-base balance should be maintained.
Tuberculous pleurisy
The treatment goal of tuberculous pleurisy is not only to treat and control tuberculosis, but also to minimize the residual pleural thickening after the reabsorption of pleural effusion, prevent the reduction of lung function, and reduce the sequelae caused by pleural thickening.
General measures include rest, nutritional support, and symptomatic treatment.
Tuberculous pleural effusion is prone to cause pleural adhesion due to its high protein content. In principle, the effusion in the pleural cavity should be aspirated promptly or thoracic catheter drainage should be performed to reduce or relieve the compression of the heart and lungs by the pleural effusion, reduce fibrin deposition, and relieve the symptoms of tuberculosis. The first aspiration should not exceed 800ml, and each subsequent aspiration should not exceed 1,000ml. The aspiration should not be too fast to avoid shock and reexpansion pulmonary edema caused by sudden drop in thoracic pressure, manifested by severe cough, tachypnea, excessive foamy expectoration, moist crackles throughout both lungs, decreased PaO2, and signs of pulmonary edema on x-ray or CT. Treatment includes immediate oxygen therapy, glucocorticoids and diuretics, control of fluid intake, and close monitoring of the condition and acid-base imbalance. Sometimes, tracheal intubation and mechanical ventilation may be required. If there are dizziness, pallor, diaphoresis, palpitations, and cold extremities during the fluid aspiration process, pleural reaction should be considered. The fluid aspiration should be stopped immediately, the patient should be in supine position, and if necessary, 0.5ml of 0.1% epinephrine should be injected subcutaneously. The condition and blood pressure changes should be closely observed. Generally, after aspiration of the pleural effusion, it is not necessary to inject anti-tuberculosis drugs into the pleural cavity, but urokinase or streptokinase can be injected to prevent pleural adhesion.
The treatment principle of tuberculous pleurisy is the same as that of active pulmonary tuberculosis, and early anti-tuberculosis treatment is particularly important.
The efficacy of glucocorticoids is not certain. If the systemic symptoms are severe and there are large amounts of pleural effusion, glucocorticoids can be added to anti-tuberculosis treatment. Common treatment is prednisone 20 - 30mg/d. When the body temperature returns to normal, the systemic symptoms are reduced or absent, and the amount of pleural effusion is significantly reduced, the dose should be gradually reduced until discontinuation. The general course of treatment is 4 - 6 weeks.
In the treatment of tuberculous empyema, pyopneumothorax, and pleural bronchial fistula, most patients require surgical treatment. Preoperative closed thoracic drainage can be performed while systemic treatment is in progress to gradually reduce its area and create conditions for pleurectomy or pneumonectomy.
Malignant pleural effusion
The primary disease and pleural effusion should be treated. The most common causes of malignant pleural effusion are lung cancer and breast cancer. Active treatment of the primary tumor (chemotherapy, targeted therapy, application of anti-angiogenic drugs, immunotherapy, and radiotherapy) has a certain effect. Pleural effusion is mostly a complication of advanced malignant tumors. If patients have no symptoms of dyspnea, pleural effusion drainage is not necessary, and close follow-up can be conducted while treating the primary tumor. If patients have dyspnea, thoracentesis and drainage are recommended to help clarify whether the symptoms are related to the pleural effusion and determine whether the lung can be reexpanded. In patients whose lungs can be reexpanded, either thoracic catheter drainage or pleurodesis can be first-line treatment. In patients whose lungs cannot be reexpanded, thoracic catheter drainage is preferred.
Chemotherapeutic drugs, anti-angiogenic drugs, and biological agents can be injected into the thoracic cavity to help control the effusion. Common chemotherapeutic drugs include cisplatin and lobaplatin. Anti-angiogenic drugs include recombinant human vascular endothelial inhibitor and bevacizumab. Biological agents include IL-2, tumor necrosis factor, interferon, and tumor-infiltrating lymphocytes.