Pleural Thickening: Etiology, Radiologic Assessment, and Surgical Management

2.1.1. Inflammatory/infectious

Infections are a leading cause of benign pleural thickening. The inflammatory response to various pathogens can lead to fibrin deposition and subsequent fibrosis of the pleural layers. Empyema, a collection of pus in the pleural space, is a particularly potent cause of significant pleural thickening [1]. Organizing empyema, if inadequately drained, leads to fibroblast-driven collagen deposition and the formation of a dense fibrous pleural peel (fibrothorax) that encases the lung, causing a “trapped lung” and severe restrictive dysfunction [4, 7, 8].

The most common cause of chronic diffuse pleural thickening (DPT) is parapneumonic empyema or complicated pleural infection, where inadequate drainage leads to fibrous peel formation (fibrothorax) that restricts lung expansion [4, 9]. Tuberculous pleurisy remains a significant global cause of pleural disease, often presenting as exudative effusion that can resolve with residual thickening and calcification. Studies have reported that 10–72% of patients develop such sequelae despite standard anti-TB therapy [10]. Other infections, including fungal empyema and chronic hemothorax with organizing clots, can similarly produce a dense fibrous pleural rind as a healing response. In post-infectious cases, pleural thickening is typically diffuse, often associated with calcifications and hemithorax volume loss (trapped lung), features that radiologically favor a benign etiology [4, 9].

2.1.2. Trauma and surgery

Trauma and post-pleural injury syndromes, such as hemothorax or post-surgical pleuritis, are common causes of pleural thickening. Blood in the pleural space triggers inflammation and fibrin deposition; if not fully evacuated, it can organize into a dense fibrous peel, often causing localized thickening that may require surgical decortication to restore lung function [11, 12].

2.1.3. Asbestos-related benign pleural disease

Asbestos exposure is a well-established cause of various pleural abnormalities, including benign pleural thickening. This can manifest in several ways.

Pleural plaques: Pleural plaques are the most common benign manifestation of asbestos exposure, appearing as discrete, circumscribed areas of hyalinized collagen on the parietal pleura, typically along the ribs or diaphragm [2, 13]. They often calcify over time and are usually asymptomatic, serving as a biomarker of prior asbestos inhalation without malignant potential. On imaging, they present as focal pleural thickening and therefore enter the differential diagnosis for pleural thickening; their prevalence has been reported to be 1.5% in CT-based cohort studies and up to 50–60% among heavily exposed individuals [2, 4, 13].

Diffuse pleural thickening (DPT): In contrast to plaques, DPT is a more extensive, often non-calcified fibrotic reaction that primarily affects the visceral pleura and can extend to the parietal pleura, resulting in the fusion of pleural layers [2, 14]. DPT commonly develops following a benign asbestos-related pleural effusion, with epidemiologic data indicating that approximately 5–14% of exposed individuals develop sufficient thickening to obliterate the costophrenic angles on chest radiography [2]. Unlike plaques, DPT can cause significant restrictive lung disease and dyspnea, particularly when widespread and circumferential, owing to chronic inflammation and progressive fibrosis in response to inhaled asbestos fibers.

Benign asbestos pleural effusion (BAPE): BAPE can resolve with residual pleural thickening. It is often the earliest manifestation of asbestos-related pleural disease and can occur several years after exposure.

Benign asbestos-related pleural diseases, including plaques, diffuse thickening, and round atelectasis, warrant evaluation for coexisting asbestosis and mesothelioma. They typically present as bilateral smooth thickening or calcified plaques without invasive features but can mimic tumors on imaging.

2.1.4. Drug-induced pleural thickening

Certain medications can induce pleural reactions, including effusions and subsequent pleural thickening. Historically, methysergide has been associated with retroperitoneal and pleural fibrosis. More recently, drugs such as amiodarone, methotrexate, and some beta-blockers have been implicated in drug-induced pleurisy, which can lead to pleural thickening [15]. The mechanism often involves a hypersensitivity reaction or direct toxicity to the pleura.

2.1.5. Drug-induced pleural thickening

Connective tissue diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), can cause pleuritis that leads to chronic pleural thickening. Rheumatoid pleurisy, more common in middle-aged men with longstanding seropositive RA, may produce exudative effusions that organize into fibrous scars, sometimes showing granulomas and a characteristic “gritty” pleura on thoracoscopy [16, 17]. Recurrent effusions can cause diffuse thickening and occasional calcification, whereas SLE-related pleuritis may result in similar chronic pleural changes, albeit less frequently.

2.1.6. Other rare causes

Uremic pleuritis: Seen in patients with renal failure, it often resolves with dialysis but can leave residual thickening.

Post-radiation pleuritis: Thoracic radiation therapy is a known iatrogenic cause of localized pleural thickening. Patients treated with radiation for breast cancer, lung cancer, or lymphoma often develop unilateral pleural fibrosis within the irradiated field years later [4].

Spontaneous pneumothorax: Recurrent spontaneous pneumothorax can lead to localized pleural adhesions and thickening due to the inflammatory response to air in the pleural space.

Familial mediterranean fever (FMF): This genetic disorder can cause recurrent episodes of serositis, including pleuritis, which may result in chronic pleural thickening [18].

Benign tumors and tumor-like conditions: Certain benign neoplasms or tumor-like processes can appear as pleural thickening on imaging. The most notable is the solitary fibrous tumor of the pleura (SFTP), a mesenchymal neoplasm previously termed benign pleural fibroma or localized fibrous mesothelioma. Approximately 80% of SFTPs are benign and typically present as well-defined, focal pleural-based masses that may produce an obtuse angle with the chest wall on imaging but do not encase the lung. They are often incidental findings, although larger lesions can cause symptoms such as cough, chest pain, or paraneoplastic syndromes, such as hypertrophic osteoarthropathy or hypoglycemia (Doege–Potter syndrome) [4].

In benign conditions, pleural thickening is usually diffuse and smooth rather than nodular, can be unilateral or bilateral, and often shows signs of volume loss, such as an elevated hemidiaphragm or rib crowding if chronic [4]. Calcifications strongly suggest a benign process, particularly post-tuberculous or old empyema [4, 19]. A history of prior infection or asbestos exposure supports this diagnosis. Recognizing benign thickening helps avoid unnecessary invasive procedures, although a biopsy may still be needed to rule out early malignancy.

2.2.1. Malignant pleural mesothelioma (MPM)

MPM is the most concerning cause of DPT. It is an aggressive neoplasm strongly linked to asbestos exposure, with approximately 80% of cases having significant exposure and a latency of 30–50 years [1, 3, 4, 21]. Although rare, its incidence remains notable worldwide due to past industrial asbestos use, causing approximately 30,000 new cases annually [3]. MPM typically presents in older adults with diffuse, nodular, circumferential pleural thickening that encases the lung, mediastinum, and diaphragm, often accompanied by a large effusion, chest pain, dyspnea, and weight loss [22]. Pathologically, it spreads diffusely along the pleura, forming a rind, with three subtypes: epithelioid (most common), sarcomatoid, and biphasic. Imaging, especially CT and positron emission tomography (PET-CT), is key for suspicion; features include circumferential nodular thickening >1 cm, mediastinal and diaphragmatic involvement, and possible invasion of adjacent structures. However, early disease can mimic benign fibrosis; therefore, a definitive diagnosis requires biopsy. Other risk factors include prior chest irradiation, chronic tuberculous pleuritis, and rare genetic mutations (e.g., BAP1). The prognosis remains poor, with a median survival of approximately 12–18 months [1, 3, 4].

2.2.2. Metastatic pleural disease

Metastatic pleural involvement is far more common than mesothelioma and is the leading cause of malignant pleural effusions, often presenting with pleural thickening. Common primary cancers include lung, breast, ovarian, and gastrointestinal cancers [23, 24]. Metastatic pleural thickening can be focal or diffuse, nodular, and is typically accompanied by effusion and sometimes lymphadenopathy. Imaging often shows multiple discrete nodules or irregular thickening, unlike the symmetric circumferential rind of mesothelioma. For example, lung adenocarcinoma metastases tend to form discrete pleural implants, whereas breast cancer may cause diffuse thickening with effusion but less uniform visceral pleural involvement. Elevated carcinoembryonic antigen (CEA) levels in pleural fluid or blood favor metastatic adenocarcinoma over mesothelioma, which usually does not raise CEA [24]. Accurate distinction is crucial, as management aligns with the primary cancer and often requires immunohistochemistry (IHC) on biopsy.

2.2.3. Lymphoma

Beyond mesothelioma, the pleura can rarely harbor other primary malignancies. Primary pleural lymphoma, often linked to chronic empyema or pyothorax (pyothorax-associated lymphoma), may present as mass-like thickening, typically in immunocompromised patients. Both Hodgkin and non-Hodgkin lymphomas can involve the pleura, causing effusions and nodular or diffuse thickening, usually requiring biopsy for diagnosis.

Other rare primaries include pleural sarcomas (e.g., angiosarcoma, synovial sarcoma), diffuse pleural spread of thymoma or germ cell tumors (sometimes called “drop metastases”), and pleural epithelioid hemangioendothelioma – a vascular tumor of intermediate malignancy. These entities are uncommon and are diagnosed only after excluding more frequent causes with histopathologic confirmation.

In summary, malignant pleural thickening is most often due to diffuse malignant mesothelioma or metastatic carcinomatosis. Radiologically, features favoring a malignant cause include nodular pleural thickening exceeding 1 cm in thickness, circumferential involvement of the hemithorax, involvement of the mediastinal pleural surface, and extension into the fissures or chest wall [4, 21]. The presence of a concomitant pleural effusion is common in malignancy (although benign effusions can coexist with inflammation as well). Because clinical and radiographic findings can overlap between benign and malignant causes, tissue biopsy is usually required for definitive diagnosis when malignant disease is suspected. The following sections will delve into the imaging characteristics that help differentiate these etiologies and the diagnostic procedures used to obtain tissue for histopathologic evaluation.

3.1.1. Chest radiography (X-ray)

Chest radiography is often the first imaging modality for detecting pleural disease but has limited sensitivity for assessing pleural thickening [1, 9, 20]. Diffuse thickening may appear on a posteroanterior (PA) radiograph as a smooth, continuous pleural density extending over at least 25% of the chest wall, with possible blunting or obliteration of the costophrenic angle that does not shift with patient position, indicating fibrosis rather than fluid [4, 25]. Focal calcified plaques can be seen as curvilinear opacities along the ribs, diaphragm, or lateral chest wall, while an apical cap is common with aging; however, thickening over ~2 cm should raise suspicion for prior tuberculosis or malignancy.

A classic radiographic clue is the “extrapleural sign,” where a pleural-based lesion creates an opacity with smooth, tapered margins forming obtuse angles with the chest wall, suggesting a pleural or extrapleural origin rather than a parenchymal mass. Both benign and malignant processes can produce this sign; for example, a chronic calcified empyema or a pleural tumor [4]. However, chest radiography often underestimates the true extent of thickening and cannot reliably distinguish benign from malignant causes. Small nodules (<5 mm) may be entirely missed, and diffuse thickening from mesothelioma may mimic fibrotic changes from old TB empyema. Therefore, significant pleural abnormalities on radiography should prompt further cross-sectional imaging for definitive characterization [20, 21].

3.1.2. Computed tomography (CT)

Chest CT is the gold-standard imaging modality for the detailed assessment of pleural thickening [22]. It provides high-resolution cross-sectional images that allow precise evaluation of pleural thickness, extent, morphology, and relationship with adjacent structures [22]. Key features assessed on CT include the following [4, 19, 21, 22, 26–28]:

Location and extent: CT differentiates between localized and diffuse thickening and identifies involvement of the parietal, visceral, diaphragmatic, and mediastinal pleura. The normal pleura is only approximately 1–2 mm thick, and any visible thickening suggests pathology.

Morphology: CT distinguishes smooth, uniform thickening (more typical of benign fibrosis) from nodular or irregular thickening, which is concerning for malignancy. Nodules >1 cm, circumferential encasement of the lung, and mediastinal pleural involvement strongly suggest malignancy, particularly mesothelioma.

Calcification: The pattern of calcification helps identify benign causes, such as asbestos plaques or old empyema. Chronic benign thickening often shows associated pleural calcification.

Associated findings: CT can identify associated pleural effusions, parenchymal lung abnormalities, lymphadenopathy, and chest wall invasion, all of which are crucial for differential diagnosis.

Benign versus malignant patterns: Malignant pleural disease (e.g., mesothelioma) typically shows nodular or irregular thickening >1 cm, circumferential pleural rind encasing the lung, mediastinal pleural surface involvement, fissure and chest wall invasion, and enhancement after IV contrast. Benign thickening usually appears smooth and uniform, less than ~10 mm thick except in localized areas, spares the mediastinal pleura or shows mild involvement, displays volume loss, rib crowding, diaphragmatic elevation, and may exhibit the “extrapleural fat sign”—hypertrophy of extrapleural fat adjacent to chronic fibrosis. Quantitative criteria such as continuous thickening >5 cm in length, >8 cm vertically, and >3 mm thick can support a benign diagnosis but are not absolute.

Role in biopsy and staging: CT is essential for planning image-guided pleural biopsies, targeting areas of maximum nodularity or thickness. Non-contrast CT can detect subtle pleural changes in high-risk patients (e.g., asbestos exposure), whereas contrast-enhanced CT better characterizes suspicious lesions and enhancement patterns. For mesothelioma, CT helps to stage local tumor spread (T stage) and assess nodal involvement.

Limitations: CT may underestimate chest wall or diaphragmatic invasion due to limited soft tissue contrast and may miss small metastases. There is also inter-observer variability in interpreting subtle pleural changes, reinforcing the need for correlation between clinical history and other modalities.

3.1.3. Magnetic resonance imaging (MRI)

MRI offers excellent soft tissue contrast and is increasingly utilized in the evaluation of pleural thickening, particularly when differentiating between benign and malignant etiologies, assessing chest wall invasion, or evaluating diaphragmatic involvement [28]. MRI can provide functional information through diffusion-weighted imaging (DWI) and dynamic contrast-enhanced (DCE) sequences, which can help distinguish between active tumors and fibrous tissue. Although not routinely used as a first-line imaging modality for pleural thickening, MRI is valuable in specific scenarios, such as in patients with contraindications to iodinated contrast or when a detailed assessment of soft tissue invasion is required.

3.1.4. Ultrasound

Thoracic ultrasound is a readily available, non-invasive, and radiation-free imaging modality that is highly valuable for the assessment of pleural diseases [20]. It is particularly useful for the following reasons:

Detection of pleural effusions: Ultrasound can detect small pleural effusions, even those not visible on chest X-ray, and characterize their nature (e.g., anechoic, septated, complex).

Guidance for procedures: It is indispensable for guiding thoracentesis and pleural biopsy, minimizing the risks of complications.

Assessment of pleural thickening: Ultrasound can visualize pleural thickening and assess its vascularity using Doppler. Although less precise than CT for detailed morphologic characterization, it can identify nodularities or masses on the pleural surface and differentiate between fluid and solid components [29].

3.1.5. Positron emission tomography (PET-CT)

PET-CT, typically performed with 18F–fluorodeoxyglucose (FDG), provides functional metabolic information that complements anatomical imaging in the evaluation of pleural thickening [4, 21, 30].

Differentiating benign versus malignant: Malignant pleural lesions show increased glucose metabolism and, therefore, high FDG uptake (The maximum standardized uptake value [SUVmax]), whereas benign fibrous thickening generally has low or absent uptake. Qualitative and quantitative PET analysis can help distinguish tumors from scar tissue; for example, SUVmax values above 2.0–2.5 may suggest malignancy. However, false positives can occur because of inflammation (e.g., post-talc pleurodesis), and some early-stage mesotheliomas may have low uptake, risking false negatives.

Staging: PET-CT is highly valuable in staging MPM and metastatic pleural disease by detecting nodal and distant metastases, which is essential for treatment planning and surgical decision-making. Pre-operative workups are routinely recommended to avoid futile surgeries in patients with unresectable disease.

Guiding biopsy: Areas of high metabolic activity can guide targeted biopsies, improving diagnostic yield by sampling the most suspicious sites.

Monitoring treatment response: Changes in FDG uptake can reflect the metabolic response earlier than visible size changes on CT, aiding in therapy monitoring.

Limitations: While PET/CT enhances diagnostic confidence, it cannot alone confirm or exclude malignancy due to overlapping uptake in inflammation and cancer. Findings must always be interpreted in the context of other imaging, clinical history, and histopathology [21, 31].

3.2.1. Imaging features suggestive of malignancy

Nodularity: The presence of discrete nodules or irregular, lumpy thickening within the pleura is a strong indicator of malignancy, particularly in the context of mesothelioma or metastatic disease [1].

Circumferential thickening: Involvement of the entire circumference of the pleura encasing the lung is highly suggestive of MPM [22]. DPT is defined as thickening of the pleura (>5 mm) with a combined area of involvement [4].

Mediastinal pleural involvement: Thickening of the mediastinal pleura, especially if nodular, is a concerning sign of malignancy.

Parietal and visceral pleural involvement: Malignant processes often involve both layers of the pleura, leading to a rind-like appearance.

Associated pleural effusion: While benign conditions can cause effusions, a large, rapidly reaccumulating, or hemorrhagic effusion in conjunction with pleural thickening raises suspicion for malignancy.

Chest wall or diaphragmatic invasion: Direct extension of pleural thickening into the chest wall, diaphragm, or mediastinal structures is a definitive sign of malignancy.

Contralateral pleural involvement: While less common, bilateral malignant pleural thickening can occur with metastatic disease.

High FDG uptake on PET-CT: As discussed, increased metabolic activity on PET-CT is a strong indicator of malignancy.

3.2.2. Imaging features suggestive of benignity

Smooth, non-nodular thickening: Benign thickening often appears smooth and uniform, without discrete nodules.

Localized thickening: Benign processes tend to cause localized thickening, such as apical caps or focal areas related to prior inflammation.

Calcification: The presence of calcification, particularly in the form of discrete pleural plaques or diffuse calcification from old empyema or TB, is characteristic of a benign etiology [13]. However, calcification rarely occurs in mesothelioma.

Stable appearance over time: Benign pleural thickening typically remains stable or shows slow progression over long periods, whereas malignant thickening often demonstrates rapid progression.

Absence of associated mass or lymphadenopathy: The lack of a discrete pleural mass or regional lymph node involvement favors a benign process.

Radiologic findings can strongly suggest the cause of pleural thickening but are not definitive. Histopathologic evaluation of pleural tissue remains the gold standard for differentiating benign from malignant processes and for diagnosing specific conditions such as tuberculosis or distinct tumor types. Therefore, pleural biopsy, which provides tissue for histologic and sometimes microbiologic analysis, is essential when imaging and clinical features raise the suspicion of malignancy or when the etiology is unclear. This section outlines biopsy techniques, characteristic histopathologic features of major causes, and the role of ancillary tests such as IHC and molecular markers in diagnosis.

5.1.1. Diagnostic purposes

When imaging and less invasive procedures (e.g., thoracentesis and closed pleural biopsy) fail to yield a definitive diagnosis, surgical biopsy becomes necessary. VATS is the gold standard for obtaining adequate pleural tissue for histopathologic examination, particularly in cases of suspected malignancy (e.g., mesothelioma, metastatic disease) or chronic inflammatory conditions where a specific diagnosis is elusive [35]. VATS allows for direct visualization of the pleura and targeted biopsies of suspicious areas and often provides a larger tissue sample than percutaneous methods.

5.1.2. Therapeutic purposes

Therapeutic indications for the surgical management of pleural thickening primarily aim to alleviate symptoms, restore lung function, or remove diseased tissue.

Symptomatic relief: Significant pleural thickening, especially DPT, fibrothorax, or organized empyema, can cause severe dyspnea due to restrictive lung physiology. Surgical decortication can free the trapped lung, allowing it to re-expand and improve respiratory mechanics (e.g., vital capacity <50–70% predicted) [6–8]. Decortication removes the inelastic fibrous peel, allowing full lung re-expansion and symptomatic relief.

Lung re-expansion: In cases of trapped lung secondary to organized hemothorax or empyema, the fibrous peel prevents the lung from re-expanding. Decortication is performed to remove the peel and facilitate full lung expansion [8].

Tumor debulking/resection: In MPM, surgery aims for macroscopic complete resection (MCR) of visible tumors as part of a multimodality treatment plan that includes chemotherapy and/or radiotherapy [36]. Surgery alone is not curative because of microscopic spread; however, cytoreduction can improve local control, symptom relief, and possibly survival in selected patients. Pleurectomy/decortication (P/D) and extrapleural pneumonectomy (EPP) are the principal surgical options, with P/D now preferred in many centers due to lung preservation and lower morbidity [19, 20].

Management of recurrent pleural effusions: While not directly treating thickening, pleurodesis or placement of indwelling pleural catheters (IPCs) controls recurrent effusions often associated with pleural malignancy or chronic exudates. Pleurodesis induces pleural adhesion to obliterate the pleural space and prevent fluid reaccumulation [37]. IPCs allow outpatient drainage, improving the quality of life in patients unfit for surgery [33].

5.2.1. Thoracentesis and pleural drainage (brief mention for context)

While not strictly surgical management of thickening, thoracentesis (diagnostic or therapeutic) and chest tube drainage are often the initial steps in managing pleural effusions that may lead to or be associated with pleural thickening. They are crucial for fluid analysis and temporary symptom relief but do not address the underlying thickening directly [15].

5.2.2. Video-assisted thoracoscopic surgery (VATS)

VATS has revolutionized thoracic surgery, offering a minimally invasive approach for both diagnostic and therapeutic interventions for pleural diseases. For pleural thickening, VATS is widely used for:

Diagnostic biopsy: As mentioned, VATS provides excellent visualization and allows for multiple targeted biopsies, significantly increasing diagnostic yield compared to blind or image-guided percutaneous biopsies [38].

Pleurodesis: Chemical or mechanical pleurodesis can be performed via VATS to prevent the recurrence of pleural effusions, particularly in malignant cases. This involves inducing inflammation and adhesion between the parietal and visceral pleura [39].

Decortication/debridement: In early or localized cases of organized empyema or hemothorax, VATS can be used for debridement and removal of fibrinous material, facilitating lung re-expansion [12].

Advantages of VATS include smaller incisions, reduced pain, shorter hospital stays, and faster recovery compared to open thoracotomy.

5.2.3. Decortication

Decortication involves the surgical removal of the dense fibrous pleural peel that restricts lung expansion and is indicated for symptomatic trapped lung in chronic empyema, organized hemothorax, or fibrothorax. It can be performed via VATS for early-stage disease or open thoracotomy for dense, mature peels [7, 40, 41]. Outcomes are excellent: lung function typically improves by approximately 10–15% in forced expiratory volume in the first second/forced vital capacity (FEV₁/FVC, Tiffeneau-Pinelli index), with >90% achieving full re-expansion in well-selected patients. Mortality is low (<2% in modern series) [7, 8, 41].

5.2.4. Pleurectomy

Pleurectomy involves the surgical removal of the pleura. It can be partial or complete, involving either the parietal pleura (lining the chest wall) or the visceral pleura (covering the lung), or both. This is often performed in the context of the following:

Recurrent pleural effusions: Parietal pleurectomy can be performed to achieve permanent pleurodesis and prevent fluid reaccumulation, particularly in benign recurrent effusions or when chemical pleurodesis has failed.

Malignant pleural mesothelioma (MPM): Pleurectomy is a key component of the surgical management of MPM [36]. Parietal pleurectomy involves the removal of the parietal pleura, while visceral pleurectomy involves stripping the visceral pleura from the lung surface. In many cases of MPM, extended P/D is performed, which involves the removal of both parietal and visceral pleura, along with any gross tumor, from the lung, diaphragm, and pericardium, while preserving the lung [42]. This procedure aims to achieve complete macroscopic resection of the tumor.

5.2.5. Extrapleural pneumonectomy (EPP) and pleurectomy/decortication (P/D) in malignant pleural mesothelioma (MPM)

For patients with MPM, two main surgical approaches are considered for curative intent [36]:

Extrapleural Pneumonectomy (EPP): This is a radical procedure involving en bloc removal of the ipsilateral lung, parietal and visceral pleura, ipsilateral diaphragm, and pericardium. EPP aims for complete microscopic resection and is associated with significant morbidity and mortality. It is typically reserved for highly selected patients with early-stage disease, good performance status, and no evidence of nodal or distant metastases [43].

Pleurectomy/decortication (P/D): As described above, P/D is a lung-sparing procedure that involves the extensive removal of all macroscopic tumors from the pleura, diaphragm, and pericardium, while preserving the lung. P/D is generally associated with lower morbidity and mortality than EPP and is increasingly favored, especially for patients who may not tolerate EPP or have more advanced disease where lung preservation is desirable. The goal of P/D is MCR, which has been shown to improve survival in selected patients [40]. In one study, P/D had a median 30-day mortality of 2.2% and a median overall survival of 21 months [44].

Both EPP and P/D are typically part of a multimodal treatment strategy that includes chemotherapy and/or radiation therapy.

5.2.6. Other surgical considerations

Pleurodesis: This procedure induces adhesion between the parietal and visceral pleura to obliterate the pleural space and prevent fluid reaccumulation. It can be achieved chemically (e.g., talc slurry, doxycycline) or mechanically (e.g., pleural abrasion during VATS). It is commonly used for recurrent malignant pleural effusions [39].

Indwelling pleural catheters (IPCs): For patients with recurrent symptomatic pleural effusions who are not candidates for pleurodesis or more invasive surgery, IPCs offer a palliative option for outpatient drainage and symptom control. While not a surgical treatment for thickening, they manage the associated effusion [34].