Mesothelioma and other pleural tumours

• Malignant pleural mesothelioma (MPM) is an aggressive cancer of the pleura, the serous membrane that lines the chest wall and covers the lung. It is overwhelmingly a disease of people exposed to asbestos fibres.
• It usually announces itself slowly, years after exposure, with breathlessness or chest pain from a pleural effusion, often bloody, together with loss of weight and sweating. There is no early warning sign that patients notice on their own.
• A chest radiograph followed by contrast CT of the thorax is the first imaging; the diagnosis rests on pleural tissue, and thoracoscopy is the preferred way to obtain it where an effusion is present.
• Under the microscope MPM is epithelioid (the commonest form), biphasic (about 10 to 15% of cases) or sarcomatoid, and the subtype drives both prognosis and the choice of surgery. Rare localized forms can be cured by excision, but diffuse MPM is not. ^[4][5]
• For fit patients with unresectable disease, current first-line options are cisplatin plus pemetrexed (with folic acid and vitamin B12 support) or nivolumab plus ipilimumab; surgery is no longer radical pneumonectomy by default, and the outlook overall remains poor.

By the end of this page you should be able to:

1. Explain the link between asbestos and mesothelioma, including dose, latency and the types of fibre.
2. Recognise the pleural presentation of mesothelioma and plan a diagnostic pathway from effusion to tissue.
3. Interpret pleural fluid cytology, immunohistochemistry and CT or PET-CT findings in suspected MPM.
4. Describe the 2015 WHO histological subtypes and what the subtype implies for prognosis and treatment.
5. Apply the 8th edition TNM staging system as revised by the IASLC and IMIG.
6. Weigh first-line cisplatin plus pemetrexed against nivolumab plus ipilimumab and know the supportive measures each requires.
7. Offer patients accurate information about compensation, palliative care and follow-up.
8. Outline the rare other primary and secondary tumours of the pleura and how they differ from MPM.

Malignant pleural mesothelioma is one form of pleural tumour. By contrast, metastatic cancer to the pleura is far commoner overall, and a handful of rare primary pleural tumours (localized mesothelioma, solitary fibrous tumour and other spindle-cell lesions) also occur. These are discussed in the section on other pleural tumours.

Classification by histology (2015 WHO classification of tumours of the lung, pleura, thymus and heart) divides diffuse MPM into three principal subtypes ^[1][4]:

• Epithelioid (about 60 to 80% of cases): the commonest form. The cells resemble epithelium; numerous architectural patterns (solid, tubulopapillary, tubular, trabecular, micropapillary, adenomatoid, microcystic, clear-cell, transitional, pleomorphic) may be seen, and more than one pattern is usual ^[4][5].
• Sarcomatoid (under 10% of cases): spindle cells in an infiltrative pattern. A special form, desmoplastic mesothelioma, contains at least 50% dense hyalinized stroma between bland tumour cells and occurs in under 2% of patients ^[4].
• Biphasic (10 to 15% of diffuse cases): at least 10% epithelioid and at least 10% sarcomatoid component, with an intermediate prognosis ^[4].

Two rare localized forms behave differently from diffuse MPM and are worth recognising ^[4]:

• Localized malignant mesothelioma, a solitary nodular lesion without diffuse pleural involvement, with epithelioid, sarcomatoid or biphasic histology. It has a much better prognosis than diffuse MPM and may be curable by complete excision.
• Well-differentiated papillary mesothelioma (WDPM), an exceptionally rare pleural tumour of bland papillary epithelioid cells, usually with very indolent behaviour. It must be distinguished from diffuse epithelioid MPM with a papillary pattern.

The AJCC 8th edition staging system applies to diffuse malignant pleural mesothelioma only; localized mesothelioma and other primary pleural tumours are not staged by it ^[5].

Malignant pleural mesothelioma is rare but has been increasing in the countries that used asbestos heavily in the mid twentieth century. In the UK, mesothelioma was systematically recorded from the late 1960s, and current projections expect about 2,500 deaths per year for the rest of this decade before numbers begin to fall ^[1]. In 2014, pleural mesothelioma accounted for 2,179 of 2,249 mesothelioma cases (97%) diagnosed in the UK, with 70 peritoneal cases (about 3%) ^[1].

Epidemiological points that clinicians need ^[1][5]:

• Sex. About 83 per cent of patients are male, reflecting occupational exposure; women are usually exposed para-occupationally or environmentally. ^[1]
• Age. Median age at diagnosis in the UK is 73 years. ^[1]
• Asbestos attribution. Eighty-five per cent of male mesotheliomas are attributable to occupational asbestos exposure in the UK; in North American series a history of asbestos exposure is reported in about 70 to 80 per cent of cases. The difference in the two figures is best read as regional variation in how exposure is assessed, not as disagreement about causation ^[1][5].
• Incidence. In the UK, 8,740 cases were seen in hospitals in England and Wales between 2008 and 2012; 67 per cent received active anticancer treatment (chemotherapy, radiotherapy or surgery). ^[1]
• Survival. Overall median survival in that UK cohort was 9.5 months, with 1-year and 3-year survival rates of 41 and 12 per cent. ^[1]
• Side. The right hemithorax is affected more often, by a ratio of about 1.6 to 1, possibly reflecting the larger pleural surface area ^[1].
• Bilateral pleural disease is rare, accounting for as few as 3 per cent of cases; a pleural effusion is present on the affected side in about 94 per cent of cases of pleural malignancy ^[2]. ^[1]

Regional variation matters. Death rates in countries that banned asbestos early are now falling, while countries still using or recycling asbestos (and countries with weak industrial regulation) are seeing rising or under-recognised incidence. ^[5]

The overwhelming cause of malignant pleural mesothelioma is inhalation of asbestos fibres. The fibres deposit in the distal parenchyma, migrate to the pleura, and produce repeated low-grade inflammation and mesothelial injury over decades. The outline below is the practical content a clinician needs ^[1][5]:

• Fibres. The amphibole fibres (blue crocidolite and brown amosite asbestos) carry a higher risk than serpentine chrysotile (white asbestos, the commonest form). No form is safe. ^[1]
• Dose and latency. Risk is related to cumulative fibre burden but there is no threshold below which the risk is zero. The latency between first exposure and disease is very long: about 40 years for pleural and 46 years for peritoneal disease, and typically 30 to 40 years overall. Disease can appear decades after a brief exposure, including Para-occupational exposure ^[1].
• High-risk occupations. Historic production of asbestos sheeting, brake and clutch linings, construction and demolition, shipbuilding and ship repair, insulation work, boiler repair, carpentry, electrical work, plumbing, and laundering of contaminated clothing. For British men born in the 1940s, more than 10 years of work before age 30 carried a predicted lifetime risk of 5.9 per cent for carpenters, 2 per cent for plumbers, electricians and painters, and 0.8 per cent for other construction workers ^[1].
• Non-occupational exposure. Living with a contaminated worker (Para exposure), living near an asbestos plant, and environmental contamination all occur ^[1].
• Genetic susceptibility. Rare familial cases are linked to germline mutation of BAP1 (BRCA-associated protein 1), an autosomal dominant tumour-predisposition gene. These carriers also develop uveal melanoma, renal cell carcinoma, and other malignancies. WDPM can also carry germline BAP1 mutation ^[1][4].

• Simian virus 40 (SV40) contaminating early polio vaccine was once believed to cause mesothelioma; this has not held up in human studies and should not be attributed.
• Radiation (therapeutic irradiation of the thorax) and chronic pleural inflammation are reported but very rare.
• Erionite (a naturally occurring fibre) accounts for clusters of disease in some regions (for example, parts of Turkey).

Everything the disease does follows from three facts: asbestos fibres are biopersistent in the pleura, the pleura has a huge surface area with lymphatic stomata that concentrate fibres, and mesothelial cells are easily pushed into proliferation and genomic instability.

1. Fibre deposition. Inhaled fibres migrate from terminal airspaces along lymphatic routes to the parietal pleura, where they lodge at stomatal openings. Local reactive oxygen species and macrophage frustration produce chronic inflammation.
2. Mesothelial transformation. Repeated injury drives mesothelial proliferation. Key genomic events include loss of CDKN2A/p16 (in most epithelioid and many sarcomatoid tumours), loss of BAP1 (in a proportion, often the epithelioid form), and NF2/Merlin mutations. Unlike many solid cancers, MP has few druggable driver mutations, which is why targeted therapy has been slow to arrive ^[4].
3. Pleural effusion. Tumour seedlings and reactive fibrosis obstruct lymphatic drainage of the pleura, and tumour-related vascular permeability produces an exudative, often heavily blood-stained effusion. The effusion is the presenting feature in the great majority of patients and explains the breathlessness.
4. Local invasion rather than distant spread. Early disease spreads diffusely along pleural surfaces and invades locally (chest wall, diaphragm, mediastinum). Distant metastases occur later, particularly in the sarcomatoid form, which has a high rate of metastasis at diagnosis ^[4].
5. Immunology. MPM modulates the immune microenvironment; programmed death-ligand 1 (PD-L1) expression is more common in sarcomatoid and biphasic disease and is associated with poorer survival ^[4].

Symptoms are nonspecific and develop insidiously. Chest pain and dyspnoea are the commonest presenting symptoms; other symptoms include weight loss, fever and sweats ^[1]. Patients rarely arrive early. Typical features:

• Dyspnoea on exertion, the commonest symptom, from the effusion and from the rigid, entrapped lung.
• Chest wall pain, often described as a nagging, vague ache that is hard to localize; it arises from chest-wall invasion rather than from obstruction.
• Systemic symptoms of weight loss, sweats and fatigue.
• Cough, usually mild.
• A history of occupational or Para-occupational asbestos exposure, often decades earlier. A thorough occupational history covering every occupation throughout life, including relatives' and partners' occupations, is essential ^[1].

• Physical signs of a pleural effusion: stony dullness to percussion, reduced breath sounds, and reduced expansion on the affected side.
• Pleural mass or thickened pleura: may be palpable or visible.
• Fixed chest wall: reduced expansion that does not improve with drainage.
• Digital clubbing, lymphadenopathy or finger clubbing are uncommon and should suggest other diagnoses such as lung cancer ^[1].
• The right side is affected more often (ratio about 1.6 to 1) ^[1].

• A pleural effusion in an older adult with any asbestos exposure, particularly one that is blood-stained, exudative and persistent, should be treated as malignant until proven otherwise.
• Chest-wall pain that is poorly controlled suggests invasion and unresectability.
• Rapid unilateral findings in a previously well patient with known asbestos exposure can herald advanced disease.

The principal challenge is not mesothelioma versus health, but mesothelioma versus other pleural disease. The key separators:

Key principles:

• Mesothelioma is usually a unilateral exudative effusion with circumferential pleural thickening and involvement of the mediastinal pleura and interlobar fissures. A non-expandable (trapped) lung after drainage is common.
• Any unexplained unilateral pleural effusion in a person with asbestos exposure should be investigated on the assumption that it may be malignant, even with a normal CT ^[2].
• Where the imaging, clinical picture and cytology are equivocal, the diagnosis is tissue, obtained by thoracoscopy or image-guided needle biopsy ^[1][2].

No blood test diagnoses mesothelioma. Erythrocyte sedimentation rate, C-reactive protein and anaemia may be present, and interleukin-6 can be raised in constitutionally symptomatic patients ^[1]. None should guide treatment on its own.

• Chest radiograph is usually the trigger for referral. Urgent chest X-ray is offered to patients with symptoms and signs as set out in the NICE guideline for suspected cancer ^[1].
• Contrast-enhanced CT of the thorax, optimised for pleural evaluation, is the initial cross-sectional imaging of choice for diagnosis and staging. It shows pleural thickening (often more than 1 cm, nodular, mediastinal), fissural thickening, effusion, chest-wall or diaphragmatic invasion ^[1].
• PET-CT is valuable where excluding distant metastases would change management; it can support diagnosis when CT or clinical features are suspicious but biopsies are negative or not feasible. It is unreliable after talc pleurodesis and in areas where tuberculosis is common ^[1].
• MRI is superior to CT where differentiating T stage (invasion through chest wall, diaphragm, mediastinal fat, pericardium) would change a management decision ^[1].
• Thoracic ultrasound guides drainage, supports the diagnosis of pleural malignancy at presentation and records whether the lung is trapped ^[2].

The BTS pleural disease (2023) and mesothelioma (2018) guidelines set out the pathway ^[1][2]:

• Pleural aspiration: send 25 to 50 mL of fluid for cytology. Sensitivity for MPM is highly variable, from 16 to 73 per cent, and depends heavily on the cytologist ^[1][2]. Cytology alone should not be relied on unless biopsy is impossible or unrequired for treatment ^[1].
• Image-guided pleural biopsy has high yield and low complication rate when CT shows a focal area of abnormal pleura ^[1].
• Thoracoscopy (local anaesthetic or VATS) is the preferred investigation where a symptomatic exudative effusion remains non-diagnostic on aspiration; it allows multiple biopsies, inspection and talc poudrage ^[1][2].
• Blind non-image-guided pleural biopsy should not be performed ^[2].
• Biopsies should be reviewed by a pathologist experienced in MPM, with a second opinion if uncertain ^[1].

• IHC is recommended on biopsy and cytology specimens. A combination of at least two positive mesothelial markers (calretinin, cytokeratin 5/6, Wilms tumour 1, D-240) and at least two negative adenocarcinoma markers (TTF1, CEA, Ber-EP4) is used in the differential. Marker performance falls in sarcomatoid MPM ^[1].
• Pancytokeratin stains positive in nearly all mesotheliomas; calretinin, D2-40, WT-1 and cytokeratin 5/6 are particularly useful in epithelioid disease ^[5].
• BAP1 loss on IHC supports malignancy and separates MPM from reactive mesothelial proliferation.
• Subtype must be reported in every case; non-epithelioid histology is associated with much shorter survival ^[1].
• Biomarkers (soluble mesothelin, fibulin-3, osteopontin) are not primary tests: serum SMRP sensitivity 60% and specificity 81%; pleural fluid SMRP 75% and 76%. They may support diagnosis in patients unfit for invasive testing ^[1].

There are no imaging or blood criteria that diagnose MPM. Diagnosis rests on compatible clinical and imaging findings, histological confirmation from adequate biopsy, and subtyping ^[1]. Where biopsy is impossible or declined, cytology plus IHC in an experienced centre can provide a diagnosis, but this is discouraged as routine ^[1].

Staging should be recorded by the 8th edition TNM, derived from the international IASLC database and accepted by IMIG, AJCC and UICC ^[1][3]:

• T1a and T1b merged into T1, removing the distinction between parietal-only and visceral pleural involvement. Pleural thickness over 5.1 mm is associated with shorter survival ^[3].
• N1 + old N2 collapsed into new N1 (all ipsilateral intrathoracic nodal stations); old N3 becomes new N2 (contralateral or supraclavicular nodes).
• Stage IV means distant metastasis (M1) only. T4 or new N2 disease without metastasis is stage IIIB ^[3].

8th edition stage groups ^[3][5]:

• CT is least reliable for T4 and N stage; MRI if T-stage assignment changes management; PET-CT if excluding distant metastasis changes management ^[1].
• Lymph nodes that would change treatment still require mediastinoscopy or EBUS-TBNA ^[1].

Staging alone predicts poorly. Validated scores (EORTC, CALGB, mGPS, LENT where effusion present, and decision tree analysis) are used for counselling, but no score should decide treatment ^[1][5]. The EORTC score uses WBC above 8.3 x 10^9/L, performance status 1 or worse, unproven histology, nonepithelioid type and male sex, and divides patients into low risk (score 1.27 or lower, 0 to 2 risk factors, 40% 1-year survival) and high risk (above 1.27, 3 to 5 factors, relative risk of death 2.9, 12% 1-year survival) ^[5]. Decision tree analysis is the most useful in routine practice ^[1].

MPM is not curable in diffuse form. Aims are symptom relief, prolongation of survival where appropriate, and quality of life. Every case should go to a regional mesothelioma MDT with sufficient case volume and a named clinical nurse specialist, with early palliative care referral ^[1].

Covered by BTS pleural (2023) and BTS mesothelioma (2018) ^[1][2]:

• Talc pleurodesis (slurry or poudrage) and indwelling pleural catheters are the standard options, chosen by patient preference. Talc is preferred over VATS partial pleurectomy ^[1][2].
• VATS partial pleurectomy should not be performed for fluid control in preference to talc ^[1].
• Offer IPC or pleurodesis first line where the lung expands; IPC is better supported with non-expandable (trapped) lung ^[2].
• In MPE, definitive pleural intervention should not be deferred until after systemic therapy ^[2].

First-line options are summarised below; details from NCI PDQ (updated 2025) and the ESMO guideline ^[5][6].

Chemotherapy. For WHO 0 to 1 performance status, cisplatin plus pemetrexed is the established backbone ^[1][5]:

• Pemetrexed 500 mg/m2 plus cisplatin 75 mg/m2 every 21 days improved median survival versus cisplatin alone (12.1 versus 9.3 months; P = 0.020; HR 0.77) and median time to progression (5.7 versus 3.9 months). ^[5]
• Folic acid (350 to 1000 micrograms daily, 1-3 weeks before the first dose until 1-3 weeks after) and vitamin B12 (1000 micrograms intramuscularly, 1-3 weeks before, every 9 weeks) are mandatory with each course; dexamethasone 4 mg twice daily surrounds pemetrexed to prevent rash. ^[5]
• Carboplatin plus pemetrexed where cisplatin is contraindicated; raltitrexed is an alternative to pemetrexed.
• Bevacizumab added to pemetrexed-cisplatin improved median OS from 16.1 to 18.8 months (HR 0.77; P = 0.0167) but with more hypertension and thrombosis. ^[5]
• Durvalumab with platinum-pemetrexed (PrE0505) reported median OS 20.4 versus 12.1 (historical control) and response 56.4%, grade 3+ toxicity 65.5%. ^[5]
• Maintenance gemcitabine after platinum-pemetrexed delayed progression (median PFS 6.2 versus 3.2 months) without significantly improving OS. ^[5]

Immunotherapy. Nivolumab plus ipilimumab is an established first-line option for unresectable MPM and an alternative to chemotherapy ^[5][6]. CheckMate 743 (605 patients) showed median OS 18.1 versus 14.1 months (HR 0.74; P = 0.002), grade 3-4 toxicity 30% versus 32%, and three treatment-related deaths ^[5]. PD-L1 is not a reliable selection biomarker in MPM; better results are sometimes seen in sarcomatoid disease ^[4].

Pemetrexed monotherapy, vorinostat and untrialled second-line chemotherapy are not recommended; second-line treatment should be offered in a trial ^[1].

• Extrapleural pneumonectomy is not recommended (operative mortality 6 to 30 per cent).
• Extended pleurectomy decortication outside a trial is not recommended.
• VATS partial pleurectomy is not superior to talc for effusion control.
• Palliative surgery (pleurectomy and decortication) can relieve effusion, pain and tumour burden, with operative mortality under 2 per cent ^[5].
• For operated patients, epithelioid histology, negative nodes and negative margins predict longer survival ^[5].

• Prophylactic radiotherapy to chest wall procedure tracts is not recommended. ^[1]
• Hemithorax and routine pre/post-operative radiotherapy are not standard.
• Palliative radiotherapy is appropriate for localised pain matching areas of underlying disease.

• Compensation matters must be raised early and often; patients and carers need accurate, understandable information about compensation because claims are time-limited ^[1].
• In the UK, a full occupational history (including relatives' and armed forces employment) should be recorded, and patients signposted to the Diffuse Mesothelioma Payment Scheme and industrial injuries benefit (within a RegionNote below).
• Review by specialist palliative care, pain teams and respiratory nurses, with 3 to 4 monthly follow-up, is standard ^[1].

• Pleural effusion and trapped lung with progressive breathlessness and loculation after drainage.
• Chest wall invasion with severe localized pain (unresectable).
• Mediastinal invasion causing dysphagia, superior vena cava obstruction, or nerve palsies.
• Distant metastasis, more common in sarcomatoid disease.
• Treatment complications: antifolate toxicity without B12/folate supplementation; bevacizumab hypertension and thrombosis; pneumonitis with immunotherapy; operative mortality with radical surgery.

Diffuse MPM remains a poor-prognosis cancer: median survival 9.5 months in the UK 2008-2012 cohort (1-year survival 41%, 3-year 12%) ^[1]. Modern first-line systemic therapy raises these figures for fit patients (median OS 18.1 months with nivolumab plus ipilimumab in CheckMate 743; 18.8 months with pemetrexed, cisplatin and bevacizumab) ^[5]. ^[6]

Consistent prognostic factors ^[4][5]:

• Histological subtype: epithelioid best, biphasic intermediate, sarcomatoid worst.
• Stage (stage I notably better than advanced stages, though precise stage-by-stage survival is uncertain in a rare cancer).
• Performance status, nodal status, epithelioid fraction in biphasic disease (under 50% epithelioid is worse), and PD-L1 expression.

• Asbestos control is the only effective prevention. There is no safe threshold for exposure; current exposure in buildings and industry must be encapsulated or removed under regulated conditions ^[1].
• No validated screening test exists. Soluble mesothelin and other candidate markers do not reach the sensitivity needed for population screening, and surveillance CT is not established practice ^[1].
• Record a full occupational history in every respiratory or oncology patient, including household or Para-occupational exposure, because disease can appear four decades later.

Diffuse MPM is only one of several pleural tumours:

• Metastatic pleural disease is by far the commonest pleural malignancy (lung, breast, ovary, kidney, GI tract, melanoma, haematological). Management targets the primary and leans on drainage plus systemic therapy.
• Localized malignant mesothelioma behaves as a solitary nodule, has a better prognosis than diffuse MPM and may be cured by excision; solitary fibrous tumour (benign and malignant variants) is variably indolent ^[4].
• Rare primary pleural malignancies (mesenchymal and epithelial tumours) are not staged by the MPM TNM system ^[5].
• Benign pleural disease (asbestos plaques, diffuse pleural fibrosis, benign asbestos effusion) mimics malignancy and must be excluded before accepting a benign label ^[1][5].

The commonest diagnostic puzzle is "metastatic carcinoma versus mesothelioma"; immunohistochemistry separates them, and the initial steps (drain, biopsy, MDT) are the same ^[1][5].

• Older and frail patients. Performance status shapes every decision; in patients unfit for invasive tests, serum or fluid biomarkers can support a probable diagnosis but must not be offered alone ^[1]. Best supportive care, with effusion control, is appropriate for many.
• Women and younger patients. A substantial minority of younger cases have a family history and signal BAP1 or other tumour-predisposition syndromes; ask about other cancers and refer for genetic counselling ^[1][4].
• Pregnancy. MPM in pregnancy is rare. Management is individual and specialist; no standard evidence-based protocol is cited here.

• Occupational history and CT are the anchors; a plain radiograph shows the effusion, while contrast CT showing circumferential pleural thickening or rind is strongly suggestive; thoracoscopic biopsy is the most cost-effective diagnostic method where available ^[1][2].
• Where thoracoscopy is unavailable, image-guided cutting-needle biopsy of focal abnormal pleura is specifically recommended ^[1].
• Cytology alone can suffice in experienced hands, reserved for patients who will not undergo further treatment or cannot tolerate biopsy ^[1].
• Systemic therapy: cisplatin plus pemetrexed is off-patent and relatively cheap but needs blood monitoring and antiemetics; immunotherapy and bevacizumab are much less available. Where no oncology service exists, prioritise effusion control, pain relief, oxygen and palliative care.
• Compensation: disparities are widest where claims cannot be pursued; recording the exposure history and giving a written diagnosis remain essential.

• MPM is a diffuse pleural malignancy, almost always after asbestos exposure; amphibole fibres carry higher risk than chrysotile and no threshold of exposure is safe.
• Latency is long (about 40 years pleural) and the exposure history must include family (Para-occupational) and armed forces exposure.
• Presentation is usually a unilateral exudative (often blood-stained) effusion with chest pain, breathlessness and weight loss; the right side is more often affected; bilateral disease is rare.
• Chest X-ray leads to contrast CT thorax; diagnosis rests on pleural tissue obtained by image-guided biopsy or thoracoscopy, with an immunohistochemistry panel and BAP1/p16 assessment.
• Histological subtypes are epithelioid, biphasic and sarcomatoid; epithelioid carries the best prognosis and sarcomatoid the worst. Localized forms can be cured by excision.
• Stage by the 8th edition IASLC/IMIG TNM: T1a/T1b merged, new N1/N2, stage IV only for distant metastasis. ^[3]
• First-line systemic therapy for fit patients (WHO 0 to 1): cisplatin plus pemetrexed with mandatory folic acid and vitamin B12, or nivolumab plus ipilimumab for unresectable disease; bevacizumab may be added where licensed.
• EPP is not performed; EPD remains restricted to trials; prophylactic radiotherapy to tracts is not recommended; palliative radiotherapy is for local pain.
• Effusion control is by talc pleurodesis or indwelling pleural catheter, chosen by the patient and by whether the lung is trapped.
• Offer early palliative care, MDT review and accurate compensation information; follow up every 3 to 4 months.
• No validated screening test exists; prevention is asbestos control.

• lung cancer
• pleural effusion
• pneumothorax
• asbestos-related disease
• thoracentesis and pleural procedures
• palliative care and symptom control