malignancy

1. MALIGNANT PLEURAL EFFUSION

2. DEFINITION:
 By detecting exfoliated malignant cells in pleural fluid or demonstrating
these cells in pleural tissues - by percutaneous pleural biopsies,
thoracoscopy, thoracotomy or at autopsy.
 22% of all pleural effusions
 42% of exudative pleural effusions

4. LUNG MALIGNANCIES:
 All type of lung carcinoma
 M/C ADENOCARCINOMA
 Lung carcinoma - anti-p53 antibodies are more likely
 Lung carcinoma + Pleural effusion is M1a , stage IV
 Presence of pleural effusion at the time of diagnosis adversely affect
the prognosis.

5. BREAST CARCINOMA:
 2nd most common cause of MPE
 More common with lymphangitic spread
 Determination of steroid receptors in the effusion is useful in
planning the therapy.

6. LYMPHOMAS
 Lymphomatous invasion of pleura is an uncommon and late finding in HODGKIN’S
DISEASE but seen with increased frequency in NON HODGKIN’S LYMPHOMA
 Responsible for 75% of chylothoraces secondary to malignant diseases
 Approximately 40% of the patients with AITL [Angioimmunoblastic T Cell Lymphoma]
have pleural effusion

7. LYMPHOMAS
HODGKIN’S DISEASE
Incidence at presentation - 7 to 21%
Intrathoracic lymph node involvement without
microscopic pleural involvement
HD and pleural effusion have NODULAR
SCLEROSIS type.
NON HODGKIN’S LYMPHOMA
Incidence - 6 to 50%
20 to 70% have evidence of mediastinal
disease.
LARGE CELL LYMPHOMAS are more frequently
associated with pleural effusion than small cell
lymphomas

8. MULTIPLE MYELOMA:
 MPE in patients with multiple myeloma - 1%
 Develops after an average of 12 months after the diagnosis
 Associated pleural or chest wall plasmacytomas

9. MALIGNANT MESOTHELIOMA:
 Less common cause of MPE
 M/C primary malignant tumor of the pleura
 Risk factor- Inhalational exposure to asbestosis
 Usually unilateral but in <10% cases it is bilateral.
 Epithelial type is associated with large pleural effusion and regional lymh node metastases.
 Sarcomatous type is associated with distant metastases but there is no or very little pleural
effusion.

10. PATHOPHYSIOLOGICAL MECHANISM:

11. CLINICAL MANIFESTATIONS:
* Dyspnoea (> 50% of patients)
* Chest pain ( 34% patients)
* Dry and non productive Cough
* Cachexia and lymphadenopathy (1/3rd patients)

12. Dyspnea:
• Decrease in compliance of chest wall.
• Contralateral shift of mediastinum
• Inversion of ipsilateral diaphragm
• Decrease in ipsilateral lung volume modulated by neurogenic
reflexes from lung and chest wall.
• Post obstructive pneumonia or Atelectasis due to central
bronchial lesion

13. CHEST PAIN:
•Due to involvement of parietal pleura , ribs and chest wall.
•Patients with MPE - dull chest pain
•Patients with benign disease - more intense pleuritic chest pain
•Malignant mesothelioma chest pain is the M/C presenting symptom
•Pleuritic chest pain is referred to abdomen as intercostal nerves are also distributed to
abdomen.
•Pleuritic pain felt simultaneously in lower chest and ipsilateral shoulder is
pathognomonic of diaphragmatic involvement(due to involvement of phrenic
nerve;C3,4,5)

14. DRY & NON PRODUCTIVE COUGH:
•Due to pleural inflammation
•Lung compression by the fluid - bring opposing bronchial walls into contacts
stimulating the cough reflex

15. Chest radiographs:
Malignant pleural effusions:
◦ Typically unilateral
◦ Ipsilateral to the primary tumor
Bilateral - 10% to 15%

16. Chest radiographs:

17. USG THORAX
Suggestive of malignant disease
• Parietal pleural thickening (>10 mm)
• Pleural nodularity, and/or
• Diaphragmatic nodularity or thickening (>7 mm)
Guide pleural procedures

18. CT THORAX:
Undiagnosed pleural effusions - CT scan - benign or malignant etiology
Following 4 findings are suggestive of malignancy:
i. Pleural nodularity
ii. Pleural rind (Fibrous swelling of the pleura causing retraction of thoracic wall )
iii. Mediastinal pleural involvement
iv. Pleural thickening greater than 1 cm.

21. Pleural fluid characteristics:
Malignant pleural effusion -exudate following LIGHT’S CRITERIA
• Fluid protein : serum protein > 0.5
• Fluid LDH : serum LDH > 0.6
• Fluid LDH > 2/3rd the upper limit of normal value of serum LDH.
Serous, serosanguineous, or grossly bloody
Limitation: Misidentifies 25% of transudative effusions as exudative effusions

22. Grossly bloody pleural fluid - RBC count >100,000/mm3 >> malignant pleural disease
Either lymphocytes or mononuclear cells (greater than 50% lymphocytes)
WBC count - is variable : 1000 - 10,000/mm3
Low PH (less than 7.3) and glucose (less than 60 mg/dL) - greater burden of tumor
within the pleural space
10% - elevated pleural fluid amylase level
◦ Salivary isoenzyme rather than the pancreatic isoenzyme
◦ Amylase isoenzyme analysis -differentiate pancreatic effusion V/S malignant effusion
Pleural fluid characteristics:

23. Pleural Biopsy
•“closed” biopsy technique
• Minimally invasive, and low-cost method
• Image guided
• Medical thoracoscopy
• Surgical thoracoscopy
• VATS - gold standard for the diagnosis of malignant pleural disease

24. CYTOLOGIC EXAMINATION OF PLEURAL FLUID:
As a definite diagnosis
Important features of malignant cells:
◦ Large cells
◦ Nuclei of malignant cells may exceeds 50µm in diameter in contrast with
mesothelial cell nuclei which rarely exceeds 20µm in diameter.
◦ Malignant cells have high nucleocytoplasmic ratio.

25. IHC MARKERS

26. MANAGEMENT OF MALIGNANT PLEURAL EFFUSION
[ATS & ERS GUIDELINES]

27. PROGNOSIS IN MALIGNANT PLEURAL EFFUSION:
MPE management depends upon prognosis
Certain factors i.e. tumor type, stage and performance status(PS) are accepted prognostic factors in
malignancy, including MPE
Lung cancer carries the worst prognosis
Longer survival - gynaecological tumors d/t underlying sensitivity to treatment
Specific MPE related prognostic factors include:
 Effusion size
 massive MPE, defined as fluid occupying the entire hemithorax, associated with worse survival in large
prospective study.
 Pleural fluid pH ≤7.28 is associated with shorter survival
 High serum and pleural fluid VEGF levels -worse outcomes in MPE - effects of inflammation, angiogenesis and
tumor necrosis.

29. Performance status [ecog]:
0 Asymptomatic
1 Symptomatic but ambulatory (able to carry out light work)
2 In bed < 50% of the day (unable to work but able to live at home
with some assistance)
3 In bed >50% of the day (unable to care for the self)
4 Complete bedridden

31. Therapeutic pleural aspiration
High rate of recurrence
Aspiration is not recommended - life expectancy >1 month
Caution should be taken if removing >1.5 litre on a single occasion

33. Pleurodesis
• Small-bore (10-14 F) intercostal catheters - drainage and administration of sclerosing agents
• Large pleural effusions - drained in a controlled fashion - reduce the risk of re-expansion
pulmonary oedema
• Once effusion drainage and lung re-expansion have been radiographically confirmed,
pleurodesis should not be delayed
• Suction to aid pleural drainage before and after pleurodesis is usually unnecessary
• High-volume low-pressure system is recommended
• Partial pleural apposition - chemical pleurodesis may still be attempted - symptomatic relief
• Symptomatic cases - pleural apposition cannot be achieved (‘trapped lung’)- indwelling pleural
catheters

34. • Talc is the most effective sclerosant available for pleurodesis
• Graded talc > ungraded talc - as it reduces the risk of arterial hypoxaemia
• Talc pleurodesis – by slurry or by insufflation
• Bleomycin, Povidone iodine, Tetracycline, Doxycycline
• S/E Pleuritic chest pain and fever
• Patient rotation is not necessary after intrapleural instillation of sclerosant
• The intercostal tube should be clamped for 1 h after sclerosant administration
• In the absence of excessive fluid drainage (>250 ml/ day) - removed within 24 -48 h of
sclerosant administration

35. •Malignant seeding at intercostal tube or port site
•Patients with proven or suspected mesothelioma - prophylactic radiotherapy to the site of
thoracoscopy, surgery or large-bore chest drain insertion
•Not in pleural aspirations or pleural biopsy

36. Intrapleural fibrinolytics
• Relief of distressing dyspnoea due to multiloculated malignant effusion resistant to simple
drainage
• Streptokinase/ Urokinase
• Septations -broken up under direct vision at thoracoscopy(medical/surgical)
• Thoracic surgery -access multiple loculations, especially those positioned on the mediastinum

37. Re-expansion pulmonary oedema
Maximum of 1.5 l on the first occasion
Remaining fluid - drained 1.5 l at a time at 2 h intervals
◦ Stopping if the patient develops chest discomfort, persistent cough or vasovagal symptom
Reperfusion injury of the underlying hypoxic lung
Increased capillary permeability
Local production of neutrophil chemotactic factors such as interleukin-8

38. Indwelling pleural catheter
•PleurX catheter - 15.5 F silicone rubber catheter , 66 cm in
length with fenestrations along the proximal 24 cm.
•Inserted into the pleural space using the Seldinger
technique under local anesthesia
•Catheter is maintained in place with a chest wall tunnel 5
to 8 cm in length.
•It has a special valve on its distal end that prevents fluid or
air from passing in either direction through the catheter

39. Pleurectomy
•Pleurectomy
•Abrasion pleurodesis

40. Para-malignant effusions
 Not the direct result of neoplastic involvement of the pleura
 Still related to the primary tumor

42. Thank you