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 Classification of pleural effusions.
 Causes of pleural effusions.
 Clinical presentation.
 Management options.
 Pleurx drain.
 Complications of Pleurx drain.
 A pleural effusion is an abnormal build-up of fluid in the pleural space.
 Pleural effusions may be classified as being either a transudate or exudate
according to the protein concentration.
Transudate (< 30g/L protein) Exudate (> 30g/L protein)
• heart failure (most common transudate cause)
• hypoalbuminaemia (liver disease, nephrotic
syndrome, malabsorption)
• hypothyroidism
• infection: pneumonia (most common exudate
cause), TB, subphrenic abscess
• connective tissue disease: RA, SLE
• neoplasia: lung cancer,
mesothelioma, metastases
• pancreatitis
• pulmonary embolism
• yellow nail syndrome
If the protein level is between 25-35 g/L, Light's criteria should be applied.
An exudate is likely if at least one of the following criteria are met:
 pleural fluid protein divided by serum protein >0.5
 pleural fluid LDH divided by serum LDH >0.6
 pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
 Occurs when either a lung cancer or another type of cancer spread to the pleural space.
 These cancer cells;
 increase the production of pleural fluid
 cause decreased absorption of the fluid
 Who gets malignant pleural effusions?
 carcinomas of the lung & mesothelioma (36%)
 breast (25%)
 lymphoma (10%)
 ovary (5%)
 Median survival following diagnosis ranges from 3 to 12 months.
 Dependent on the stage and type of the underlying malignancy.
 The shortest survival time is observed in malignant effusions secondary to lung
cancer, and the longest in ovarian cancer.
The majority of malignant effusions are symptomatic.
 Dyspnoea is the most common presenting symptom.
 Chest pain/ pressure.
 Cough.
 Constitutional symptoms including weight loss, malaise and anorexia generally
accompany respiratory symptoms.
Confirmation by:
 CXR
 CT
 Ultrasound
Observation:
 Observation is recommended if the patient is asymptomatic and the tumour type is known.
 Advice should be sought from the respiratory team for symptomatic malignant effusions.
Therapeutic pleural aspiration:
 Pleural effusions treated by aspiration alone are associated with a high rate of recurrence of
effusion at 1 month, so aspiration is NOT recommended if life expectancy is >1 month.
 Caution should be taken if removing >1.5 L on a single occasion.
Intercostal tube drainage and intrapleural instillation of sclerosant:
 Other than in patients with a very short life expectancy, small-bore chest tubes
followed by pleurodesis are preferable to recurrent aspiration.
 Talc is the most effective sclerosant available for pleurodesis.
 Large pleural effusions should be drained in a controlled fashion to reduce the
risk of re-expansion pulmonary oedema.
 IPC-related pleural infection – Antibiotics, MIST2 trial.
 Catheter tract metastasis - Simple analgesia and external beam radiotherapy.
 Symptomatic loculations - Pleural aspiration, removal of the ineffective IPC and
insertion of a second catheter targeting the residual locules, intrapleural
fibrinolysis.
 Catheter blockage - Saline flush and manipulation along the catheter.
https://thorax.bmj.com/content/65/Suppl_2/ii32

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Malignant Pleural Effusion.pptx

  • 1.
  • 2.  Classification of pleural effusions.  Causes of pleural effusions.  Clinical presentation.  Management options.  Pleurx drain.  Complications of Pleurx drain.
  • 3.  A pleural effusion is an abnormal build-up of fluid in the pleural space.  Pleural effusions may be classified as being either a transudate or exudate according to the protein concentration. Transudate (< 30g/L protein) Exudate (> 30g/L protein) • heart failure (most common transudate cause) • hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption) • hypothyroidism • infection: pneumonia (most common exudate cause), TB, subphrenic abscess • connective tissue disease: RA, SLE • neoplasia: lung cancer, mesothelioma, metastases • pancreatitis • pulmonary embolism • yellow nail syndrome
  • 4. If the protein level is between 25-35 g/L, Light's criteria should be applied. An exudate is likely if at least one of the following criteria are met:  pleural fluid protein divided by serum protein >0.5  pleural fluid LDH divided by serum LDH >0.6  pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
  • 5.  Occurs when either a lung cancer or another type of cancer spread to the pleural space.  These cancer cells;  increase the production of pleural fluid  cause decreased absorption of the fluid  Who gets malignant pleural effusions?  carcinomas of the lung & mesothelioma (36%)  breast (25%)  lymphoma (10%)  ovary (5%)
  • 6.  Median survival following diagnosis ranges from 3 to 12 months.  Dependent on the stage and type of the underlying malignancy.  The shortest survival time is observed in malignant effusions secondary to lung cancer, and the longest in ovarian cancer.
  • 7. The majority of malignant effusions are symptomatic.  Dyspnoea is the most common presenting symptom.  Chest pain/ pressure.  Cough.  Constitutional symptoms including weight loss, malaise and anorexia generally accompany respiratory symptoms. Confirmation by:  CXR  CT  Ultrasound
  • 8.
  • 9. Observation:  Observation is recommended if the patient is asymptomatic and the tumour type is known.  Advice should be sought from the respiratory team for symptomatic malignant effusions. Therapeutic pleural aspiration:  Pleural effusions treated by aspiration alone are associated with a high rate of recurrence of effusion at 1 month, so aspiration is NOT recommended if life expectancy is >1 month.  Caution should be taken if removing >1.5 L on a single occasion.
  • 10. Intercostal tube drainage and intrapleural instillation of sclerosant:  Other than in patients with a very short life expectancy, small-bore chest tubes followed by pleurodesis are preferable to recurrent aspiration.  Talc is the most effective sclerosant available for pleurodesis.  Large pleural effusions should be drained in a controlled fashion to reduce the risk of re-expansion pulmonary oedema.
  • 11.
  • 12.  IPC-related pleural infection – Antibiotics, MIST2 trial.  Catheter tract metastasis - Simple analgesia and external beam radiotherapy.  Symptomatic loculations - Pleural aspiration, removal of the ineffective IPC and insertion of a second catheter targeting the residual locules, intrapleural fibrinolysis.  Catheter blockage - Saline flush and manipulation along the catheter.

Editor's Notes

  1. The discovery of malignant cells in pleural fluid and/or parietal pleura signifies disseminated or advanced disease and a reduced life expectancy in patients with cancer.1
  2. Dyspnoea is the most common presenting symptom, reflecting reduced compliance of the chest wall, depression of the ipsilateral diaphragm, mediastinal shift and reduction in lung volume. Chest pain is less common and is usually related to malignant involvement of the parietal pleura, ribs and other intercostal structures.
  3. Treatment options for malignant pleural effusions are determined by several factors: symptoms and performance status of the patient, the primary tumour type and its response to systemic therapy, and degree of lung re-expansion following pleural fluid evacuation.  The majority of these patients will become symptomatic in due course and require further intervention. There is no evidence that initial thoracentesis carried out according to standard techniques will reduce the chances of subsequent effective pleurodesis after tube drainage. However, repeated thoracentesis may limit the scope for thoracoscopic intervention as it often leads to the formation of adhesions between the parietal and visceral pleura. Repeated therapeutic pleural aspiration provides transient relief of symptoms and avoids hospitalisation for patients with limited survival expectancy and poor performance status. It is appropriate for frail or terminally ill patients.  The amount of fluid evacuated by pleural aspiration will be guided by patient symptoms (cough, chest discomfort)27 and should be limited to 1.5 l on a single occasion. Pleural aspiration alone and intercostal tube drainage without instillation of a sclerosant are associated with a high recurrence rate and a small risk of iatrogenic pneumothorax and empyema.28–36 Therapeutic pleural aspiration should take place under ultrasound guidance
  4. Intercostal drainage should be followed by pleurodesis to prevent recurrence unless lung is significantly trapped. Large pleural effusions should be drained incrementally, draining a maximum of 1.5 l on the first occasion. Any remaining fluid should be drained 1.5 l at a time at 2 h intervals, stopping if the patient develops chest discomfort, persistent cough or vasovagal symptoms. Re-expansion pulmonary oedema is a well-described serious but rare complication following rapid expansion of a collapsed lung through evacuation of large amounts of pleural fluid on a single occasion and the use of early and excessive pleural suction. Pathophysiological mechanisms include reperfusion injury of the underlying hypoxic lung, increased capillary permeability and local production of neutrophil chemotactic factors such as interleukin-8.52 53
  5. Talc pleurodesis has been, for many decades, the preferred treatment for MPEs. Data from recent years, however, have raised doubts on its efficacy and safety.3 The indwelling pleural catheter (IPC) provides a revolutionary alternative for achieving long-term control of recurrent effusions, especially MPEs.  Pleurodesis is only useful in patients with fully expanded lungs after fluid evacuation. It is increasingly realised that non-expandable (or ‘trapped’) lungs are common in MPEs.5 A recent study using pleural ultrasound as a screening tool found 50–60% of MPE patients had non-expandable lungs and poor performance not suitable for talc pleurodesis.6 IPC, however, can be used for all MPE patients whether the lung is expandable or trapped.  Interventional radiologist will make 2 small incisions (surgical cuts), one into pleural space and another one a few inches away (see Figure 2). This will make a tunnel under the skin between the 2 openings. The catheter will be passed through this tunnel.
  6. The standard diagnostic criteria for pleural infection include the relevant clinical signs and symptoms of infection, presence of low pleural fluid pH (and/or glucose), or presence of pus or bacteria in the pleural fluid.24 In patients fitted with an IPC, the diagnosis of pleural infection can be challenging. Malignant effusions often have low pleural fluid pH and high lactate dehydrogenase, and fever related to underlying tumour is not uncommon. Akin to long-term urinary catheter use, bacterial ‘colonisation’ can occur in IPC-treated patients whose pleural fluid yields positive microbiology but without clinical manifestation of empyema or the typical biochemical profile of infected pleural fluid Cutaneous flora, including Staphylococcus spp (especially S. aureus), accounts for most of the reported cases, followed by Pseudomonas aeruginosa and Enterobacteriaceae. Most cases resolved with antibiotic treatment . Removal of the IPC is not necessary unless the infection fails to respond. The IPC provides ready access to drainage of infected material. MIST2 trial on respiratory wards - Intrapleural Use of Tissue Plasminogen Activator and Dnase which is an intrapleural fibrinolytic therapy which facilitates drainage of infected fluid. Patients with catheter tract metastasis (CTM) typically present with a new, and often painful, subcutaneous nodule/mass near the IPC insertion site or its subcutaneous tract.  Unknown aetiology. Patients with CTM can usually be treated effectively with simple analgaesics and external beam radiotherapy without the need to remove the IPC.  The presence of an IPC could facilitate ‘spontaneous pleurodesis’ in approximately 40% of patients Catheter may induce fibrin deposition within the pleural cavity,. However, fibrin deposition, whether stimulated by the IPC or underlying tumour, can also unfavourably induce septations and pleural fluid loculation, thus limiting effective IPC drainage. Intrapleural fibrinolysis provides a feasible alternative. This may help to lyse adhesions, restores drainage via IPC and thus avoids a second invasive pleural procedure  Catheter blockage The formation of dense fibrinous tissue around and within the IPC can occasionally lead to blockage. Saline flush and manipulation along the catheter may dislodge occluding materials and re-establish patency. Non-draining blocked catheters with little residual pleural fluid should be removed to prevent infection.