A pleural effusion refers to a collection of fluid with the pleural space. The pleural space is the anatomical ‘potential space’ between the thoracic wall and the lung parenchyma. The normal small volume of pleural fluid is maintained by the balance of:
Starling’s forces – the hydrostatic and oncotic pressures within the pleural vessels
Lymphatic drainage
The development of a pleural effusion is due to a disruption of one component of this balance and can be categorised as:
Increased intravascular hydrostatic pressure e.g. cogenstive cardiac failure
Decreased intravascular oncotic pressure e.g. hypoalbumineamia
Obstruction to lymphatic drainage e.g. thoracic duct injury
Increased negative pleural hydrostatic pressure e.g. ‘trapped lung’ where the lung can’t expand
Increased pleural oncotic pressure e.g. from existing pleural effusion
Increased permeability of the vessel/pleural membranes e.g. pneumonia
The pathophysiology is helpful as it is the basis for differentiating the two main types of pleural effusion: transudate vs exudate.
Transudative effusions have a low protein composition (<30g/L) usually represent an imbalance of the Starling forces. Exudative effusions have a high protein composition (>30g/L) and represent a distortion of the semipermeable capillary membranes by an inflammatory process. Lights criteria can help differentiate between the two categories when the protein value is close (which is common). Pleural fluid is an exudate if one or more of the below criteria are met:
Pleural fluid divided by serum protein is >0.5
Pleural fluid LDH divided by serum LDH is >0.6
Pleural fluid LDH is >2/3rd the upper normal limits
Pleural aspiration is therefore required to obtain the biochemical values. This is indicated if the cause is uncertain or the effusion is unresponsive to treatment. Aspiration should be done under ultrasound guidance, taking of 50ml of fluid with a needle and a syringe. Samples should be sent for:
Biochemistry – protein and LDH
Microbiology – Gram stain & culture
Cytology
Further possible tests include; pH, glucose, amylase, haematocrit.
Treatment is dependent on the underlying cause of the effusion. Drainage is usally only required for symptomatic reasons i.e. significant respiratory strain. Complicated parapneumonic effusions require rapid drainage to reduce the risk of fibrotic complications. The indications for urgent drainage include:
Frank pus
Pleural fluid pH <7.2
Bacteria on gram stain or culture
Long Notes
A pleural effusion refers to a collection of fluid with the pleural space. The pleural space is the anatomical ‘potential space’ between the thoracic wall and the lung parenchyma. The inner surface of the thoracic cavity is lined with the parietal pleura, whilst the lungs are covered with the visceral pleura. The pleura slide over each other allowing effective movement of the lungs during respiration. This is usually aided by a very small volume of fluid (approximately 10ml in an adult) which acts as a lubricant.
Pathophysiology
The normal small volume of pleural fluid is maintained by the balance of:
Starling’s forces – the hydrostatic and oncotic pressures within the pleural vessels
Lymphatic drainage
As with other vessels, the Starling forces govern net movement of fluid across their semipermeable membranes. The relatively high hydrostatic pressure within the vessel ‘forces’ fluid out of the vessel as it is higher than the hydrostatic pressure outside the vessel. The oncotic pressure exerted by the plasma proteins that remain within the vessels act to ‘pull’ fluid back in. The net effect is a slight outward movement of fluid out of the vessels. This excess fluid is taken up by the lymphatic system and returned to the circulation.
The development of a pleural effusion is due to a disruption of one component of this balance and can be categorised as:
Increased intravascular hydrostatic pressure e.g. cogenstive cardiac failure
Decreased intravascular oncotic pressure e.g. hypoalbumineamia
Obstruction to lymphatic drainage e.g. thoracic duct injury
Increased negative pleural hydrostatic pressure e.g. ‘trapped lung’ where the lung can’t expand
Increased pleural oncotic pressure e.g. from existing pleural effusion
Increased permeability of the vessel/pleural membranes e.g. pneumonia
The pathophysiology is helpful as it is the basis for differentiating the two main types of pleural effusion: transudate vs exudate.
Transudate
Transudative effusions are caused when there is an imbalance in the Starling’s forces acting around the pleural space i.e. the hydrostatic and oncotic pressures. Though the semipermeable mebrane is still intact, there is a change in the balance of the net movement of fluid across it. They have a low protein composition and a relatively small number of causes:
Congestive cardiac failure – bilateral 81%
Cirrhosis (hepatic hydrothorax) – migration of ascitic fluid - right sided 70%, bilateral 15%
Hypoalbuminaemia – bilateral >90%
Nephrotic syndrome – usually bilateral
Peritoneal dialysis – similar to hepatic hydrothorax
Atelectasis – causing lung trapping and resulting negative pressure
Urinothorax – from obstructive uropathy with urine tracking retroperitoneally.
Constrictive pericarditis
CSF leak to the pleura – usually related to neurosurgery
Myxoedema
Superior vena cava syndrome – can also include thoracic duct injury
Exudate
Exudative effusions are caused by disruption of the integrity of local vessel walls semipermeable membrane, usually by an inflammatory process. With the loss of integrity of the semipermeable membrane, protein is able to escape the vessel and so these effusions have a higher protein concentration.
Pneumonia – parapneumonic effusion
Malignancy – lung, pleural and breast the most common
Meig’s syndrome – ovarian tumour with ascites and resultant pleural effusion
Other considerations for pleural effusion include:
Haemothorax – the fluid in the pleural space is primarily blood. This is generally related to trauma or a coagulopathy
Empyema – the fluid is pus. This can be a complication of pneumonia or surgical interventions
Iatrogenic – causes by misplaced lines e.g. CVC
Chylothorax – milky white effusion. High in triglycerides caused by thoracic duct injury
Presentation/Investigation
Some effusions may be incidental, but many are discovered after patients present with respiratory symptoms:
Dyspnoea – most common symptom, often relating to the impact of the fluid on diaphragm mechanics
Chest pain – often pleuritic in nature due to pleural irritation. Can vary greatly in severity.
Cough – often mild if present at all, and generally non-productive.
The clinical assessment should include a careful history. This must include consideration of the important risk factors for some causes e.g. drug history, occupational history.
The extent of clinical signs will depend on the size of the effusion. Typical findings on chest examination include:
Reduced air entry
Dullness to percussion
Reduced chest wall expansion
Reduced tactile vocal fremitus
Egophony at the top of the effusion
Pleural rub
A chest x-ray is a vital first line investigation for pleural effusions. It requires around 200ml of pleural fluid to cause radiographic changes on a plain film.
Management
The workup of a patient with a pleural effusion is initially centred on establishing the cause. The wide variety of causes with different pathophysiology means that this is essential to guide management. In general, transudative causes are less concerning, whereas the causes of exudative effusions need carefully investigation. If the history and investigative features strongly suggest a transudative cause then this should be treated first e.g. optimisation of diuretics for CCF. No further investigation is needed unless there is a failure to respond, and this approach is recommended by the British Thoracic Society (BTS) guidelines.
If there is suggestion that the cause is exudative, or if a presumed transudative cause isn’t responding to treatment, then further investigation is warranted. The first next step in pleural aspiration, to establish the exact nature of the effusion.
Pleural Aspiration
This involves needle aspiration of the pleural fluid for sampling. Patients should be consented as to the risks and benefits beforehand. The procedure employs full ANTT with careful consideration to asepsis. Bedside ultrasound guidance is recommended to maximise the success of the procedure and minimise the risk of complications. After full cleaning, there is infiltration of the skin and subcutaneous tissues with local anaesthetic before the pleural fluid is then sampled. This is done by a small gauge needle (21g preferably) and a 50ml syringe.
Biochemistry – sample of at least 2-5ml in a plain container. Parallel serum samples should be sent to allow calculation of Light’s criteria. The requests should be:
Protein
LDH
Microscopy and Culture – 5ml of fluid in a plain container. If there is high suspicion of an infective process then a further 5ml should be put into blood culture bottles. Cytology – The maximum amount of aspirated fluid should be sent to maximise the chances of a positive yield. Ideally at least 50ml should be sent. It will need refrigeration if sent out of hours.
Further tests may be needed depending on the suspicion of specific disease processes:
pH – taken into a blood gas syringe if not purulent
Glucose – can be helpful for rheumatoid effusions
Triglycerides – if considering chylothorax versus pseudochylothorax
Amylase – can be helpful for pancreatitis related effusions
Haematocrit – if considering haemothorax
Acid-fast bacilli – if high suspicion for TB
Interpretation
Appearance
Frankly purulent fluid suggests an empyema Milky fluid suggests a chylothorax or pseudochylothorax Grossly bloody fluid suggests trauma, malignancy, pulmonary embolism or asbestos related disease. A haematocrit of over 50% of the peripheral haematocrit is used to define a haemothorax.
Light's Criteria
Classically the cut off for differentiation between a transudate and a exudate was a pleural fluid protein level of 30g/l. Above this value was an exudate, below this value was a transudate. However, it is common to have values close to this, and so Light’s criteria is recommended to determine what the underlying pathophysiology is. It has an accuracy of 93-96%. Pleural fluid is an exudate if one or more of the below criteria are met:
Pleural fluid divided by serum protein is >0.5
Pleural fluid LDH divided by serum LDH is >0.6
Pleural fluid LDH is >2/3rd the upper normal limits
Of notes, there is the potential for Light’s criteria to misclassify some transudates as exudates. This is usually in patients with CCF on long term diuretics because of the concentrating effect of diuretics on protein and LDH levels.
Cell Counts
If the cell count shows a predominantly lymphocytosis (>50% lymphocytes) the common causes are malignancy, TB and CCF. Neutrophil predominant effusions are more common in acute processes, including parapneumonic effusion, pulmonary embolism, and acute TB. An eosinophilic effusion is when eosinophils make up >10% of the cell count. The most common cause is blood or air in the pleural space but is a relatively non-specific finding. It can be seen in drug induced, parapneumonic, benign asbestos, lymphoma, PE and parasitic related effusions.
pH
Pleural acidosis (pH < 7.30) represents an accumulation of metabolic by-products (CO2, Lactate). It occurs in malignant disease, complicated pleural infections, connective tissue disease and oesophageal rupture. In malignant pleural disease, a low pH has been associated with more extensive disease and worse survival outcomes. In general, parapneumonic effusions with a pH below 7.2 have a higher rate of complications and warrant chest drain insertion. The measured pH can be affected by the exposure to air (raising the pH) and the contamination with local anaesthetic (lowering it), so care is needed to avoid these artefacts.
Glucose
Glucose usually diffuses freely in to pleural space and is the same as plasma glucose normally. Low pleural glucose levels are found in complicate parapneumonic effusions, empyema, rheumatoid effusions, TB, and malignancy.
Cytology
Cytological examination of the pleural fluid is often a quick and effective way for establishing the diagnosis if malignant disease is suspected. The yield is around 60%, but an adequate sample size is needed. The advice is to send as much as possible from the remaining sample after other tests have been sent off (often 20-40ml). In general, the evidence that aiming for over 50ml isn’t worth the risks associated with using a venflon and a 3-way tap.
There are a number of other more advanced tests that can be performed. This includes further pleural fluid testing, alternative biopsy methods and additional imaging.
Drainage
In general, treatment of the underlying cause will be the mainstay of management, with little need for drainage unless there are significant symptoms. Clearly significant respiratory demand is an indication for drainage. Chest drain insertion will be required rather than a single drainage episode. Drainage of over 1.5L at a single time should be avoided because of the risk of re-expansion pulmonary oedema.
Complicated parapneumonic effusions are the most common indication for rapid drainage due to the high risk of fibrotic changes, sometimes needing surgical decortication to allow resolution. The indications for urgent drainage are: