CHAPTER 4 Clare E. Hooper Worcestershire NHS Trust, UK Pleural effusions are a common presentation with a large number of possible causes. They may result from systemic disease or processes local to the pleura and lung. The guiding principle of investigation should be to minimise the number of invasive tests performed by selecting procedures with the best diagnostic yield and both diagnostic and therapeutic benefits. As malignancy accounts for a substantial proportion of symptomatic unilateral pleural effusions, it is important that it is robustly excluded. Figure 4.1 details a suggested algorithm for investigating pleural effusions in countries of low tuberculosis (TB) prevalence (such as the UK).
Investigation of Pleural Effusions
Figure 4.1
Bilateral pleural effusions in patients with a clear history or clinical features suggesting a transudate (i.e. congestive cardiac failure, renal failure, hypoproteinaemia) do not require specific investigation with aspiration or cross‐sectional imaging unless they fail to respond to appropriate medical management. Although the division of pleural effusions by their unilateral or bilateral appearance on chest X‐ray and their protein content (exudates or transudates) is helpful in focusing initial tests, some effusions are of multi‐factorial origin and present with a mixed picture, requiring a particularly flexible approach to investigation.
Clinical presentation
Pleural effusions are associated with dyspnoea, pleuritic chest pain and cough (caused by extrinsic bronchial compression by a large effusion) but patients may also present with an asymptomatic chest X‐ray finding. Whether an effusion is associated with dyspnoea is determined by its size, the degree of associated pleural thickening and the presence of coexistent parenchymal lung disease or the respiratory reserve of the patient.
History taking
The following aspects of the history are particularly important:
- Duration of symptoms.
- Severity of dyspnoea (is a therapeutic pleural aspiration indicated urgently for symptomatic relief?)
- Preceding lower respiratory tract infection.
- Systemic symptoms of sepsis or malignancy (fevers, sweats, weight loss).
- History of cardiac or respiratory disease.
- Past history of malignant disease.
- Risk factors for TB: ethnic origin, contacts, immunocompromise.
- Drug history, including new drugs with a possible association with the onset of symptoms, change to diuretic dosage and any anticoagulants/antiplatelet agents (which require consideration before invasive procedures).
- Symptoms or history of connective tissue disease.
- Occupational history with an emphasis on asbestos exposure.
- Smoking.
- Performance status (to determine appropriateness of more invasive and physically stressful diagnostic and management strategies).
Examination
A thorough multi‐system examination is important. This should include the following:
- Confirmation of clinical signs of a pleural effusion.
- Assessment of dyspnoea at rest and on minor exertion.
- Examination for signs of disseminated malignancy (lymph nodes, abdominal organomegaly, breast examination).
- Joints and skin.
- Signs of cardiac failure.
- Joints and skin.
Initial imaging
Chest X‐ray
Costophrenic angle blunting or loss of diaphragmatic contour is seen on erect postero‐anterior (PA) chest X‐ray in the presence of 200 mL or more of pleural fluid. In the erect position, simple pleural effusions have a surface meniscus as shown in Figure 4.2(a). Loculated effusions can appear as discrete smooth sub‐pleural opacities and loculated pleural infection or empyema is often seen as a classic D‐shaped opacity (Figure 4.2b).
Figure 4.2 Chest X‐rays: (a) meniscus of left pleural effusion; (b) D‐shaped appearance of loculated pleural empyema; (c) asbestos‐related pleural plaques.
A useful convention for classifying the size of effusion on PA chest X‐ray is the proportion of the hemithorax that is occupied by fluid: small <1/3; moderate 1/3 to 1/2; large >1/2. Massive pleural effusions, occupying the entire hemithorax and causing mediastinal shift to the contralateral side, are most often seen with pleural malignancy.
In a supine patient, particularly on antero‐posterior (AP) chest X‐ray (e.g. in the critical care setting), pleural effusions distribute posteriorly and appear as a general haze over the hemithorax with preservation of vascular markings.
Other important observations that may provide clues to the cause of effusion include the presence of parenchymal consolidation or masses, bulky hila and abnormal mediastinal contours, cardiomegaly and evidence of previous cardiac surgery, diffuse pleural thickening and pleural plaques (associated with asbestos exposure; Figure 4.2c).
Thoracic ultrasound
Ultrasound is the next essential step after chest X‐ray for patients who require further investigation. It should be performed by the physician who will plan and perform any subsequent invasive investigations.
Ultrasound is more sensitive than chest X‐ray in detecting small effusions, allows accurate characterisation of the nature and distribution of pleural fluid, guidance of safe pleural aspiration and often the detection of signs of malignancy or underlying lung consolidation.
Pleural fluid may appear anechoic (simple), echogenic/complex or septated on ultrasound (Figure 4.3). The presence of echogenicity or septation positively confirms that the effusion is an exudate, while anechoic appearances can occur with either transudates or exudates.
Figure 4.3 Thoracic ultrasound image of a complex septated pleural effusion.
The observation of significant pleural or diaphragmatic thickening or nodularity on thoracic ultrasound has a high specificity (95–100%) for identifying a malignant cause for the pleural effusion (Figure 4.4).
Figure 4.4 Thoracic ultrasound demonstrating large anechoic pleural effusion (a) and nodularity and thickening of the diaphragmatic pleura (b).
Real‐time ultrasound guidance of diagnostic pleural aspiration has been shown to improve success rates and reduce the risk of organ puncture and iatrogenic pneumothorax.
A visual assessment of pleural fluid volume on ultrasound along with an impression of patient dyspnoea is helpful in determining what volume of fluid to remove at initial aspiration while awaiting more definitive procedures.
Pleural fluid tests
All unilateral pleural effusions of unknown cause should be sampled and sent for assessment of protein and lactate dehydrogenase (LDH), cytological examination and microscopy and culture. Additional tests are useful in specific circumstances. The aspiration procedure is described elsewhere in this book.
Fluid appearance
Pleural fluid appearance can provide some information regarding the likely cause of effusion but is often non‐specific. Straw coloured fluid may indicate a transudate or a paucicellular exudate. Blood‐tinged fluid is non‐specific but frankly bloody pleural effusions suggest malignancy, benign asbestos effusion, post cardiac injury syndrome, pulmonary infarction or haemothorax. Brown fluid is usually a marker of a long‐standing bloody effusion. Milky fluid suggests a lipid effusion (chylous or pseudochylous) but can be difficult to distinguish from the turbid or purulent fluid of empyema.
Distinguishing exudates and transudates
The dichotomous division of pleural effusions into exudates and transudates is a standard approach that is useful in focusing investigations towards a smaller number of diagnostic possibilities. Table 4.1 lists causes of pleural exudates and transudates.
Table 4.1 Causes of pleural exudates and transudates.
| Exudates | Transudates |
| Common | Common |
| Simple parapneumonic effusion | Left ventricular failure |
| Pleural infection | Hepatic failure (hepatic hydrothorax) |
| Malignant pleural effusion | Renal failure |
| Hypo‐albuminaemia | |
| Less common | Less common |
| Post CABG effusion | Peritoneal dialysis |
| Benign asbestos effusion | Hypothyroidism |
| Tuberculous pleuritis | Nephrotic syndrome |
| Rheumatoid arthritis | |
| Post myocardial infarction | |
| Haemothorax | |
| Pulmonary embolism with infarction | |
| Pancreatitis | |
| Rare | Rare |
| Drug reaction | Constrictive pericarditis |
| Sarcoidosis | Urinothorax |
| Other connective tissue disease (SLE, Sjögren syndrome) | Meigs syndrome |
CABG, coronary artery bypass graft; SLE, systemic lupus erythematosus.
Pleural fluid protein alone gives a rough guide: >30 g/L suggests an exudate and <30 g/L a transudate. This division is not accurate when fluid protein approaches the cut‐off or in the presence of abnormal serum protein.
Light’s criteria have been shown to be the most accurate method of dividing exudates and transudates. The system requires the concurrent measurement of paired serum and pleural fluid protein and LDH (Box 4.1).
Full access? Get Clinical Tree
