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Pleural diseases 

Pleural diseases

Pleural diseases

Robert J.O. Davies

, Fergus V. Gleeson

, Y.C. Gary Lee

, Jose Porcel

, and Fraser Brims



Investigation—enhanced discussion of distinction between transudative and exudative effusions, use of measurement of ADA activity in diagnosis of tuberculosis, and tumour biomarkers.

Specific causes of effusion and pleural diseases—expanded notes on rheumatoid arthritis, SLE, benign asbestos pleural effusion, benign asbestos-related pleural plaques, and rounded atelectasis.

Pneumothorax—comments on use of diagnostic ultrasound, the role of suction for continuing air leak, the timing of surgery, and use of endobronchial valves.

A relevant case history from Oxford Case Histories in Respiratory Medicine has been added to this chapter.

Updated on 30 May 2013. The previous version of this content can be found here.
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date: 30 March 2017

Pleural effusion—general considerations

This is a common clinical problem which can complicate a range of lung and systemic diseases. Most cases can be diagnosed by pleural fluid analysis and pleural biopsy, with Light’s criteria making it possible to discriminate between transudates and exudates. These state that a pleural effusion is an exudate if any of the following are present: (1) pleural fluid to serum protein ratio greater than 0.5; (2) pleural fluid lactate dehydrogenase (LDH) greater than two-thirds of the upper limit of normal serum LDH; (3) pleural fluid to serum LDH ratio greater than 0.6.

Aetiology—common causes of a transudative effusion are heart failure and liver cirrhosis; common causes of an exudative effusion are malignancy, empyema/parapneumonic effusion, and tuberculosis.

Diagnosis—a low pH and low glucose are found in pleural fluid caused by very inflammatory processes, most commonly pleural infection or malignancy. A single cytological test of pleural fluid for malignant cells is about 50% sensitive for malignancy, with a second sample increasing sensitivity to about 60%. Where cytology is negative, image-guided pleural cutting needle biopsy or thoracoscopy are the most sensitive techniques to identify malignancy (c.80%) and are superior to closed pleural biopsy (c.45%). A high pleural fluid adenosine deaminase (ADA) activity strongly supports the diagnosis of tuberculosis in TB endemic regions. Alternatively, tuberculosis can be diagnosed by pleural biopsy (closed biopsy c.80% sensitive vs thoracoscopy c.100%). Where an effusion remains undiagnosed, specifically treatable conditions such as pulmonary embolism and drug-induced pleuritis should be reconsidered.

Pleural effusion—particular diseases

Pyogenic pleural infection—community-acquired infection is usually due to Streptococci (50% of cases, including milleri group, and pneumoniae), enterobacteria, anaerobes, and Staphylococci; hospital-acquired infection is most commonly due to Staphylococcus aureus (50% of cases, of which many can be methicillin-resistant (MRSA)), enterobacteria, or enterococci. Clinical features can range from fulminant sepsis to an indolent presentation with weight loss. Diagnosis depends on sampling pleural fluid to identify purulence, the presence of bacteria or low pleural pH/glucose. Treatment depends on effective chest tube drainage, appropriate antimicrobials (usually for at least 3 weeks), adequate nutrition, and prompt thoracic surgical drainage where clinical recovery is delayed. Mortality is greater than 20%. A recent randomized trial has suggested the usefulness of intrapleural administration of tissue plasminogen activator (tPA) and deoxyribonuclease (DNase) in improving radiographic and clinical outcomes.

Tuberculous pleural effusion and empyema—hypersensitivity tuberculous pleurisy is due to a delayed hypersensitivity reaction to mycobacteria in the pleural space, occurs in cases of primary infection, and is associated with a low pleural mycobacterial load. Diagnosis is often dependent on pleural histology revealing caseating granulomas. Tuberculous empyema is caused by rupture of cavitating tuberculosis into the pleural space and usually involves coinfection with mycobacteria and pyogenic bacteria (due to inoculation of the pleural space from the infected lung tissue). Treatment is as for tuberculosis elsewhere. Corticosteroids may have an adjuvant role in hastening pleural fluid reabsorption. Antibiotics for pyogenic bacteria are required in addition to antituberculous treatment in tuberculous empyema.

Chylothorax and pseudochylothorax—turbid or white pleural fluid has three common causes, with diagnosis established by lipid analysis of pleural fluid: (1) true chylothorax—due to leaking of chyle from a damaged thoracic duct, which usually caused by lymphoma, other cancers and trauma (including surgery); treatment is of the underlying disease where possible, and talc pleurodesis or thoracic duct repair for fluid control; nutrition is a high priority; (2) pseudochylothorax—due to chronic pleural inflammation; and (3) atypical empyema.

Haemothorax—most commonly caused by chest trauma or iatrogenically, haemothorax is distinguished from heavily blood stained pleural effusion by the pleural fluid haematocrit being greater than 0.5 of that in blood. Traumatic haemothorax is not detectable on a presentation chest radiograph in 20% of cases, when it subsequently evolves over a few days. Initial treatment is by large bore chest tube drainage. About 20% of patients require surgery (video-assisted thoracoscopic surgery, or thoracotomy) to control blood loss, repair organ injury, and evacuate the blood. Failure to evacuate a large haemothorax can lead to late extensive pleural fibrosis (‘fibrothorax’).

Benign asbestos-induced pleural disease

The commonest benign asbestos-induced pleural disease is pleural plaque. These are fibrotic and sometimes calcified pleural thickenings on the lateral chest wall and the dome of the diaphragm that have no clinical significance. Diffuse pleural fibrosis is less common and occurs due to asbestos-mediated pleural inflammation, sometimes following benign asbestos pleural effusion. There is no specific treatment and care is supportive. When visceral pleural thickening causes the lung to enfold it forms a characteristic lesion known as ‘rounded atelectasis’.


Pneumothoraces, defined as air in the pleural space, are classified as traumatic (including iatrogenic) or spontaneous, with the latter being primary (where the lung is largely normal) or secondary (where the pneumothorax is due to an underlying lung disease, most commonly chronic obstructive pulmonary disease). The diagnosis is usually established by visualization of a lung edge—a pleural line—on the chest radiograph. Treatment involves removing air from the pleural cavity and preventing recurrence.

Primary pneumothorax—associated with smoking, tall stature, and the presence of macroscopic subpleural apical lung blebs; generally a benign disease; usually treated conservatively. Supplementary oxygen can be given (where the patient is an inpatient) to hasten reabsorption. Aspiration is recommended for pneumothorax of greater than 15% of hemithorax volume, with chest tube drainage required if this fails. Recurs in 40% of cases, with video-assisted thoracic surgery typically recommended to prevent recurrence in patients who have had three events. All should be advised to stop smoking.

Secondary pneumothorax—diagnosis can be difficult if the chest radiograph is very abnormal due to the underlying lung disease; CT is used in this setting. Most patients require chest tube drainage and recurrence prevention.

Tension pneumothorax—a rare but important variant of pneumothorax where a ‘flap valve’ mechanism at the visceral pleural surface results in the development of increasing positive pressure in the pleural space. Diagnosis is based on the clinical features of a large pneumothorax with mediastinal shift away from the affected side, cardiovascular compromise, and severe progressive dyspnoea. Treated by urgent thoracic decompression, followed by placement of a chest tube.

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