Pleural effusion is a common clinical problem and may present to a wide range of specialties. Accurate aetiological diagnosis is key to subsequent management, requiring a multidisciplinary approach and knowledge of the correct investigation pathway. This article will focus on appropriate staged investigations for the patient presenting with pleural effusion rather than on its causes or treatment.
Clinical syndromesPleural effusion is often detected on plain chest radiography as an incidental finding and patients may be asymptomatic. Clinical symptoms are variable, depending on the size and aetiology of the effusion and rarely specific enough to suggest a diagnosis in the absence of further investigations. Large effusions are likely to be associated with dyspnoea, but this is often a late finding and oxygen saturations may not be severely lowered. Dyspnoea is the result of impaired mechanics and increased intrapleural pressure swings.The presence of chest pain implies involvement of the parietal pleura which is heavily innervated. Inflammation, infection and malignant involvement may produce pain, including shoulder tip symptoms associated with diaphragmatic involvement. Weight loss, anorexia and malaise may imply malignancy or infection (eg empyema).
CausesPleural effusions are divided into transudative and exudative (Table 1). They are diagnosed according to pleural fluid biochemical characteristics (see below). However, transudates occur with structurally normal pleura, in which oncotic or hydrostatic pressure results in fluid leak. In contrast, exudates occur with damaged or altered pleura, resulting in loss of tissue fluid and protein causing fluid formation. 1 Differentiation of transudate from exudate is key to further management. Treatment for transudative effusion relies on treatment of the underlying disease, and uncommonly requires specific pleural intervention. In contrast, exudative effusion usually needs further investigation and often requires intervention.
Initial diagnostic approachThe presence of bilateral, symmetrical effusions in the appropriate clinical context is highly suggestive of transudative effusion, and in general requires no further investigation. 2 However, it should be noted that about 50% of heart failure CME Respiratory medicine • pleural fluid protein/serum protein >0.5• pleural fluid LDH/serum LDH >0.6• pleural fluid LDH more than two-thirds of the upper limit of normal serum LDH * If pleural fluid protein is 25-35 g/l or serum protein level is abnormal, apply Light's criteria. LDH = lactate dehydrogenase; TB = tuberculosis.