Pleural effusion is common in heart failure and tends to be more frequent and larger on the right.
All types of pericardial disease may be associated with pleural effusion, which is predominantly left-sided. Pleural effusion is a characteristic finding in the postcardiac injury syndrome, seen in about 80% of patients. It may be bilateral or unilateral and is commonly accompanied by consolidation and pericardial effusion. Pulmonary embolism is commonly associated with pleural effusion, which is seen in 25–50% of cases.
A number of drugs have been described as causing pleural effusions. The most common agents are cytotoxics (methotrexate, procarbazine, mitomycin, busulfan, bleomycin and interleukin-2), nitrofurantoin, antimigraine drugs (ergotamine, methysergide), amiodarone, propylthiouracil, bromocriptine and gonadotrophins. With a number of these agents pleural thickening is more common than a pleural effusion.
Pleural effusion is also a recognised complication of hepatic cirrhosis. The principal mechanism of its production is the transdiaphragmatic passage of ascites, though other factors such as hypoalbuminaemia may contribute in a small number of cases.
Both acute and chronic pancreatitis are associated with pleural effusions which have high amylase levels. In acute pancreatitis, exudative and often blood-stained effusions form in 15% of patients, particularly on the left side where the diaphragm is closely related to the pancreatic tail. Associated elevation of the hemidiaphragm and basal lung consolidation are common. In chronic pancreatitis, effusions tend to be large and recurrent and patients present with dyspnoea, unlike effusions in acute pancreatitis in which abdominal symptoms predominate. The pathogenesis of pleural effusion in chronic pancreatitis is fistula formation following ductal rupture.
Pleural effusion is common with subphrenic abscess and occurs in about 80% of patients. The effusion is often accompanied by basal lung collapse and consolidation, an elevated hemidiaphragm and a subdiaphragmatic air–fluid level.
Pleural effusion may occur in a number of renal conditions. Exudative effusions may be seen in uraemia and are often accompanied by pericarditis. Effusions can be large or small and are often unilateral, behaving in a rather indolent fashion. In common with other hypoproteinaemic states, bilateral effusions develop in about 20% of patients with nephrotic syndrome. Peritoneal dialysis can produce pleural effusions by the direct transdiaphragmatic passage of fluid, as occurs with cirrhotic ascites. In common with other ascites-related effusions they are predominantly right-sided, but these effusions have a diagnostically high level of glucose.
Patients with acquired immune deficiency syndrome are at risk for a variety of pleural infections and neoplasms that can be associated with pleural effusion. These effusions are most frequently caused by pneumonic infections but can also be the result of non-Hodgkin's lymphoma. Empyema is a suppurative exudate usually parapneumonic. Less commonly it is caused by transdiaphragmatic extension of a liver abscess or by broncho pleural fistula (Fig. 1)
FIGURE 1 ■ Empyema. (A) Chest X-ray shows an encapsulated pleural effusion on the right and a free pleural effusion on the left. (B, C) An enhanced CT confirms this bilateral fluid collection. However, the pleura on the right is thickened but smooth and enhancing while subpleural fat is infiltrated and widened, which is the result of oedema. The empyema followed pneumonia, which can be seen in the middle lobe (C). Compare with non-complicated left pleural effusion.
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