Pathophysiology

An increased amount of fluid (an effusion) accumulates in the pleural space whenever the rate of fluid formation exceeds the rate of fluid absorption. Numerous conditions may lead to pleural effusions, including viral and bacterial infections, neoplasms, thromboemboli, cardiovascular dysfunction, and immunologic dysfunction (Box 110-1). Mechanisms that contribute to increased pleural fluid accumulation include an increase in microvascular pressure (e.g., CHF), a decrease in plasma osmotic pressure (e.g., hypoalbuminemia), an increase in the permeability of microcirculation (e.g., pneumonia), a decrease in pleural pressure (e.g., atelectasis), an impaired lymphatic drainage from pleural spaces (e.g., malignant effusions), and the movement of fluid across the diaphragm from the peritoneal cavity (e.g., inflammation from acute pancreatitis). Parapneumonic effusions are the most common type of effusion and are associated with bacterial infections such as pneumonia, lung abscesses, and bronchiectasis.⁵ Malignant pleural effusions are a common problem encountered in persons with advanced cancer. Lung cancer in men and breast cancer in women are the most common causes of malignant pleural effusions.⁶ Other common causes of malignant pleural effusions include lymphomas and genitourinary tract and gastrointestinal tract tumors.⁶

Pleural effusions are often categorized as transudates and exudates on the basis of the amount of protein detected in the pleural fluid. Exudative pleural effusions result primarily from pleural and lung inflammation (e.g., pneumonia) or impaired lymphatic drainage of the pleural space (e.g., malignant disease). In fact, a variety of disease mechanisms, including pneumonia and other infections, malignant carcinomas, immunologic and lymphatic abnormalities, and iatrogenic factors, can cause exudates. Transudative effusions develop when systemic factors alter the formation or absorption of pleural fluid, rather than from pleuritic disease. They are produced by imbalances in hydrostatic and osmotic pressures across the pleural membrane and are usually bilateral. Transudates have a lower specific gravity and lower concentrations of protein and lactate dehydrogenase compared with exudative effusions.¹ CHF is probably the most common cause of transudative pleural effusions, but other disease processes that cause movement of fluid from the peritoneal space or retroperitoneal space, such as cirrhosis, nephrosis, and glomerulonephritis, can cause transudates.²

Age-related changes affecting the respiratory system play an important role in the development of pleural effusions. In addition to the expected changes related to aging, years of exposure to particulate matter, dust, occupational toxins, and episodic respiratory infections increase the risk for development of a pleural effusion.²

Clinical Presentation

Persons with pleural effusions often are asymptomatic when they are seen initially. When symptoms do occur, the most common presenting complaints include dyspnea, nonproductive cough, pleuritic chest pain, and activity intolerance. Dyspnea is the most common complaint and often increases with recumbent positions.² Cough tends to worsen as the size of the effusion increases. Pleuritic pain is associated with inflammation of the parietal pleura and is caused by irritation of its sensory fibers. This pain is often sharp, unilateral, and localized to the affected area, although it may also be experienced in the lower chest and ipsilateral shoulder or referred to the abdomen. Exacerbating factors include deep inspiration, cough, and other movement of the upper body. Constrictive pericarditis is a relatively common cause of pleural effusions, and chest pain and dyspnea are common associated symptoms.⁷

Malignant tumors involving the parietal pleura generally cause steady, dull pain compared with the sharp, intermittent pain associated with an acute inflammatory process. Pleural effusions cause compression of adjacent lung tissue and reduce the amount of possible lung expansion, which may result in varying degrees of dyspnea, depending on the size and functional status of the underlying lung and the rate of fluid accumulation. However, dyspnea does not necessarily correlate with blood oxygen levels or the size of the pleural effusion but rather seems to be related to the increased thoracic cage size, which affects respiratory muscle function. Dyspnea is a common presenting symptom associated with malignant pleural effusions and is occasionally accompanied by chest pain and cough. Chest pain is usually related to involvement of the parietal pleura, ribs and intercostal muscles, and other structures. The nonproductive cough is most likely a result of lung compression and bronchial irritation.² Associated constitutional symptoms include weight loss, malaise, and anorexia.

A thorough history is important and can be helpful in discriminating between the symptoms associated with the effusion and those of the primary underlying pathophysiologic process. Information about the presence of fever, cough, sputum production, dyspnea, or abdominal pain should be elicited. Past medical history, including systemic and chronic illnesses, previous surgeries, prior exposures (such as to tuberculosis and asbestos), and previous alcohol abuse, is important.

Physical Examination

Several findings on physical examination are suggestive of a pleural effusion; however, the clinical manifestations of the effusion may be overshadowed by the underlying disease process.⁸ Common physical examination findings include decreased or absent breath sounds over the effusion, decreased respiratory excursion, dullness to percussion, reduced or absent tactile fremitus, and decreased or absent bronchial breath sounds, sometimes with egophony (E-to-A change) at the upper fluid borders. Pleural inflammation is often accompanied by a friction rub that is transitory and that generally disappears as fluid accumulates in the pleural space. Small effusions (<500 mL) may be associated with minimum or no findings. In situations in which effusions are greater (>1500 mL) or pulmonary compromise is more substantial, the use of accessory muscles of respiration, inspiratory lag, cyanosis, bulging intercostal margins, mediastinal shift, and jugular vein distention may be evident. In addition to assessing the respiratory status, the provider needs to perform a complete physical examination to identify signs that may be manifestations of systemic or acute illness and suggest the cause of the effusion. For example, nonthoracic signs such as jugular vein distention and an S₃ gallop are suggestive of CHF. A right ventricular heave or thrombophlebitis suggests pulmonary embolus. Lymphadenopathy or hepatosplenomegaly may be associated with hepatic disease, and ascites may be indicative of a hepatic cause.