Epidemiology

Because pleural effusions are harbingers of underlying disease, their precise incidence is difficult to determine. The incidence in the United States is estimated to be at least 1.5 million cases annually.¹ In industrialized countries worldwide, the incidence approaches 320 cases per 100,000 people—with heart failure, bacterial pneumonia, cirrhosis, malignancy, and pulmonary embolism representing the most common causes. The morbidity and mortality associated with pleural effusion are directly related to cause, stage of disease at the time of diagnosis, and biochemical findings in the pleural fluid. Because pleural effusions are manifestations of underlying diseases, age, sex, race, and socioeconomic status reflect the variation in incidence of the causative disease state or disorder.

Pathophysiology

Under normal physiologic conditions, the parietal and visceral pleurae are in close apposition, with only a small potential space between them. This potential space contains a small amount of pleural fluid (1 mL) to minimize friction from continuous movement of the appositional lining. The accumulation of pleural fluid (whether osmotic or hydrostatic in nature) can usually be explained by either increased pleural fluid formation or decreased pleural fluid absorption, or both.

Pleural effusions caused by an increase in pleural fluid formation can be further subdivided into elevation in hydrostatic pressure (e.g., congestive heart failure), decreased colloid osmotic pressure (e.g., cirrhosis, nephrotic syndrome), increased capillary permeability (e.g., infection, neoplasm), passage of fluid through openings in the diaphragm (e.g., ascites), or reduction of pleural space pressure (e.g., atelectasis). An effusion caused by decreased pleural fluid absorption can be qualified further as either lymphatic obstruction or elevation of systemic venous pressure resulting in impaired lymphatic drainage (e.g., superior vena cava syndrome).

The presence of fluid in the normally negative pressure environment of the pleural space has a number of consequences for respiratory physiology. Pleural effusions produce a restrictive ventilatory defect and also decrease total lung capacity, functional residual capacity, and forced vital capacity. They may cause ventilation-perfusion mismatches and, when large enough, compromise cardiac output.²

The classic work of Light et al.³ in 1972 demonstrated that 99% of pleural effusions could be classified into these two general categories, transudative and exudative (Box 52.1). A basic difference is that transudates generally reflect a systemic process whereas exudates usually signify underlying local pleuropulmonary disease.³

Presenting Signs and Symptoms

In many cases, pleural effusions are asymptomatic when discovered. Physical findings of pleural effusions are unlikely to be manifested until an effusion exceeds 300 mL. Dyspnea, the most common symptom associated with pleural effusion, is related more to distortion of the diaphragm and chest wall during respiration than to hypoxemia. Less commonly, symptoms of pleural effusions consist of a mild, nonproductive cough and chest pain. Pleuritic chest pain indicates inflammation of the parietal pleura because the visceral pleura is not innervated. In many patients, drainage of pleural fluid alleviates the symptoms despite limited improvement in gas exchange. Findings on lung examination such as decreased breath sounds, dullness to percussion, pleural friction rub, egophony, and reduced tactile fremitus have all been described.^1,2 Auscultation alone can miss up to 600 mL of fluid in the lung.^4–6

The emergency physician should assess for the cause of the effusion. If a patient complains of fever, weight loss, and a progressively worsening cough with associated dyspnea, an oncologic or infectious cause is likely. Constant chest wall pain may reflect chest wall invasion by bronchogenic carcinoma or malignant mesothelioma. Pleuritic chest pain suggests either pulmonary embolism or an inflammatory pleural process. An effusion can mimic the classic symptoms of acute coronary syndrome, such as chest pain, dyspnea, and shoulder pain (Box 52.2).

Differential Diagnosis and Medical Decision Making

A pleural effusion is frequently identified during evaluation of the underlying chief complaint of the patient. Because the etiology of pleural effusion is myriad, a thorough history and physical examination may narrow the differential diagnosis substantially. Box 52.3 lists the common causes of pleural effusion. Frequently, effusion is identified on physical examination or with basic chest radiography, but additional imaging modalities, including radiography, ultrasonography, and computed tomography (CT), may identify the cause and provide additional insight about the effusion.^1,3,6

Diagnostic Considerations