Malignant pleural effusions (MPEs) cause considerable morbidity for patients afflicted with cancer. Metastatic breast, lung, and ovarian cancers account for the majority of cases. An estimated 150,000 new patients are diagnosed annually with dyspnea secondary to MPE.1,2 Both diagnostic and therapeutic goals can be achieved with thoracentesis. Initial malignant diagnosis can be established in 50–60% of patients by means of thoracentesis.1,2 However, in almost all cases, the malignant effusions recur, and patients require long-term palliation. The ideal therapy permits expedient, low-cost management of the pleural effusion with minimal morbidity because many of these patients have terminal disease. Operative management includes drainage through the use of video-assisted thoracic surgery (VATS) techniques combined with sclerosis, as well as operative placement of indwelling drainage catheters.2–4 The operative techniques are described in Chapter 101. Nonoperative management of MPEs, the focus of this chapter, includes systemic chemotherapy and several methods of mechanical drainage, which may be combined with pleural sclerosing agents.
Lung cancer is the leading cause of MPE and accounts for as many as 40% of cases, followed by metastatic breast (25%), ovarian (5%), and gastric cancers (5%). Another 10% of patients have lymphoma-induced effusions, leaving 10% without identifiable primary malignancy.2,5 Metastatic pleural spread is a complex mechanism that requires a series of mutational events leading to the sequential expression and coordination of numerous growth factors and cell surface adhesion molecules.6
Pleural seeding either by direct tumor extension or by hematogenous or lymphangitic spread initiates a series of pathophysiologic events that cause the development of effusions. These mechanisms include (1) the production of angiogenic growth factors that cause increased vascular permeability, including vascular endothelial growth factor, among others, (2) lymphatic obstruction, which perturbs the normal absorption cycle of 2–3 L of pleural fluid daily, (3) direct production of fluid by the tumor, which often occurs with ovarian malignancies, and rarely, (4) tumor invasion and blockage of venous structures, which results in venous hypertension and the ensuing alternating Starling's forces that culminate in the effusion.2
All or some of these mechanisms contribute to the effusion, which then causes dyspnea, the principal and most disturbing symptom. The dyspnea tends to be progressive, if untreated, and eventually leads to symptoms at rest, underscoring the need for palliative treatment. The severity or degree of symptoms is related to the underlying cardiopulmonary function, the size of the effusion, or the rate of accumulation. Large effusions compress the lung and alter chest wall compliance, which together cause shortness of breath not only by altering the breathing mechanics, that is, decreasing the forced expiratory volume in 1 second (FEV1) and tidal volume, but also by stimulating neurologic reflexes that lead to a subjective and uncomfortable sense of shortness of breath.2
The development of MPE portends a dismal prognosis because it is a sign of advanced disease. After diagnosis, patients with ...