Pleural Effusion in Congestive Heart Failure

Abstract

Pleural effusions are commonly seen in patients with congestive heart failure. They are usually bilateral or right sided and are rarely left sided. An important step in the evaluation of any pleural effusion is the classification of the fluid into a transudate or an exudate. Transudative effusions develop when there is a change in systemic factors such as an increase in capillary hydrostatic pressure or a decrease in colloid oncotic pressure. Exudates are the result of pleural inflammation, infection, injury, or lymphatic obstruction. An exudative process always requires a more extensive and often invasive workup and often a search for occult malignancy.1Health and Public Policy Committee, American College of PhysiciansDiagnostic thoracentesis and pleural biopsy in pleural effusions.Ann Intern Med. 1985; 103: 799-802Crossref PubMed Scopus (43) Google Scholar It is believed that congestive heart failure causes transudative effusions.In the past, specific gravity and protein concentration of the fluid were used to separate transudates from exudates. More than 50 years ago, Gilligan et al2Gilligan DR Volk MC Blumgart HS Observations of the chemical and physical relationship between blood serum and body fluids.J Clin Invest. 1934; 13: 365-381Crossref PubMed Google Scholar studied the effect of diuresis on the protein concentration of pleural effusion. A decrease in the volume of the fluid and a small increase in the protein concentration were reported. Pillay3Pillay VKG Total proteins in serous fluids in cardiac failure.S Afr Med J. 1965; 39: 142-143PubMed Google Scholar studied six patients with pleural effusion due to heart failure at the time of hospital admission and after diuresis with mercurials. The mean fluid protein concentration increased from 1.5 to 2.0 g/dl. In one patient it rose from 1.3 to 3.1 g/dl.Criteria proposed by Light et al4Light RW MacGregor MI Luchsinger PC Ball WC Pleural effusions: the diagnostic separation of transudates and exudates.Ann Intern Med. 1972; 77: 507-513Crossref PubMed Scopus (1178) Google Scholar are now used to classify effusions. The fluid is classified as an exudate if the pleural fluid/serum protein ratio is greater than 0.5, or the pleural fluid lactate dehydrogenase (LDH) is greater than 200 IU, or the pleural fluid/serum LDH ratio is greater than 0.6. Even when these criteria are used, effusions due to heart failure may be misclassified. Peterman and Speicher5Peterman TA Speicher CE Evaluating pleural effusions: a two stage laboratory approach.JAMA. 1984; 252: 1051-1053Crossref PubMed Scopus (40) Google Scholar studied 495 pleural effusions to evaluate the criteria of Light et al. Of the 57 patients with heart failure and no other cause for pleural effusion, 19 (33 percent) had exudative effusions. Recently we studied eight patients with pleural effusion due to heart failure. Thoracentesis was performed at the time of hospital admission and after diuretic therapy. Significant increase in the protein level (2.2 to 3.2 g/dl) and the fluid/serum ratio of LDH (0.39 to 0.64) was found. In three patients the fluid was classified as a transudate at the initial study (by the criteria of Light et al) but met the criteria for an exudate after treatment of heart failure.6Chakko SC Caldwell SH Sforza PP Treatment of congestive heart failure and its effect on pleural fluid chemistry.Chest. 1989; 95: 798-802Abstract Full Text Full Text PDF PubMed Scopus (77) Google Scholar It is clear that treatment of heart failure causes significant changes in the pleural fluid chemistry; in some cases a transudate may be converted into a “pseudoexudate.” It is likely that with diuresis, water from the effusion is reabsorbed more rapidly than other molecules and the concentrations of protein and LDH rise.Since pleural effusions are common in heart failure, thoracentesis of all such effusions is not practical. The health and public policy committee of the American College of Physicians noted that “the indication for a diagnostic thoracentesis is the presence of any pleural effusion of unknown cause. An exception would be a patient presenting with clear clinical manifestations of recurrent left ventricular failure. In this circumstance, a trial of diuresis may precede consideration of thoracentesis.”1Health and Public Policy Committee, American College of PhysiciansDiagnostic thoracentesis and pleural biopsy in pleural effusions.Ann Intern Med. 1985; 103: 799-802Crossref PubMed Scopus (43) Google Scholar However, the physician faces the dilemma that diuresis will alter the pleural fluid chemistry.In this issue (see page 546), Roth et al used the serum-effusion albumin gradient in the evaluation of pleural effusions. The criteria of Light et al4Light RW MacGregor MI Luchsinger PC Ball WC Pleural effusions: the diagnostic separation of transudates and exudates.Ann Intern Med. 1972; 77: 507-513Crossref PubMed Scopus (1178) Google Scholar misclassified five effusions due to heart failure as exudates, but the serum-effusion albumin gradient classified them correctly. However, the gradient misclassified two malignant effusions as transudates. The criteria of Light et al are very sensitive for diagnosing exudates and the gradient appears to be more specific. However, only 15 patients with heart failure were studied. In this and other studies, if a patient with heart failure had pleural effusion, it was assumed that the effusion was secondary to failure; an associated silent pulmonary embolism is difficult to exclude. If the serum-effusion albumin gradient is confirmed to be a useful test in larger numbers of patients with heart failure, it may become a useful clinical tool. Clinicians should be aware of the fact that diuresis may convert a transudative effusion of heart failure into a pseudoexudate. Thoracentesis is not indicated in every patient with heart failure and pleural effusion; however, if a comorbid condition is suspected, thoracentesis should be done early and not after a trial of diuretic therapy. Pleural effusions are commonly seen in patients with congestive heart failure. They are usually bilateral or right sided and are rarely left sided. An important step in the evaluation of any pleural effusion is the classification of the fluid into a transudate or an exudate. Transudative effusions develop when there is a change in systemic factors such as an increase in capillary hydrostatic pressure or a decrease in colloid oncotic pressure. Exudates are the result of pleural inflammation, infection, injury, or lymphatic obstruction. An exudative process always requires a more extensive and often invasive workup and often a search for occult malignancy.1Health and Public Policy Committee, American College of PhysiciansDiagnostic thoracentesis and pleural biopsy in pleural effusions.Ann Intern Med. 1985; 103: 799-802Crossref PubMed Scopus (43) Google Scholar It is believed that congestive heart failure causes transudative effusions. In the past, specific gravity and protein concentration of the fluid were used to separate transudates from exudates. More than 50 years ago, Gilligan et al2Gilligan DR Volk MC Blumgart HS Observations of the chemical and physical relationship between blood serum and body fluids.J Clin Invest. 1934; 13: 365-381Crossref PubMed Google Scholar studied the effect of diuresis on the protein concentration of pleural effusion. A decrease in the volume of the fluid and a small increase in the protein concentration were reported. Pillay3Pillay VKG Total proteins in serous fluids in cardiac failure.S Afr Med J. 1965; 39: 142-143PubMed Google Scholar studied six patients with pleural effusion due to heart failure at the time of hospital admission and after diuresis with mercurials. The mean fluid protein concentration increased from 1.5 to 2.0 g/dl. In one patient it rose from 1.3 to 3.1 g/dl. Criteria proposed by Light et al4Light RW MacGregor MI Luchsinger PC Ball WC Pleural effusions: the diagnostic separation of transudates and exudates.Ann Intern Med. 1972; 77: 507-513Crossref PubMed Scopus (1178) Google Scholar are now used to classify effusions. The fluid is classified as an exudate if the pleural fluid/serum protein ratio is greater than 0.5, or the pleural fluid lactate dehydrogenase (LDH) is greater than 200 IU, or the pleural fluid/serum LDH ratio is greater than 0.6. Even when these criteria are used, effusions due to heart failure may be misclassified. Peterman and Speicher5Peterman TA Speicher CE Evaluating pleural effusions: a two stage laboratory approach.JAMA. 1984; 252: 1051-1053Crossref PubMed Scopus (40) Google Scholar studied 495 pleural effusions to evaluate the criteria of Light et al. Of the 57 patients with heart failure and no other cause for pleural effusion, 19 (33 percent) had exudative effusions. Recently we studied eight patients with pleural effusion due to heart failure. Thoracentesis was performed at the time of hospital admission and after diuretic therapy. Significant increase in the protein level (2.2 to 3.2 g/dl) and the fluid/serum ratio of LDH (0.39 to 0.64) was found. In three patients the fluid was classified as a transudate at the initial study (by the criteria of Light et al) but met the criteria for an exudate after treatment of heart failure.6Chakko SC Caldwell SH Sforza PP Treatment of congestive heart failure and its effect on pleural fluid chemistry.Chest. 1989; 95: 798-802Abstract Full Text Full Text PDF PubMed Scopus (77) Google Scholar It is clear that treatment of heart failure causes significant changes in the pleural fluid chemistry; in some cases a transudate may be converted into a “pseudoexudate.” It is likely that with diuresis, water from the effusion is reabsorbed more rapidly than other molecules and the concentrations of protein and LDH rise. Since pleural effusions are common in heart failure, thoracentesis of all such effusions is not practical. The health and public policy committee of the American College of Physicians noted that “the indication for a diagnostic thoracentesis is the presence of any pleural effusion of unknown cause. An exception would be a patient presenting with clear clinical manifestations of recurrent left ventricular failure. In this circumstance, a trial of diuresis may precede consideration of thoracentesis.”1Health and Public Policy Committee, American College of PhysiciansDiagnostic thoracentesis and pleural biopsy in pleural effusions.Ann Intern Med. 1985; 103: 799-802Crossref PubMed Scopus (43) Google Scholar However, the physician faces the dilemma that diuresis will alter the pleural fluid chemistry. In this issue (see page 546), Roth et al used the serum-effusion albumin gradient in the evaluation of pleural effusions. The criteria of Light et al4Light RW MacGregor MI Luchsinger PC Ball WC Pleural effusions: the diagnostic separation of transudates and exudates.Ann Intern Med. 1972; 77: 507-513Crossref PubMed Scopus (1178) Google Scholar misclassified five effusions due to heart failure as exudates, but the serum-effusion albumin gradient classified them correctly. However, the gradient misclassified two malignant effusions as transudates. The criteria of Light et al are very sensitive for diagnosing exudates and the gradient appears to be more specific. However, only 15 patients with heart failure were studied. In this and other studies, if a patient with heart failure had pleural effusion, it was assumed that the effusion was secondary to failure; an associated silent pulmonary embolism is difficult to exclude. If the serum-effusion albumin gradient is confirmed to be a useful test in larger numbers of patients with heart failure, it may become a useful clinical tool. Clinicians should be aware of the fact that diuresis may convert a transudative effusion of heart failure into a pseudoexudate. Thoracentesis is not indicated in every patient with heart failure and pleural effusion; however, if a comorbid condition is suspected, thoracentesis should be done early and not after a trial of diuretic therapy.