Pericardial effusion: a continuing drain on our diagnostic acumen

Effusive pericardial disease is a relatively rare cause of hospital admission. Its presenting clinical symptoms are frequently non-specific, and the treating physicians may not suspect the diagnosis. Although the clinical course may be benign, pericardial effusions can be associated with substantial morbidity and mortality. Even when the condition is recognized, clinicians are often frustrated in their attempts to determine its underlying etiology and to treat a persistent effusion. The indication for drainage of an effusion is clear if there is cardiac tamponade, but is less certain in the absence of hemodynamic instability. Pericardiocentesis is not without risk, and the diagnostic yield of pathological examination of the fluid is frequently low, even when pericardial tissue is obtained by surgical biopsy. Clinicians have benefitted from the work of a small group of clinical investigators who became ardent “students” of the pericardium. The authors of the article in this issue of The Green Journal, “Large pericardial effusion in a general hospital: clinical clues to etiologic diagnosis”, are members of that small circle (1). In 1977, Drs. Sagrista-Sauleda, Permanyer-Miralda and Soler-Soler from the Hospital General Universitari Vall d’Hebron in Barcelona established one of the first “clinical pathways” in cardiology for the diagnosis and treatment of pericardial disease. Their prospective application of this systematic and logical approach, and their careful data collection, are excellent examples of this special breed of clinical investigation. Not only have they written some of the seminal papers in the field, but they have also provided young clinician-investigators with an important model for ongoing “grassroots” hospital and patient-based research. In an era of advanced technology, innovative therapeutics, and the randomized trial, we often forget that there is still much to be learned about the natural history of a disease. The protocol developed by these investigators consists of three stages, which involve progressively more invasive diagnostic tests (1). Stage I consists of the basics: history, physical examination, electrocardiogram (EKG), and chest radiograph. Laboratory tests in this stage include sputum for acid-fast bacilli, anti-nuclear antibody assays, and thyroid studies as well as others suggested by the history and physical examination. In Stage II, pericardiocentesis is performed for tamponade, suspicion of purulent pericarditis, or large effusions. Finally, in Stage III, the authors proceed to open pericardial biopsy if tamponade recurs following the pericardiocentesis or if there is a persistent effusion and no diagnosis after 3 weeks. In the paper in this issue (1), that protocol was used in 322 hospitalized patients with moderate and large effusions identified in the echocardiography laboratory during a 6-year period. Patients were divided into three groups: 124 with moderate effusions (10 to 20 mm in diastole); 79 with large effusions (.20 mm in diastole) and 119 with tamponade. The investigators hypothesized that clinical data, including the size of the effusion, the presence of tamponade, and the presence of inflammatory signs (chest pain, friction rub, fever, and EKG signs of diffuse ST elevation) would point to the etiology of the effusion. An underlying condition was identified on this basis after the first stage of their investigation in 60% of their patients. Of the remaining 130 patients, 76 had inflammatory signs; after a careful laboratory examination, the majority of these patients (n 5 61) were classified as “acute idiopathic pericarditis.” Of the 54 without inflammatory signs, there were 19 with tamponade and 35 without. Nine of those with tamponade and without inflammation had neoplastic pericarditis. Moreover, tamponade was most common in those with neoplastic disease. Still, among the patients without an underlying diagnosis apparent on presentation, the majority in each clinical category had idiopathic pericarditis, confirming the diagnostic importance of noninvasive tests in the exclusion of underlying disease. The authors reported that the incidence of acute inflammatory signs varied among the final diagnostic categories in the 130 patients with no diagnosis after Stage I. Not surprisingly, they were most frequent (98%) among those with a final diagnosis of acute idiopathic pericarditis and uncommon among those with chronic idiopathic pericarditis or other etiologies. The importance of this finding is uncertain, since acute idiopathic pericarditis was diagnosed when “clinical symptoms subsided with bed rest and nonsteroidal anti-inflammatory drugs” in the absence of any other specific diagnosis. Thus, the observation that inflammatory signs were frequent in this group seems self-evident. However, inflammatory signs were not uncommon among patients with neoplastic effusions (33%) and, importantly, their presence did not exclude malignancy. Am J Med. 2000;109:169 –170. From the Associate Professor of Clinical Medicine, Director, Adult Echocardiography Laboratory, University of California, San Francisco, California. Correspondence should be addressed to Elyse Foster, MD, University of California, San Francisco, 505 Parnassus Avenue, San Francisco, CA 94143-0214.