The workup of moderate-to-large pericardial effusion should focus on its hemodynamic impact and potential cause. A structured approach to diagnostic evaluation of pericardial effusion is needed. We retrospectively studied a contemporary cohort of 103 patients with moderate-to-large pericardial effusion hospitalized at St. Luke’s Roosevelt Hospital Center from July 2009 till August 2013. Diagnosis of pericardial effusion was independently ascertained by chart review. We applied a stepwise parsimonious approach to establish the cause of pericardial effusion. In the studied cohort, the mean age was 61 years, 50% were men, and 65 patients (63%) underwent pericardial effusion drainage. Using the structured approach, the cause of the effusion was ascertained in 70 patients (68%) by noninvasive targeted testing. Malignant effusion was confirmed in 19 patients (19%). All patients with malignant effusion had either history of malignancy or suggestive noninvasive findings. In conclusion, a structured approach can help to ascertain the diagnosis in patients with moderate-to-large pericardial effusion and guide the need for pericardial drainage or sampling.
Pericardial effusion is relatively common in routine clinical practice. It can be recognized based on clinical suspicion or can be an incidental finding on chest or cardiac imaging. Once pericardial effusion is recognized, the further diagnostic workup should focus on the potential cause of the effusion and its hemodynamic impact. Although draining pericardial effusion due to tamponade is a well-established indication, routine pericardial drainage for diagnostic purposes is not indicated. The present study assesses the impact of a structured and practical approach to establish the cause of pericardial effusion in a modern cohort of inner city patients with moderate-to-large pericardial effusion.
Materials and Methods
We conducted a retrospective study of patients with moderate-to-large pericardial effusion hospitalized at St. Luke’s Roosevelt Hospital Center from July 2009 till August 2013. After exclusion of patients with trivial and small effusions, 124 patients were identified. A total of 103 patients were included in our final analysis after excluding 21 patients due to incomplete or unobtainable data or terminal illness on palliative care.
Pericardial effusion was considered moderate if the largest dimension of pericardial fluid at end-diastole in any echocardiographic view was at least 1 cm but ≤2 cm; large effusion was defined as the largest pericardial fluid pocket measuring >2 cm. Right atrial collapse was defined as right atrial invagination in any echocardiographic view with duration of >1/3 of the cardiac cycle. Right ventricular collapse was defined as failure of the right ventricle to expand during the early phase of diastole. Confirmatory signs of hemodynamically significant pericardial effusion included respiratory variation across the atrioventricular valves and inferior vena cava engorgement. The pericardial effusion scoring index was calculated based on the size of the effusion at end-diastole, echocardiographic hemodynamic findings, and presumed cause as previously described.
Demographic, clinical, laboratory, imaging, procedural, and pathologic data were obtained by chart review. The final diagnosis for the cause of pericardial effusion was verified by 3 independent reviewers (EA, GEH, and PC). The diagnosis of acute pericarditis was ascertained if the patient met at least 2 of 4 following criteria: (1) characteristic chest pain, (2) friction rub on physical examination, (3) typical electrocardiographic changes, and (4) presence of pericardial effusion. All patients with pericarditis had elevated inflammatory markers (C-reactive protein >10 mg/L and/or erythrocyte sedimentation rate >50 mm/hr). The diagnosis of pericardial effusion due to congestive heart failure or pulmonary hypertension was ascertained when evidence for right ventricular dilation and hypokinesia was present on echocardiogram, and/or the tricuspid regurgitation velocity exceeded 3.5 m/s. Connective tissue disease was diagnosed based on clinical features and autoimmune antibody titers. Malignant effusions were confirmed by pericardial fluid cytology or pathology of the sampled pericardium. Two cases were assumed malignant because of highly suggestive computed tomographic scan findings. Postprocedural and postsurgical effusions were divided into early (diagnosed within 7 days of the procedure or surgery) and late (>7 days).
Means and proportions are reported for patients who did and did not undergo pericardial effusion drainage. Comparison between the groups was performed using the t test or Mann-Whitney U test for continuous variables and chi-square or Fisher’s exact test for categorical variables. Analysis was performed using a standard statistical package (SPSS 16.0 for Windows; SPSS, Inc, Chicago, Illinois). All statistical tests were 2-sided, and a p value of <0.05 was considered to indicate statistical significance.
Results
One hundred three patients with moderate-to-large pericardial effusion were included in the analysis. The mean age was 61 years, and 50% were men ( Table 1 ). The common symptoms at the time of presentation included dyspnea and chest pain. Patients who underwent pericardial effusion drainage were more likely to have known malignancy, larger effusions, and evidence of chamber collapse on echocardiogram and a greater mean pericardial effusion scoring index. The causes of pericardial effusion are listed in Table 2 . Malignant effusion comprised 19% of all effusions, which is similar to older studies of moderate-to-large pericardial effusion. Patients with malignant effusions were younger than patients with idiopathic effusion (mean age 56 [14] vs 66 [12] years, p = 0.03). We report a greater incidence of postprocedural and surgical effusions (19%) compared with some other studies that probably reflect contemporary medical practice. Other causes in Table 2 include purulent pericarditis (1), liver cirrhosis (1), drug-induced pericardial effusion (1), ascending aortic dissection (1), and peripneumonic nonpurulent effusion (1). No case of tuberculous pericarditis was identified.
| Characteristics | Overall (n = 103) | Drained | P Value | |
|---|---|---|---|---|
| Yes (n = 65) | No (n = 38) | |||
| Age (years), mean ± SD | 61 ± 19 | 59 ± 17 | 64 ± 21 | 0.21 |
| Male gender | 51 (50%) | 32 (49%) | 19 (50%) | 0.94 |
| Presenting complaint | 0.28 | |||
| Dyspnea | 61 (59%) | 41 (63%) | 20 (53%) | |
| Chest pain | 19 (19%) | 12 (19%) | 7 (18%) | |
| Syncope | 7 (7%) | 3 (5%) | 4 (11%) | |
| Other or incidental finding | 16 (16%) | 9 (14%) | 7 (18%) | |
| Known malignancy | 19 (19%) | 17 (26%) | 2 (5%) | <0.01 |
| Immunosuppressive therapy | 12 (12%) | 10 (15%) | 2 (5%) | 0.12 |
| HIV infection | 7 (7%) | 5 (8%) | 2 (5%) | 0.64 |
| Known ESRD | 11 (11%) | 6 (9%) | 5 (13%) | 0.53 |
| Large effusion | 71 (69%) | 54 (83%) | 17 (45%) | <0.01 |
| Effusion size (cm), mean ± SD | 2.2 ± 0.5 | 2.4 ± 0.5 | 1.9 ± 0.4 | <0.01 |
| Chamber collapse | 63 (61%) | 52 (80%) | 11 (29%) | <0.01 |
| Pericardial effusion scoring index, mean ± SD | 4.7 ± 1.9 | 5.5 ± 1.6 | 3.1 ± 1.4 | <0.01 |
| Etiology | Overall (n = 103) | Drained | P Value | |
|---|---|---|---|---|
| Yes (n = 65) | No (n = 38) | |||
| Idiopathic | 21 (20%) | 13 (20%) | 8 (21%) | 0.90 |
| Malignant | 19 (19%) | 17 (26%) | 2 (5%) | <0.01 |
| Post-procedural or surgery | 19 (19%) | 15 (23%) | 4 (11%) | 0.11 |
| Renal failure | 12 (12%) | 5 (8%) | 7 (18%) | 0.12 |
| Pericarditis | 9 (9%) | 5 (8%) | 4 (11%) | 0.72 |
| Heart failure and pulmonary hypertension | 8 (8%) | 3 (5%) | 5 (13%) | 0.14 |
| Hypothyroidism | 5 (5%) | 1 (2%) | 4 (11%) | 0.06 |
| Connective tissue disorder | 5 (5%) | 2 (3%) | 3 (8%) | 0.36 |
| Other causes ∗ | 5 (5%) | 4 (6%) | 1 (3%) | 0.65 |
∗ See Results section for details.
We retrospectively applied a stepwise parsimonious approach to laboratory testing and imaging in patients with pericardial effusion ( Figure 1 ) as modified from the previous algorithm. History, physical examination, and medical chart review often provide clues to the cause of pericardial effusion. Thorough breast examination for masses is an important component of physical examination in women. Transthoracic echocardiography is the standard test in establishing the presence of pericardial effusion, quantifying the size of the effusion, and assessing its hemodynamic impact. Postprocedural effusions, congestive heart failure with right ventricular failure or pulmonary hypertension, and typical acute pericarditis can be ascertained at this stage if there are no atypical features. The initial tier of testing includes complete blood count, complete metabolic panel, coagulation studies, inflammatory markers (erythrocyte sedimentation rate and C-reactive protein), cardiac biomarkers, thyroid-stimulating hormone level, and chest x-ray. Advanced renal disease and profound hypothyroidism can be ascertained at this stage. Elevated inflammatory markers are common in pericarditis, and elevated cardiac biomarkers suggest myocardial involvement. Chest x-ray may reveal infiltrates or mass lesions. The next tier of testing is tailored to the individual patient scenario. In appropriate clinical settings, human immunodeficiency virus testing, autoantibodies, and blood cultures are obtained. Advanced chest imaging (such as computed tomographic scan, positron emission tomography, and magnetic resonance imaging) can be helpful in certain clinical situations, especially when malignancy is suspected. Tuberculosis testing should also be considered in the right epidemiologic and clinical settings. Transesophageal echocardiography can diagnose loculated effusion when transthoracic echocardiography is limited (e.g., postoperative patients), and regional tamponade is considered.
