CASE
A 27-year-old man presented to the emergency department with complaints of shortness of breath that had worsened over several weeks and a dry cough that was sometimes severe. His symptoms increased when lying flat.
He denied having any chest pain. The patient had been healthy until 3 months previously, when he ruptured an Achilles tendon, which was surgically repaired. He subsequently developed postoperative deep vein thrombosis and pulmonary embolism (PE). After warfarin (Coumadin) therapy, follow-up chest CT showed resolution of the PE.
Physical examination revealed a well-nourished, well-developed young male with moderately severe shortness of breath at rest, decreased breath sounds at the right base, a regular heart rhythm (rate, 120 beats per minute), and a temperature of 101°F. Posteroanterior and lateral chest films were obtained (see Figure 1). What do these images reveal?

DISCUSSION
Figure 1 demonstrates cardiomegaly and a right pleural effusion. A pericardial fat stripe is present, and a cardiac edge can be distinguished as a separate shadow along the left border of the heart. Figure 2 shows a chest film taken 8 weeks previously, which is essentially normal. The new enlargement of the cardiac silhouette on the more recent image is suspicious for a pericardial effusion.
PERICARDIAL EFFUSION is an increase in pericardial fluid. Normally, the pericardium consists of the visceral and parietal layers separated by a small amount of fluid. The pericardial sac prevents sudden cardiac dilation during exercise and hypervolemia. The sac also minimizes friction between the heart and surrounding structures, and it reduces the risk of infection spreading from the lungs and pleural cavities to the heart. An abnormal increase in pericardial fluid may have a restrictive effect, reducing cardiac function, and may produce severe symptoms or even death from cardiac tamponade.
Acute pericarditis is the most common cause of pericardial effusion. Inflammation of the pericardium can result from viral, bacterial, fungal, and parasitic infection or from other systemic diseases. Viral infections are the most common causes of acute pericarditis. Common viruses that can lead to pericarditis include Coxsackie virus, echovirus, influenza virus, Epstein-Barr virus, varicella virus, mumps virus, and HIV. Bacterial pericarditis— the result, for example, of pneumococcal or staphylococcal infection— is rare but may occur as an extension of a pulmonary infection. Tuberculosis is a rare cause of pericarditis in the United States but is more common in countries where tuberculosis is more prevalent.
Noninfectious causes of pericarditis include recent MI (Dressler's syndrome), radiation, rheumatoid arthritis, neoplasms, uremia, trauma, sarcoidosis, myxedema, aortic aneurysm dissection with leakage, and adverse drug effects. Malignant causes of pericarditis include metastases from melanoma; sarcoma; mesothelioma; bronchogenic, breast, and ovarian carcinomas; and lymphoma (Hodgkins disease and non- Hodgkins lymphoma). Especially in young adults, acute pericarditis may be considered idiopathic, a consequence of the low diagnostic yield of invasive diagnostic procedures. That was the case in this patient.
Physical examination findings in patients with pericardial effusion depend on the size of the effusion. Findings include jugular venous distention, inspiratory elevation of jugular venous pressure (Kussmaul's sign), peripheral edema, ascites, and a pericardial knock during diastole or a pericardial friction rub. When cardiac tamponade is present, the examiner may note hypotension, distant heart sounds, jugular venous distention (Beck's triad), pulsus paradoxus, tachycardia, and evidence of poor peripheral perfusion.
Symptoms include dyspnea, pain in the center of the chest that is characteristically relieved by sitting up or leaning forward (when acute pericarditis is present), abdominal discomfort, lower extremity swelling, fatigue, palpitations, cough, and nausea. A thorough patient history, physical examination, and diagnostic studies will help to determine the etiology of the pericardial effusion. The history should include inquiry for symptoms suggesting recent infection and travel.
DIAGNOSTIC STUDIES may include pericardial fluid studies, pericardial biopsy, tuberculin skin test, blood and sputum microscopy, and cultures. The most sensitive and specific noninvasive confirmatory diagnostic study is echocardiography (see Figure 3). This will allow localization and estimation of the quantity of pericardial fluid.
Evidence of cardiac tamponade can also be observed when assessing wall motion during echocardiography, as can signs of right atrial or right ventricular diastolic collapse.
Although radiography is not diagnostic, certain findings may suggest pericardial effusion. These include an enlarged cardiac silhouette, “water bottle” configuration, pericardial fat stripe, predominantly left pleural effusion, and an increase of transverse cardiac diameter compared with a recent radiograph. Rarely, the cardiac edge can be distinguished as a separate shadow along the left cardiac border. Both MRI and CT of the chest can detect a pericardial effusion. Electrical alternans on the ECG and low voltage may also be present.
The differential diagnosis of pericardial effusion includes heart failure, myocardial infarction, valvular and/or ischemic heart disease, PE, pneumothorax, pneumonia, and severe upper respiratory infection.
TREATMENT of pericardial effusion depends on the severity. Less than severe effusions that result from acute pericarditis may be treated with NSAIDs. Drainage of pericardial fluid may be necessary to determine the etiology and thus treat the underlying condition or to relieve cardiac tamponade when hemodynamics are compromised. Drainage of pericardial fluid can be done via pericardiocentesis or surgical pericardiotomy. JAAPA
Matt Goldstein is director of the Health and Wellness Center, Health Enhancement and Cardiovascular Services, Good Samaritan Hospital, Baltimore, Maryland, and teaches in the Doctor of Health Science Program at Nova Southeastern University. He has indicated no relationships to disclose relating to the content of this article.
Julie Vajnar, PA-C, RT, department editor