A pericardial effusion refers to the accumulation of fluid in the pericardial sac surrounding the heart. The pericardial sac is composed of the thin visceral pericardium which consists of a single layer of cells adherent to the cardiac epicardium and the thicker, fibrous parietal pericardium composed of collagen and elastin which is adherent to the lungs, diaphragm, sternum, great vessels, and other mediastinal structures surrounding the heart. In a healthy individual, the pericardial sac contains between 15 mL and 50 mL of serous fluid.
The etiology of a pericardial effusion varies widely and can be divided into several categories:
Pericardial effusion is possible across all ages and populations. The predominant etiology of the effusion varies by demographic characteristics such as age, geography, and comorbidities. There is little data regarding the prevalence and incidence of pericardial effusions. Viral pericarditis leading to effusion is the most common cause in the developed world. In developing areas, pericardial effusion due to Mycobacterium tuberculosis is quite prevalent. Bacterial and parasitic etiologies are less common. Among non-inflammatory pericardial effusions, multiple malignant neoplasms can lead to pericardial effusion. In patients with pericardial effusion, malignancy ranging between 12% and 23% of pericarditis cases. In patients with HIV, pericardial effusion was reported in 5-43%, depending on the inclusion criteria, with 13% having moderate to severe effusion. According to a study in pediatric patients, post-cardiac surgery (54%), neoplasia (13%), renal (13%), idiopathic or viral pericarditis (5%) and rheumatologic (5%) were the major underlying etiologies of pericarditis and pericardial effusions in children. 
Pericardial effusion is an acute or chronic accumulation of fluid within the pericardial space. Effusion can be transudative, exudative, or sanguineous. The pericardium has limited elasticity, and in acute settings, only 100 ml to 150 mL of fluid is necessary to cause cardiac tamponade. The fluid accumulation increases pressure in the pericardial sac leading to the compression of the heart, especially the right heart due to a thinner wall. Impaired diastolic filling of the right heart causes venous congestion. Reduction in the diastolic filling of the left ventricle results in decreased stroke volume. Tachycardia and increased contractility is the initial compensatory response mediated by adrenergic stimulation to maintain cardiac output. However, eventually, blood pressure and cardiac output progressively decline. In the chronic settings, the pericardial effusion may become one to two liters in size before it causes cardiac tamponade as long as the accumulation is gradual and the parietal pericardium has adequate time to stretch and accommodate the increased volume. 
The clinical presentation of pericardial effusion is along a spectrum from a clinically irrelevant, incidental finding to life-threatening cardiac tamponade. This wide variation is due in large part to the variable rate of accumulation of the pericardial fluid. Acute accumulation may cause impaired cardiac filling and decreased cardiac output with as little as 100 mL of fluid, while chronic and slow accumulation may lead to significant effusions of one to two liters that produce no significant hemodynamic effects.
While both history and physical exam are critical components of the evaluation for pericardial effusion and cardiac tamponade, the standard of care now includes additional modalities such as echocardiography to confirm the diagnosis.
Treatment for pericardial effusion ranges from watchful waiting for emergent intervention and depends largely on the suspected etiology. Small effusions without evidence of hemodynamic compromise are watched with serial echocardiography if deemed necessary or determined to be small enough that no follow-up is necessary. Large effusions may receive a diagnostic pericardiocentesis to evaluate the etiology or drained to provide symptomatic relief if the patient has associated symptoms such as dyspnea, chest discomfort, pulmonary or lower extremity edema, or decreased exercise tolerance. Effusions that have accumulated rapidly enough or have grown to such a size as to cause hemodynamic instability or collapse are managed emergently at the bedside, the cardiac catheterization lab, or the operating room. Techniques for drainage include needle pericardiocentesis via subxiphoid or anterior thoracic approach with or without placement of a pericardial drain for serial evacuation, percutaneous balloon pericardiotomy, emergent thoracotomy, and pericardiotomy, and surgical pericardial window via subxiphoid, anterior mini-thoracotomy, or video-assisted thoracoscopic surgery (VATS) approach. The type of intervention chosen is based on the etiology of the pericardial effusion, the clinical status of the patient at the time of the intervention, and the patient's expected clinical course.
Of note, patients who have large pericardial effusions with underlying ventricular dysfunction there is a risk of development of pericardial decompression syndrome (PDS) after pericardiocentesis. Pericardial decompression syndrome (PDS) is an infrequent, life-threatening complication following an uncomplicated pericardial evacuation for cardiac tamponade physiology. PDS is characterized by a paradoxical hemodynamic instability and/or pulmonary edema following an otherwise non-complicated pericardial drainage. Physicians should be familiar with the prevention strategies for PDS and offer vulnerable patients a very close clinical monitoring, especially those undergoing pericardial drainage for large malignant effusions for suspected tamponade. A sensible strategy would not drain large quantities of pericardial fluid in a single sitting especially in case of large pericardial effusions. The most reasonable approach would be to remove the amount of pericardial fluid just enough to result in the resolution of the cardiac tamponade physiology (which can be easily achieved by hemodynamic or echo-doppler monitoring) and then place prolonged pericardial drainage to achieve a slow and gradual removal of additional pericardial fluid. Prolonged pericardial drainage may be removed when there is a daily fluid return below 30-50 ml.
Pericardial effusions are common. Unlike chronic effusions, acute effusions in symptomatic patients need emergent treatment. The management of pericardial effusions is by an interprofessional team that includes a cardiologist, radiologist, and a cardiac surgeon. While aspiration can help relieve symptoms and hemodynamic compromise in most patients, those occurring after a malignancy may require a pericardial window that can be done either open or via thoracoscopy. Symptomatic pericardial effusions that are not properly treated carry a very high mortality.
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