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Pericardial Effusion
Authors
Daniel A. Willner1; Amandeep Goyal2; Yulia Grigorova3; John Kiel4.

Affiliations
1
 Beth Israel Deaconess Medical Center
2
 Marietta Memorial Hospital
3
 Pavlov First Saint Petersburg State Medical University
4
 University of Florida College of Medicine - Jacksonville

Last Update: August 10, 2020.

Introduction
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.[1][2][3]

Etiology
The etiology of a pericardial effusion varies widely and can be divided into
several categories:
 Infectious: Pericardial effusion may be due to infection with a
multitude of viral, bacterial, fungal, and even parasitic pathogens. 
 Inflammatory/rheumatologic: Numerous auto-immune disorders,
including systemic lupus erythematosus, rheumatoid arthritis, and
Sjogren's syndrome can cause a pericardial effusion.
  Neoplastic: Both metastatic disease and primary cardiac tumors can
cause pericardial effusions. Lung cancer is the most common cause of
the malignant pericardial effusion.
 Trauma: Blunt, penetrating, and iatrogenic injury to the myocardium,
aorta, or coronary vessels can lead to the accumulation of blood within
the pericardial sac.
 Cardiac: Post-myocardial infarction (referred to as Dressler syndrome),
cardiac surgery, cardiac wall rupture.
 Vascular: Aortic dissection, type A, can be complicated by cardiac
tamponade.
 Idiopathic: Many cases of pericardial effusion are idiopathic.
 Other: There are numerous additional etiologies of pericardial effusion,
including radiation, chronic kidney disease, and renal failure,
congestive heart failure, cirrhosis, hypothyroidism leading to
myxedema, ovarian hyperstimulation syndrome, and drug-induced.

Epidemiology
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. [1]
[4][5][6]
Pathophysiology
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. [7][8][9]

History and Physical

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. 
 History: In patients with pericardial effusion due to pericarditis,
patients often present with chest pain and dyspnea with symptoms that
improve while sitting upright and worsen while lying flat due to the
inflamed pericardium contacting adjacent structures. Patients may also
present with symptoms that are not specific for pericardial effusion,
including dyspnea, edema, and fatigue. Other essential elements of
history include questions regarding recent illnesses, malignancy,
history of tuberculosis and vaccination status, auto-immune disorders,
history of chronic kidney disease or renal failure, or history of
congestive heart failure, hypothyroidism, or liver disease.
  Physical exam: Pericardial effusion leading to pericardial tamponade
should be on the differential for patients in cardiac arrest or with vital
sign abnormalities, including hypotension and tachycardia. The classic
teaching of Beck's triad (hypotension, jugular venous distension, and
muffled heart sounds) is only found in a minority of patients. Other
physical exam findings unique to pericardial effusion include Ewart's
sign (dullness to percussion at the base of the left inferior scapular
border in conjunction with tubular breath sounds and egophony). The
physical exam of patients with a concern for cardiac tamponade should
also include evaluation for pulsus paradoxus, which refers to a relative
drop in systolic blood pressure by more than 10 mmHg during
inspiration due to the collapse of the left ventricle at the expense of
right ventricle. This leads to bowing of the interventricular septum and
augmented compression of the left side of the heart with decreased
filling volumes and subsequent decreased stroke volume and systolic
blood pressure.
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.

Evaluation
Several tests can aid in evaluating a patient in whom pericardial effusion is
the differential diagnosis.[10][11][12]
 Chest X-ray: The chest X-ray may can not directly identify pericardial
effusion. If there is a significant, chronic effusion, then the heart may
appear boot-shaped, and radiology may comment on a "water bottle
sign" or a water bottle shaped heart. There may also be evidence of
pulmonary edema, engorgement of the pulmonary vessels, and/or
pleural effusions on chest x-ray - none of which are sensitive or
specific for pericardial effusion.
 ECG: The ECG findings vary from normal to non-specific ST-segment
changes for small effusions. For large effusions or tamponade, the ECG
may demonstrate electrical alternans, which is a specific but not a
sensitive finding. Electrical alternans refer to QRS complexes of
 varying heights corresponding to a back and forth motion of the heart
within the pericardial sac as it swings on its anchored base during the
cardiac cycle. If the pericardial effusion is due to pericarditis, then the
ECG may show PR depressions or diffuse ST elevations.
 Echocardiography: Transthoracic echocardiography (TTE) or
transesophageal echocardiography (TEE) is the diagnostic modality of
choice when evaluating for pericardial effusion. Echocardiography
provides a dynamic assessment of the pericardial effusion allowing for
quantification of the size of the effusion and determination of whether
there is evidence of cardiac tamponade physiology. Pericardial effusion
is identified as anechoic fluid surrounding the heart. In cases of
hemopericardium with a clot, pyogenic effusions, or exudative
effusions, there may be hypoechoic clot or debris visible within the
anechoic pericardial fluid. There are numerous criteria for the diagnosis
of cardiac tamponade by TTE or TEE. Right atrial free-wall collapse or
inversion during systole, right ventricular free wall collapse during
diastole, increased septal bowing into the left ventricle during
inspiration and the right ventricle during exhalation, a dilated inferior
vena cava without respiratory variation in a spontaneously breathing
patient in sinus rhythm, and increased flow across the mitral valve
during exhalation and the tricuspid valve during inspiration are all
potentially indicative of intrapericardial pressures that are greater than
intracardiac pressures and potential pericardial tamponade. It is
important to note that some of these echo findings are sensitive but not
specific, while others are specific but not sensitive for cardiac
tamponade.
 CT/MRI: Pericardial effusion can also be identified on CT or MRI of
the chest or heart; however, this is not the diagnostic modality of
choice.

Treatment / Management
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.[13][14]
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.[15]

Differential Diagnosis
 Acute Pericarditis
  Cardiac Tamponade
 Cardiogenic Pulmonary Edema
 Constrictive Pericarditis
 Dilated Cardiomyopathy
 Effusive-Constrictive Pericarditis
 Myocardial Infarction
 Pulmonary Embolism (PE)

Pearls and Other Issues

 Pericardial effusion is a relatively commonly encountered pathology.
 The etiology is widely varied.
 The effusion can range from incidental to life-threatening disease.
 The diagnostic modality of choice is an echocardiogram, although other
modalities can provide critical information.
 Management is driven by the size of the effusion and clinical status of
the patient.
 Cardiothoracic surgeons are the consultant of choice in patients who
are diagnosed with a pericardial effusion.

Enhancing Healthcare Team Outcomes

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.

Questions
To access free multiple choice questions on this topic, click here.

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Figures

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Large pericardial effusion, cardiac tamponade, parasternal long axis window.
Contributed by Emory EM US section
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