Pericardial Effusion

pericardial effusion

Pericardial Effusion

Practice Essentials
Pericardial effusion is the presence of an abnormal amount of fluid and/or an abnormal character to fluid in the pericardial space. It can be caused by a variety of local and systemic disorders, or it may be idiopathic. See the image below.
This echocardiogram shows a large amount of pericardial effusion (identified by the white arrows).
Signs and symptoms
Signs and symptoms of pericardial effusion include the following:
·        Chest pain, pressure, discomfort
·        Light-headedness, syncope
·        Palpitations
·        Cough
·        Dyspnea
·        Hoarseness
·        Anxiety and confusion
·        Hiccoughs
See Clinical Presentation for more detail.
Examination findings in patients with pericardial effusion include the following:
·        Classic Beck triad of pericardial tamponade: Hypotension, muffled heart sounds, jugular venous distention
·        Pulsus paradoxus
·        Pericardial friction rub
·        Tachycardia
·        Hepatojugular reflux
·        Tachypnea
·        Decreased breath sounds
·        Ewart sign: Dullness to percussion beneath the angle of left scapula
·        Hepatosplenomegaly
·        Weakened peripheral pulses, edema, and cyanosis
Lab tests
The following laboratory studies may be performed in patients with suspected pericardial effusion:
·        Electrolyte levels
·        CBC count with differential
·        Cardiac biomarker levels (eg, troponin, CK-MB, LDH)
·        Tests for other markers of inflammation (eg, ESR, CRP)
·        TSH level
·        Blood cultures
·        RF levels
·        Immunoglobulin complex tests
·        ANA tests
·        Complement levels
·        Pericardial fluid analysis
Early in the course of acute pericarditis, the ECG typically displays diffuse ST elevation in association with PR depression; the ST elevation may be present in all leads except for aVR, although in postmyocardial infarction pericarditis, the changes may be more localized.
Specific tests for infectious diseases or other conditions may also be warranted, based upon clinical suspicion, such as the following:
·        Viral cultures
·        Tuberculin skin testing or QuantiFERON-TB assay
·        Rickettsial antibodies
·        HIV serology
·        Adenosine deaminase levels
·        CEA levels
·        PCR
Imaging studies
Echocardiography is the imaging modality of choice for the diagnosis of pericardial effusion and includes the following techniques:
·        2-D echocardiography
·        M-mode echocardiography: Adjunct to 2-D echocardiography
·        Doppler echocardiography
·        Transesophageal echocardiography
·        Intracardiac echocardiography
Other radiologic studies used in the evaluation of pericardial effusion include the following:
·        Chest radiography
·        Chest CT Scanning and MRI: May be superior to echocardiography in detecting loculated pericardial effusions
Procedures that may be used in patients with pericardial effusion include the following:
·        Diagnostic and/or therapeutic pericardiocentesis
·        Diagnostic pericardioscopy
·        Placement of a pulmonary artery catheter
See Workup for more detail.
Most acute idiopathic or viral pericarditis occurrences are self-limited and respond to treatment with an NSAID. Colchicine or prednisone may be administered for severe inflammatory pericardial effusions or when NSAID treatment has failed.  Colchicine is preferred over steroids (unless specifically indicated), as the latter is associated with an increassed incidence of recurrent pericarditis. 
Autoimmune pericardial effusions may respond to treatment with anti-inflammatory medications. In general, selection of an agent depends on the severity of the patient's symptoms and the tolerability and adverse-effect profiles of the medications.
Pharmacotherapy for pericardial effusion includes use of the following agents, depending on the etiology:
·        NSAIDs (eg, indomethacin, ibuprofen, naproxen, diclofenac, ketoprofen, aspirin)
·        Corticosteroids (eg, prednisone, methylprednisolone, prednisolone)
·        Anti-inflammatory agents (eg, colchicine)
·        Antibiotics (eg, vancomycin, ceftriaxone, ciprofloxacin, isoniazid, rifampin, pyrazinamide, ethambutol)
·        Antineoplastic therapy (eg, systemic chemotherapy, radiation)
·        Sclerosing agents (eg, tetracycline, doxycycline, cisplatin, 5-fluorouracil)
Hemodynamic support for pericardial effusion includes the following:
·        Hemodynamic monitoring with a balloon flotation pulmonary artery catheter
·        IV fluid resuscitation
Surgical treatments for pericardial effusion include the following:
·        Pericardiostomy
·        Pericardotomy
·        Thoracotomy
·        Sternotomy
·        Pericardiocentesis

Pericardial effusion is the presence of an abnormal amount of and/or an abnormal character to fluid in the pericardial space. It can be caused by a variety of local and systemic disorders, or it may be idiopathic. (See Etiology.)
Pericardial effusions can be acute or chronic, and the time course of development has a great impact on the patient's symptoms. Treatment varies, and is directed at removal of the pericardial fluid and alleviation of the underlying cause, which usually is determined by a combination of fluid analysis and correlation with comorbid illnesses (see the image below). (See PresentationWorkupTreatment, and Medication.)
This image is from a patient with malignant pericardial effusion. Note the "water-bottle" appearance of the cardiac silhouette in the anteroposterior (AP) chest film.
In the human embryo, the pericardial cavity develops from the intraembryonic celom during the fourth week. The pericardial cavity initially communicates with the pleural and peritoneal cavities, but during normal development these are separated by the eighth week.
The visceral and parietal pericardium are derived from the mesoderm, albeit from different parts of the embryo. The visceral pericardium develops from splanchnic mesoderm, as cells originating from the sinus venous spread out over the myocardium. The parietal pericardium derives from lateral mesoderm that covers and accompanies the developing pleuropericardial membrane, which will eventually separate the pleural and pericardial cavities. In healthy subjects, the pericardium covers the heart and great vessels, with the exception of only partially covering the left atrium.
Congenital absence of the pericardium can occur and can be either partial or complete. This condition is often clinically silent, but it can potentially lead to excessive cardiac motion (in the case of complete absence), causing vague chest pain or dyspnea, or, in the case of partial absence with significant defects, strangulation of heart muscle and possible death. [1]
The pericardial space normally contains 15-50 mL of fluid, which serves as lubrication for the visceral and parietal layers of the pericardium. This fluid is thought to originate from the visceral pericardium and is essentially an ultrafiltrate of plasma. Total protein levels are generally low; however, the concentration of albumin is increased in pericardial fluid owing to its low molecular weight.
The pericardium and pericardial fluid provide important contributions to cardiac function, including the following:
·        The parietal pericardium contributes to resting diastolic pressure, and is responsible for most of this pressure in the right atrium and ventricle
·        Through their ability to evenly distribute force across the heart, the pericardial structures assist in ensuring uniform contraction of the myocardium
The normal pericardium can stretch to accommodate a small amount of fluid without a significant change in intrapericardial pressure, although once this pericardial reserve volume is surpassed, the pressure-volume curve becomes steep. With slow increases in volume, however, pericardial compliance can increase to lessen the increase in intrapericardial pressure.


Clinical manifestations of pericardial effusion are highly dependent on the rate of accumulation of fluid in the pericardial sac. Rapid accumulation of pericardial fluid may cause elevated intrapericardial pressures with as little as 80 mL of fluid, while slowly progressing effusions can grow to 2 L without symptoms.
Understanding the properties of the pericardium can help to predict changes within the heart under physiologic stress.
By distributing forces across the heart, the pericardium plays a significant role in the physiologic concept of ventricular interdependence, whereby changes in pressure, volume, and function in one ventricle influence the function of the other.
The pericardium plays a pivotal role in cardiac changes during inspiration. Normally, as the right atrium and ventricle fill during inspiration, the pericardium limits the ability of the left-sided chambers to dilate. This contributes to the bowing of the atrial and ventricular septums to the left, which reduces left ventricular (LV) filling volumes and leads to a drop in cardiac output. As intrapericardial pressures rise, as occurs in the development of a pericardial effusion, this effect becomes pronounced, which can lead to a clinically significant fall in stroke volume and eventually progress to the development of pericardial tamponade.
The pericardium plays a beneficial role during hypervolemic states by limiting acute cardiac cavitary dilatation.


The cause of abnormal fluid production depends on the underlying etiology, but it is usually secondary to injury or insult to the pericardium (ie, pericarditis). Transudative fluids result from obstruction of fluid drainage, which occurs through lymphatic channels. Exudative fluids occur secondary to inflammatory, infectious, malignant, or autoimmune processes within the pericardium.
In up to 60% of cases, pericardial effusion is related to a known or suspected underlying process. Therefore, the diagnostic approach should give strong consideration to coexisting medical conditions.


In many cases, the underlying cause is not identified. However, this often relates to the lack of extensive diagnostic evaluation.


Human immunodeficiency virus (HIV) infection can lead to pericardial effusion through several mechanisms, including the following:
·        Secondary bacterial infection
·        Opportunistic infection
·        Malignancy (Kaposi sarcoma, lymphoma)
·        "Capillary leak" syndrome, which is associated with effusions in other body cavities
The most common cause of infectious pericarditis and myocarditis is viral. Common etiologic organisms include coxsackievirus A and B, and hepatitis viruses. Other forms of infectious pericarditis include the following:
·        Pyogenic - Pneumococci, streptococci, staphylococci, NeisseriaLegionella species
·        Tuberculous
·        Fungal - Histoplasmosis, coccidioidomycosis, Candida
·        Syphilitic
·        Protozoal
·        Parasitic


Neoplastic disease can involve the pericardium through the following mechanisms:
·        Direct extension from mediastinal structures or the cardiac chamber
·        Retrograde extension from the lymphatic system
·        Hematologic seeding
Malignancies with the highest prevalence of pericardial effusion include lung (37% of malignant effusions) and breast (22%) malignancies, as well as leukemia/lymphoma (17%). However, patients with malignant melanoma or mesothelioma also have a high prevalence of associated pericardial effusions.


Pericardial effusions are common after cardiac surgery. In 122 consecutive patients studied serially before and after cardiac surgery, effusions were present in 103 patients; most appeared by postoperative day 2, reached their maximum size by postoperative day 10, and usually resolved without sequelae within the first postoperative month.
In a retrospective survey of more than 4,500 postoperative patients, only 48 were found to have moderate or large effusions by echocardiography; of those, 36 met diagnostic criteria for tamponade. The use of preoperative anticoagulants, valve surgery, and female sex were associated with a higher prevalence of tamponade. [2]
Early chest tube removal following cardiac surgery, around midnight on the day of surgery, may be associated with an increased risk of postoperative pleural and/or pericardial effusions requiring invasive treatment. [88This may occur even if chest tube output during the last 4 hours is below 150 mL compared with removal of the tubes next morning.
Symptoms and physical findings of significant postoperative pericardial effusions are frequently nonspecific, and echocardiographic detection and echo-guided pericardiocentesis, when necessary, are safe and effective; prolonged catheter drainage reduces the recurrence rate. [3]
Pericardial effusions in cardiac transplant patients are associated with an increased prevalence of acute rejection. [4]


Less common causes of pericardial effusion include the following:
·        Uremia
·        Myxedema
·        Severe pulmonary hypertension
·        Radiation therapy
·        Acute myocardial infarction - Including the complication of free wall rupture
·        Aortic dissection - Leading to hemorrhagic effusion from leakage into the pericardial sac
·        Trauma
·        Hyperlipidemia
·        Chylopericardium
·        Familial Mediterranean fever
·        Whipple disease
·        Hypersensitivity or autoimmune related -Systemic lupus erythematosus, [5rheumatoid arthritis, ankylosing spondylitis, rheumatic fever, scleroderma, sarcoidosis, Wegener granulomatosis
·        Drug associated - Eg, procainamide, hydralazine, isoniazid, minoxidil, phenytoin, anticoagulants, methysergide


Occurrence in the United States

Few large studies have characterized the epidemiology of pericardial effusion; however, the available data consistently show that pericardial effusion is more prevalent than is clinically evident. A higher incidence of it is associated with certain diseases.
Small pericardial effusions are often asymptomatic, and pericardial effusion has been found in 3.4% of subjects in general autopsy studies. When associated with community-acquired pneumonia (CAP), small peridcardial effusion is an independent predictor of adverse events including longer and more complicated hospital stays as well as increased mortality. [6]
A wide variety of malignant neoplasms and hematologic malignancies can lead to pericardial effusion. Data on the prevalence varies, with some studies showing the presence of pericardial effusion as high as 21% in such patients. A large study by Bussani et al showed cardiac metastases (9.1%) and pericardial metastases (6.3%) in cases of death from all causes in individuals with an underlying carcinoma at autopsy. [7As previously mentioned, malignancies with the highest prevalence of pericardial effusion include lung (37% of malignant effusions) and breast (22%) malignancies, as well as leukemia/lymphoma (17%).
Patients with HIV, with or without acquired immunodeficiency syndrome (AIDS), are also found to have an increased prevalence of pericardial effusion. [8Studies have shown the prevalence of pericardial effusion in these patients to range from 5-43%, depending on the inclusion criteria, with 13% having moderate to severe effusion. The incidence of pericardial effusion in patients infected with HIV has been estimated at 11%; however, it appears that highly active antiretroviral therapy (HAART) may have reduced the incidence of HIV-associated effusions. [9]

Race- and age-related demographics

No consistent difference among races is reported in the literature. AIDS patients with pericardial effusion are more likely to be white.
Pericardial effusion is observed in all age groups. The mean occurrence is in the fourth or fifth decades, although it is earlier than this in patients with HIV.

Pericardial Effusion Clinical Presentation


Cardiovascular symptoms in pericardial effusion can include the following:
·        Chest pain, pressure, discomfort - Characteristically, pericardial pain may be relieved by sitting up and leaning forward and is intensified by lying supine.
·        Light-headedness, syncope
·        Palpitations
Respiratory symptoms can include the following:
·        Cough
·        Dyspnea
·        Hoarseness
Neurologic symptoms of pericardial effusion can include anxiety and confusion, while hiccoughs may occur as a gastrointestinal (GI) symptom.

Physical Examination

Cardiovascular findings in pericardial effusion can include the following:
·        Classic Beck triad of pericardial tamponade - Hypotension, muffled heart sounds, jugular venous distention
·        Pulsus paradoxus - Exaggeration of physiologic respiratory variation in systemic blood pressure, defined as a decrease in systolic blood pressure of more than 10mm Hg with inspiration, signaling falling cardiac output during inspiration
·        Pericardial friction rub
·        Tachycardia
·        Hepatojugular reflux - This can be observed by applying pressure to the periumbilical region; a rise in the jugular venous pressure (JVP) of greater than 3 cm H2 O for more than 30 seconds suggests elevated central venous pressure (however, transient elevation in JVP may be normal)
Pericardial friction rub, the most important physical sign of acute pericarditis, may have up to 3 components per cardiac cycle and is high-pitched, scratching, and grating. It can sometimes be elicited only when firm pressure with the diaphragm of the stethoscope is applied to the chest wall at the left lower sternal border. The pericardial friction rub is heard most frequently during expiration with the patient upright and leaning forward.
Respiratory findings can include the following:
·        Tachypnea
·        Decreased breath sounds - Secondary to pleural effusions [10]
·        Ewart sign - Dullness to percussion beneath the angle of left scapula from compression of the left lung by pericardial fluid
Hepatosplenomegaly represents a GI symptom of pericardial effusion. Findings in the patient’s extremities can include weakened peripheral pulses, edema, and cyanosis.

Differential Diagnoses

·        Acute Pericarditis
·        Cardiac Tamponade
·        Cardiogenic Pulmonary Edema
·        Constrictive Pericarditis
·        Dilated Cardiomyopathy
·        Myocardial Infarction
·        Pulmonary Embolism (PE)

Lab Studies

The following lab studies may be performed in patients with suspected pericardial effusion:
·        Electrolytes - To assess for metabolic abnormalities (eg, renal failure)
·        Complete blood count (CBC) with differential - Leukocytosis for evidence of infection, as well as cytopenias, as signs of underlying chronic disease (eg, cancer, HIV)
·        Cardiac biomarkers
·        Other markers of inflammation, such as erythrocyte sedimentation rate and C-Reactive protein - While these do not aid in identifying specifics, they can be used to potentially assess the need for anti-inflammatory agents (ie, corticosteroids, colchicine, NSAIDs), especially in the setting of recurrent effusions. [12]
·        Thyroid-stimulating hormone - Thyroid-stimulating hormone screen for hypothyroidism [13]
·        Blood cultures in the presence of systemic inflammatory response syndrome (SIRS) or fever; in general, specific viral studies are low yield and therefore not recommended [14]
·        Rheumatoid factor, immunoglobulin complexes, antinuclear antibody test (ANA), and complement levels (which would be diminished) - In suspected rheumatologic causes
·        Specific infectious disease testing, based upon clinical suspicion, such as (1) tuberculin skin testing or QuantiFERON-TB assay; (2) rickettsial antibodies if there is a high index of suspicion for tick-borne disease; and HIV serology

Cardiac enzymes

The troponin level is frequently minimally elevated in acute pericarditis, usually in the absence of an elevated total creatine kinase level. Presumably, this is due to some involvement of the epicardium by the inflammatory process.
Although the elevated troponin may lead to the misdiagnosis of acute pericarditis as a myocardial infarction, most patients with an elevated troponin and acute pericarditis do not have findings at angiography consistent with acute coronary syndrome. An elevated troponin level in acute pericarditis typically returns to normal within 1-2 weeks and is not associated with a worse prognosis.

Pericardial fluid analysis

It should be noted that routine biochemical and cell-count analysis has a low yield in diagnosing the cause of effusion. [15In contrast, Gram stain and culture can ascertain the etiology convincingly. It is routine for the following tests to be considered part of the standard pericardial fluid analysis:
·        Lactic (acid) dehydrogenase (LDH), total protein - The Light criteria (for exudative pleural effusion) found to be as reliable in distinguishing between exudative and transudative effusions: (1) total protein fluid-to-serum ratio >0.5, (2) LDH fluid-to-serum ratio >0.6, (3) LDH fluid level exceeds two thirds of upper limit of normal serum level [16]
·        Other indicators suggestive of exudate - Specific gravity >1.015, total protein >3.0 mg/dL, LDH >300 U/dL, glucose fluid-to-serum ratio < 1
·        Cell count - Elevated leukocytes (ie, >10,000) with neutrophil predominance suggests bacterial or rheumatic cause, although unreliable
·        Gram stain - Specific (but insensitive) indicator of bacterial infection
·        Cultures - Signal and identify infectious etiology
·        Fluid hematocrit for bloody aspirates - Hemorrhagic fluid hematocrits are usually significantly less than simultaneous peripheral blood hematocrits
·        Cytology of pericardial fluid to assess for the presence of malignant cells
Special tests
These studies of the pericardial fluid should be considered individually based on the pretest probability of the suspected coexisting condition. They include the following:
·        Viral cultures
·        Adenosine deaminase; polymerase chain reaction (PCR); culture for tuberculosis; smear for acid-fast bacilli in suspected tuberculosis infection, especially in patients with HIV
A definite diagnosis of tuberculous pericarditis is based on the demonstration of tubercle bacilli in pericardial fluid or on a histologic section of the pericardium.
Probable tuberculous pericarditis is based on the proof of tuberculosis elsewhere in a patient with otherwise unexplained pericarditis, a lymphocytic pericardial exudate with elevated adenosine deaminase or gamma interferon (IFN) levels, and/or appropriate response to a trial of antituberculosis chemotherapy.
Elevated carcinoembryonic antigen (CEA) levels in pericardial fluid have a high specificity for malignant effusion.
Perform pericardial biopsy, especially if malignant pericardial effusion is suspected. [16This can be more diagnostic when combined with pericardioscopy.

Chest Radiography

Findings in chest radiography include an enlarged cardiac silhouette (so-called water-bottle heart) and a pericardial fat stripe. One third of patients have a coexisting pleural effusion. Radiography is unreliable in establishing or refuting a diagnosis of pericardial effusion. (See the image below.)
This image is from a patient with malignant pericardial effusion. Note the "water-bottle" appearance of the cardiac silhouette in the anteroposterior (AP) chest film.
Echocardiography is the imaging modality of choice for the diagnosis of pericardial effusion, as the test can be performed rapidly and in unstable patients. Most importantly, the contribution of pericardial effusion to overall cardiac enlargement and the relative roles of tamponade and myocardial dysfunction in altered hemodynamics can be evaluated with echocardiography. (See the images below.) [18]
Echocardiogram (parasternal, long axis) of a patient with a moderate pericardial effusion.
Subcostal view of an echocardiogram that shows a moderate to large amount of pericardial effusion.
This echocardiogram shows a large amount of pericardial effusion (identified by the white arrows).
Patients with viral cardiomyopathy, especially in the acute setting, may have a similar presentation to patients with pericardial effusion, with an enlarged heart being seen on chest radiographs. Echocardiography readily distinguishes the difference between enlarged cardiac chambers and a pericardial effusion.
Two-dimensional echocardiography
Pericardial effusion appears as an echo-free space between the visceral and parietal pericardium. Early effusions tend to accumulate posteriorly owing to expandable posterior/lateral pericardium.
Large effusions are characterized by excessive motion within the pericardial sac, also called swinging. Small effusions have an echo-free space of less than 10 mm and are generally seen posteriorly. Moderate-sized effusions range from 10-20 mm and are circumferential. An echo-free space of more than 20 mm indicates a large effusion. Fluid adjacent to the right atrium is an early sign of pericardial effusion. (See the image below.) [19]
This image is from a patient with malignant pericardial effusion. The effusion is seen as an echo-free region to the right of the left ventricle (LV).
Echocardiography may identify features that suggest hemodynamically significant cardiac tamponade; however, this is a clincial (not echocardiographic) diagnosis. These findings include the following:
·        Collapse of the right atrium, especially if it lasts for a third of the cardiac cycle
·        Diastolic collapse of the right ventricle
·        In hypovolemic patients, the left atrium and left ventricle may also show signs of collapse
Rarely, the cause of the effusion can also be ascertained from echocardiography. The following echocardiographic findings may be helpful:
·        Presence of a coagulum in the pericardial space indicating a bloody pericardial effusion (aortic dissection, postoperative, or after other catheter-based procedures)
·        Presence of a pacemaker lead either in the vicinity or inside an area of localized effusion, indicating lead perforation as a cause
·        Presence of tumor (primary or secondary) in the pericardial space
M-mode echocardiography
M-mode echocardiography is adjunctive to two-dimensional (2-D) imaging for the detection of pericardial effusion. Effusions can be classified using M-mode according to the following system proposed by Horowitz et al [20:
·        Type A - No effusion
·        Type B - Separation of epicardium and pericardium
·        Type C1 - Systolic and diastolic separation of pericardium
·        Type C2 - Systolic and diastolic separation of pericardium, attenuated pericardial motion
·        Type D - Pronounced separation of pericardium and epicardium with large echo-free space
In the parasternal long-axis and apical 4-chamber views, discordant changes in right and left ventricular cavity size can suggest pronounced interventricular dependence, also suggesting an echocardiographic “substrate” for tamponade. It is important to note that these changes occur independent of the cardiac cycle (as these are dependent on respiration).
Doppler echocardiography
Transmitral and transtricuspid inflow velocities should be investigated to assess for respiratory variation. Decreases in flow during inspiration (transmitral >25%) or expiration (transtricuspid >40%) should raise the suspicion of clinically significant interventricular dependence and tamponade physiology. However, these findings may be less evident or, in fact, absent in patients on mechanical ventilation, even in the presence of a hemodynamically significant pericardial effusion. [21]
Pulmonic vein inflow may show a decrease in early diastolic flow with hemodynamically significant effusions. Plethoric inferior vena cava with less than 50% collapse during inspiration may indicate elevated right atrial pressures. Hepatic vein diastolic flow reversal seen during expiration is another classic manifestation of ventricular interdependence.
Transesophageal echocardiography
Localized compressive masses, such as postoperative mediastinal hematoma, can cause tamponade without any of the classic 2-dimensional or Doppler manifestations. Transesophageal echocardiography maintains all of the advantages of transthoracic echocardiography and is useful in characterizing loculated effusions. However, this imaging study may be difficult to perform in patients with symptomatic effusions due to hemodynamic instability, with the required sedation being more difficult.
Intracardiac echocardiography
Intracardiac echocardiography (ICE) is generally reserved for the assessment of pericardial effusion in the setting of a percutaneous interventional or electrophysiologic procedure. Phased-array ICE systems can perform 2-D and Doppler interrogations.
False-positive findings
False-positive echocardiographic findings can occur in the presence of pleural effusions, pericardial thickening, increased epicardial fat tissue, atelectasis, and mediastinal lesions. Pericardial cysts, which are usually benign, can be seen classically in the right cardiophrenic angle and can be confused with pericardial effusion.
Epicardial fat tissue is more prominent anteriorly but may appear circumferentially, thus mimicking effusion. Fat is slightly echogenic and tends to move in concert with the heart, 2 characteristics that help to distinguish it from an effusion, which is generally echolucent and motionless. [182223]
In patients with pericardial effusion, imaging from low to midposterior thorax can provide additional diagnostic echocardiographic images and should be used in patients in whom conventional images are technically difficult or require additional information.

CT Scanning and MRI

Computed tomography (CT) scanning and magnetic resonance imaging (MRI) may be superior to echocardiography in detecting loculated pericardial effusions, especially when these are located anteriorly. Also, these modalities allow for greater visualization of the thoracic cavity and adjacent structures and therefore may identify abnormalities relating to the cause of the effusion.

CT scanning

CT scanning can potentially determine the composition of fluid and may detect as little as 50mL of fluid. This modality can also detect pericardial calcifications, which can be indicative of constrictive pericarditis.
CT scanning results in fewer false-positive findings than echocardiography. However, it can be problematic in patients who are unstable, given the amount of time required to transport them to and from the scanner and to perform the test.
Certain classic CT signs of tamponade have also been described, such as dilated venae cavae, reflux of contrast into the azygos vein and inferior vena cava, deformity or compression of the cardiac chambers, and bowing of the interventricular septum. [24]


MRI can detect as little as 30 mL of pericardial fluid. It may be able to distinguish hemorrhagic and nonhemorrhagic fluids, as hemorrhagic fluids have a high signal intensity on T-1 weighted images, whereas nonhemorrhagic fluids have a low signal intensity. Nodularity or irregularity of the pericardium seen on MRI may be indicative of a malignant effusion.
MRI is more difficult to perform acutely than CT scanning is, given the length of time the patient must remain in the scanner.
Late gadolinium enhancement can reveal areas of inflammation, which can potentially help decide about anti-inflammatory therapy in recurrent pericarditis and can also aid in the diagnosis of effusive-constrictive pericarditis.

Early in the course of acute pericarditis, the ECG typically displays diffuse ST elevation in association with PR depression (see the image below). The ST elevation is usually present in most leads except for aVR, although in postmyocardial infarction pericarditis, the changes may be more localized. (Patients with uremic pericarditis frequently do not have the typical electrocardiographic abnormalities.)
This electrocardiogram (ECG) is from a patient with malignant pericardial effusion. The ECG shows diffuse low voltage, with a suggestion of electrical alternans in the precordial leads.
Classically, the electrocardiographic changes of acute pericarditis evolve through 4 progressive stages, as follows:
·        Stage I - Diffuse ST-segment elevation and PR-segment depression
·        Stage II - Normalization of the ST and PR segments
·        Stage III - Widespread T-wave inversions: This is important to differentiate from myocardial infarction as T-wave inversions in pericarditis usually occur after ST-segment normalization, unlike myocardial infarction
·        Stage IV - Normalization of the T waves
Electrical alternans, which is the beat-to-beat variation in the direction and amplitude of the QRS complex, is the electrical signature of “swinging” of the heart in the pericardial fluid. In extreme cases, it can involve the P as well as the T waves. It is specific, but not sensitive, for tamponade and can also be seen in large pericardial effusions. [26]
Low-voltage QRS complexes, classically defined as total amplitude of the QRS complex less than 0.5 mv in the limb leads and less than 1 mv in the precordial leads, can also be seen in large effusions and tamponade. One study using limb lead criteria showed that it is more specific for tamponade rather than an effusion.

Pericardiocentesis and Pericardioscopy


This procedure is used for diagnostic as well as therapeutic purposes. Support for the use of echocardiographic guidance is increasing, unless emergent treatment is required. Indications for pericardiocentesis include impending hemodynamic compromise (ie, pericardial tamponade), suspected infectious or neoplastic etiology, and uncertain etiology.


This procedure is not universally available. It may increase diagnostic sensitivity in cases of unexplained pericardial effusions, especially for neoplastic disease. It allows for visualization of pericardium and for pericardial biopsies.

Approach Considerations

Pharmacotherapy for pericardial effusion may include use of the following agents, depending on etiology:
·        Aspirin/NSAIDs
·        Colchicine
·        Steroids
·        Antibiotics
Antineoplastic therapy (eg, systemic chemotherapy, radiation) in conjunction with pericardiocentesis has been shown to be effective in reducing recurrences of malignant effusions. Corticosteroids and NSAIDs are helpful in patients with autoimmune conditions.

Pericardial sclerosis

Several pericardial sclerosing agents have been used with varying success rates (eg, tetracycline, doxycycline, cisplatin, 5-fluorouracil). The pericardial catheter may be left in place for repeat instillation if necessary until the effusion resolves.
Complications include intense pain, atrial dysrhythmias, fever, and infection. Success rates are reported to be as high as 91% at 30 days.


Surgical treatments for pericardial effusion include the following:
·        Pericardiostomy
·        Pericardotomy
·        Thoracotomy
·        Sternotomy
·        Pericardiocentesis

Inpatient care

Patients with pericardial effusion who present with significant symptoms or cardiac tamponade require emergent treatment and admission to the intensive care unit (ICU). The pericardial catheter (if placed) should be removed within 24-48 hours to avoid infection. Symptomatic patients should remain hospitalized until definitive treatment is accomplished and/or symptoms have resolved

Outpatient care

Patients should be educated with regard to symptoms of increasing pericardial effusion and should be evaluated whenever these symptoms begin to occur. Indications for echocardiography after diagnosis include the following:
·        A follow-up imaging study to evaluate for recurrence/constriction - Repeat studies may be performed to answer specific clinical questions.
·        The presence of large or rapidly accumulating effusions - To detect early signs of tamponade


Symptomatic patients requiring treatment (who are surgical candidates) should receive care at an institution with cardiothoracic surgery capabilities.


A cardiologist should be involved in the care of patients with pericardial effusion. Cardiothoracic surgery may be required for recurrent or complicated cases.


Most acute idiopathic or viral pericarditis occurrences are self-limited and respond to treatment with aspirin (650 mg q6h) or another NSAID. For idiopathic or viral pericarditis, ibuprofen is preferred, given its low adverse effect profile, favorable impact on the coronary blood flow, and large dose range. Based on severity and response, the dose can range from 300-800 mg every 6-8 hours. [28]
Aspirin may be the preferred nonsteroidal agent to treat pericarditis after myocardial infarction because other NSAIDs may interfere with myocardial healing. Indomethacin should be avoided in patients who may have coronary artery disease.
In a study of 196 patients at high risk for tamponade because of pericardial effusion more than 7 days after cardiac surgery, Meurin et al found that diclofenac was not effective in reducing the size of the effusion or in preventing late cardiac tamponade. In the multicenter, randomized, double-blind trial, patients received either diclofenac (50 mg) or placebo twice daily for 14 days.


The routine use of colchicine in combination with conventional therapy is supported by results from the COlchicine for acute PEricarditis (COPE) trial. In this study, 120 patients with a first episode of acute pericarditis (idiopathic, acute, postpericardiotomy syndrome, or connective tissue disease) entered a randomized, open-label trial comparing aspirin treatment alone with aspirin plus colchicine (1-2 mg for the first day followed by 0.5-1 mg daily for 3 mo). [30]
In the study, colchicine reduced symptoms at 72 hours (11.7% vs 36.7) and reduced recurrence at 18 months (10.7% vs 36.7%). Colchicine was discontinued in 5 patients because of diarrhea, but no other adverse events were noted. Importantly, none of the 120 patients developed cardiac tamponade or progressed to pericardial constriction. The ICAP Trial (Investigation on Colchicine for Acute Pericarditis) will provide further information regarding the use of colchicine as first-line therapy. [31]
However, colchine may not be effective for patients with asymptomatic postoperative pericardial effusion. A study involving 149 patients with mild or moderate pericardial effusion on transthoracic echocardiography found no significant difference on pretreatment and posttreatment effusion values and changes in isolated coronary artery bypass graft surgery patients who received colchicine (n = 74) and those who received placebo (n = 75). [89The investigators attributed these findings to the likelihood that most of the cases of pericardial effusion were from noninflammatory causes


Steroid administration early in the course of acute pericarditis appears to be associated with an increased incidence of relapse after the steroids are tapered. In the COPE trial, steroid use was an independent risk factor for recurrence. Also, an observational study strongly suggested that the use of steroids increases the probability of relapse in patients treated with colchicine. [30]
Systemic steroids should be considered only in patients with recurrent pericarditis that is unresponsive to NSAIDs and colchicine or as needed for treatment of an underlying inflammatory disease. If steroids are to be used, an effective dose (1-1.5 mg/kg of prednisone) should be given, and it should be continued for at least 1 month before slow tapering. The European Society of Cardiology recommends that systemic corticosteroid therapy be restricted to connective-tissue diseases, autoreactive pericarditis, or uremic pericarditis. [28]
The intrapericardial administration of steroids has been reported to be effective in acute pericarditis without producing the frequent reoccurrence of pericarditis that complicates the use of systemic steroids, [32but the invasive nature of this procedure limits its use.


Purulent pericarditis

In patients with purulent pericarditis, urgent pericardial drainage combined with intravenous (IV) antibacterial therapy (eg, vancomycin 1 g bid, ceftriaxone 1-2 g bid, and ciprofloxacin 400 mg daily) is mandatory. Irrigation with urokinase or streptokinase, using large catheters, may liquify the purulent exudate, but open surgical drainage is preferable.

Tuberculous pericarditis

The initial treatment of tuberculous pericarditis should include isoniazid 300 mg daily, rifampin 600 mg daily, pyrazinamide 15-30 mg/kg daily, and ethambutol 15-25 mg/kg daily. Prednisone 1-2 mg/kg daily is given for 5-7 days and progressively reduced to discontinuation in 6-8 weeks. Drug sensitivity testing is essential. Uncertainty remains whether adjunctive corticosteroids are effective in reducing mortality or progression to constriction.
Surgical resection of the pericardium remains the appropriate treatment for constrictive pericarditis. The timing of surgical intervention is controversial, but many experts recommend a trial of medical therapy for noncalcific pericardial constriction and pericardiectomy in nonresponders after 4-8 weeks of antituberculosis chemotherapy.

Hemodynamic Support

Patients who have an effusion with actual or threatened tamponade should be considered to have a true or potential emergency. Most patients require pericardiocentesis to treat or prevent tamponade. However, treatment should be carefully individualized.
Hemodynamic monitoring with a balloon flotation pulmonary artery catheter is useful, especially in patients with tamponade or threatened tamponade in whom a decision is made to defer pericardiocentesis. Hemodynamic monitoring is also helpful after pericardiocentesis to assess reaccumulation and the presence of underlying constrictive disease. However, insertion of a pulmonary artery catheter should not be allowed to delay definitive therapy in critically ill patients.
IV fluid resuscitation may be helpful in cases of hemodynamic compromise. In patients with tamponade who are critically ill, IV positive inotropes (dobutamine, dopamine) can be used but are of limited use and should not be allowed to substitute for or delay pericardiocentesis.


As previously mentioned, pericardiocentesis is used for diagnostic as well as therapeutic purposes. Pericardial fluid drainage can be performed by percutaneous catheter drainage or open surgical approach. Individual patient characteristics (eg, loculated vs circumferential, recurrent pericardial effusion, need for pericardial biopsy and location of pericardial effusion) and local practice patterns aid in deciding the optimal method of drainage.
Percutaneous pericardial fluid drainage (pericardiocentesis) is the most common method used for pericardial fluid removal. It can be performed under fluoroscopic, echocardiographic, or CT guidance.
Echocardiographic pericardial fluid drainage has established itself as the criterion standard technique. In study of 1127 procedures performed on 977 patients, echocardiographic-guided pericardiocentesis was successful in 97%, with 1.2% major and 3.5% minor complications. [33It also established the extended drainage as a means to reduce the recurrence rate.
Use of a needle that is at least 5cm long and 16-gauge in diameter and that has a short bevel can minimize the risk of complications and should allow for adequate pericardial drainage. A system allowing placement of a catheter over the needle is preferred.
Contrast echocardiography using agitated saline is useful in cases in which bloody fluid is aspirated, to determine if the needle is in the ventricular cavity.
Attaching an ECG electrode to the pericardiocentesis needle is also useful for avoiding myocardial puncture. Electrical activity will be seen on the monitor when the needle comes into contact with atrial or ventricular myocardium. These changes may be delayed, however, and instill a false sense of security in needle placement. Sense of touch and the findings on aspiration should guide the procedure, with the clinician ultimately relying on good clinical sense.
Complications of pericardiocentesis include ventricular rupture, dysrhythmias, pneumothorax, myocardial and/or coronary artery laceration, and infection. Recurrence rates for pericardial effusion within 90 days may be as high as 90% in patients with cancer.

Pericardiotomy and Pericardiostomy

Balloon pericardotomy

In this procedure, a catheter is placed in the pericardial space under fluoroscopy. Inflation of the balloon creates a channel for passage of fluid into the pleural space, where reabsorption occurs more readily. Balloon pericardiotomy may be useful for recurrent effusions.

CT-guided pericardiostomy

Patients with effusions after cardiothoracic surgery often have limited echocardiographic windows, as well as loculated effusions, and may be on continued ventilatory support, all of which increase the difficulty of echo-guided pericardiocentesis.
CT pericardial fluid drainage has evolved as an emerging technique suited to overcome this dilemma. It has been shown as an alternative technique in patients in whom fluoroscopically or echocardiographically guided pericardiocentesis is difficult. Echocardiography can be limited due to various patient characteristics (eg, postoperative state, obesity, or chronic obstructive pulmonary disease) or due to a limitation of echocardiography in differentiating pericardial fluid from other possible surrounding structures.
In one large series, CT-directed diagnostic and therapeutic pericardiocentesis was attempted in 261 patients, with 98.4% success, 0.3% major complications and 6.9% minor complications. [34]
In 2010, Eichler et al reported their data on CT-guided pericardiocentesis in 20 patients who were poor candidates for echocardiographic drainage or pericardial fluid was not well visualized by echocardiography. All patients had successful drainage, with 0% mortality and no major complications. [35]
A report by Palmer et al suggested that, in postsurgical cases, CT-guided pericardial drainage is both safe and cost effective. The authors reported on 36 patients—33 of whom underwent major cardiothoracic surgery and 3 of whom were treated with minimally invasive procedures—whose symptomatic pericardial effusions were drained using CT-guided percutaneous placement of an indwelling pericardial catheter. [36]
There were no clinically significant complications associated with any of the placement procedures. Thirty-three patients experienced no symptom recurrence following catheter removal, although pericardial effusion did recur in the remaining 3 patients, requiring a repeat treatment.
Comparing procedure costs, the authors determined that the CT-guided tube pericardiostomies cost 89% less than intraoperative pericardial window procedures would have. No significant procedure-cost differences were found between CT-guided and ultrasonographically guided tube pericardiostomies.

Subxiphoid Pericardial Window With Pericardiostomy

This procedure is associated with low morbidity, mortality, and recurrence rates, and can be considered as a reasonable alternative diagnostic or treatment modality to pericardiocentesis in selected patients. [37]
The surgery can be performed under local anesthesia. This is advantageous because general anesthesia often leads to decreased sympathetic tone, resulting in hemodynamic collapse in patients with pericardial tamponade and shock. This procedure may be less effective when effusion is loculated.
One study indicated that the procedure may be safer and more effective at reducing recurrence rates than pericardiocentesis. However, only patients who were hemodynamically unstable underwent pericardiocentesis, and no change in overall survival rate was observed.

Thoracotomy and Median Sternotomy


This procedure should be reserved for patients in whom conservative approaches have failed. Thoracotomy allows for creation of a pleuropericardial window, which provides greater visualization of the pericardium. Thoracotomy requires general anesthesia and thus has higher morbidity and mortality rates than does the subxiphoid approach.

Median sternotomy

This procedure is reserved for patients with constrictive pericarditis. The operative mortality rate is high (5-15%).

Video-Assisted Thoracic Surgery

Video-assisted thoracic surgery (VATS) allows resection of a wider area of the pericardium than the subxiphoid approach does, without the morbidity of thoracotomy. [38The surgeon is able to create a pleuropericardial window and address concomitant pleural pathology, which is especially common in patients with malignant effusions.
One disadvantage of VATS is that it requires general anesthesia with single lung ventilation, which may be difficult in otherwise seriously ill patients.

Pericardial Effusion Medication

Medication Summary

Most acute idiopathic or viral pericarditis occurrences are self-limited and respond to treatment with an NSAID. The corticosteroid prednisone may be administered for severe inflammatory pericardial effusions or when NSAID treatment has failed.
Research indicates that the anti-inflammatory drug colchicine, when used in combination with conventional therapy, is more effective at reducing the symptoms and recurrence of pericarditis than is conventional therapy alone. [30]
Autoimmune pericardial effusions may respond to treatment with anti-inflammatory medications. In general, selection of an agent depends on the severity of the patient's symptoms and the tolerability and adverse effect profiles of the medications.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
Class Summary
These agents are used mostly for patients with active, nonhemorrhagic pericarditis with or without pericardial effusion. NSAIDS have analgesic, anti-inflammatory, and antipyretic activities.
The mechanism of action in pericarditis is not known, but NSAIDS may inhibit cyclo-oxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

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Indomethacin is the drug of choice in this class, although other NSAIDs (ie, ibuprofen, naproxen, aspirin) possess some efficacy. It is used as initial therapy for mild to moderately severe inflammatory pericardial effusions.

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Ibuprofen is a propionic acid derivative that reduces the formation of inflammatory mediators by enzyme inhibition.

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Naproxen is a propionic acid derivative that reduces the formation of inflammatory mediators by enzyme inhibition.

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Diclofenac possesses properties similar to those of the propionic acid derivatives and reduces the formation of inflammatory mediators by enzyme inhibition. The tablets are immediate-release formulations.

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Ketoprofen is used for relief of mild to moderate pain and inflammation. Small dosages are indicated initially in small patients, elderly patients, and patients with renal or liver disease. Doses higher than 75 mg do not increase the therapeutic effects. Administer high doses with caution, and closely observe the patient's response.

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Aspirin inhibits prostaglandin synthesis, preventing the formation of platelet-aggregating thromboxane A2.

Class Summary
Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. These agents modify the body's immune response to diverse stimuli.

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Prednisone is used for patients with severe inflammatory pericardial effusions or for those in whom initial treatment with NSAIDs has failed. Other agents may be used if the adverse effect profile warrants; dosages should be determined by prednisone equivalents.

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Methylprednisolone is available in IV/IM and oral form. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability. It is used for patients with severe inflammatory pericardial effusions or for those in whom initial treatment with NSAIDs has failed.

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Prednisolone is available in IV/IM and oral form. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability. It is used for patients with severe inflammatory pericardial effusions or for those in whom initial treatment with NSAIDs has failed.

Anti-inflammatory Agents
Class Summary
These agents inhibit key factors involved in inflammatory reactions.

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Colchicine is an alkaloid extract that inhibits microtubule formation and has unique anti-inflammatory properties. The drug concentrates well in leukocytes and reduces neutrophilic chemotaxis and motility. Colchicine reduces the release of lactic acid and proinflammatory enzymes. It inhibits the release of histamine-containing granules from mast cells, which may be important in the pathogenesis of elastic tissue changes found in anetoderma.
The use of colchicine in autoimmune disease is primarily empiric, and the mechanism of action in the reduction of inflammation is not clear. Colchicine is not truly an immunomodulating agent.