European Heart Journal (2013) 34, 1186–1197 REVIEW

doi:10.1093/eurheartj/ehs372

Clinical update

Management of pericardial effusion

Massimo Imazio 1* and Yehuda Adler 2
1
Department Cardiology, Maria Vittoria Hospital, Via Luigi Cibrario 72, Torino 10141, Italy; and 2Chaim Sheba Medical Center, Tel Hashomer, and Sackler University, Tel Aviv, Israel

Received 26 June 2012; revised 10 August 2012; accepted 9 October 2012; online publish-ahead-of-print 2 November 2012

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Pericardial effusion is a common finding in clinical practice either as incidental finding or manifestation of a systemic or cardiac disease. The
spectrum of pericardial effusions ranges from mild asymptomatic effusions to cardiac tamponade. The aetiology is varied (infectious, neo-
plastic, autoimmune, metabolic, and drug-related), being tuberculosis the leading cause of pericardial effusions in developing countries
and all over the world, while concurrent HIV infection may have an important promoting role in this setting. Management is guided by
the haemodynamic impact, size, presence of inflammation (i.e. pericarditis), associated medical conditions, and the aetiology whenever pos-
sible. Pericardiocentesis is mandatory for cardiac tamponade and when a bacterial or neoplastic aetiology is suspected. Pericardial biopsy is
generally reserved for cases with recurrent cardiac tamponade or persistence without a defined aetiology, especially when a bacterial or
neoplastic aetiology is suspected and cannot be assessed by other conventional and less invasive means. A true isolated effusion may not
require a specific treatment if the patient is asymptomatic, but large ones are at risk of progression to cardiac tamponade (up to one
third). Pericardiocentesis alone may be curative for large effusions, but recurrences are also common and pericardiectomy or less invasive
options (i.e. pericardial window) should be considered with recurrent cardiac tamponade or symptomatic pericardial effusion (either circum-
ferential or loculated). The aim of this paper was to summarize and critically evaluate current knowledge on the management of pericardial
effusion.
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Keywords Pericardial effusion † Aetiology † Diagnosis † Management † Pericarditis

Introduction cause of pericardial disease and concurrent HIV infection may

have an important promoting role),5 the institutional setting
(tertiary referral centre vs. secondary and general hospitals), and
Probably no serious disease is so frequently overlooked by the prac-
the availability of specific subspecialties (especially nephrology,
titioner. Postmortem experience shows how often pericarditis is not
recognized or goes to resolution and adhesion without attracting rheumatology, and oncology).
notice (Osler, The Principles and Practice of Modern Medicine, 1892). No specific guidelines and management recommendations have
been issued by medical societies beyond the 2000 national Spanish
Pericardial effusion is a common finding in clinical practice either as guidelines6 and the 2004 European Society of Cardiology guide-
incidental finding or manifestation of a systemic or cardiac disease. lines on the management of pericardial diseases,7 and some narra-
The spectrum of pericardial effusions ranges from mild asymptom- tive reviews on the topic,4,8,9 whereas no specific guidelines have
atic effusions to cardiac tamponade. Moreover, pericardial effusion been issued from the American Heart Association (AHA) and
may accumulate slowly or suddenly.1 – 3 Unfortunately, there are American College of Cardiology (ACC).
few epidemiological data on the incidence and prevalence of It is the aim of this review to critically evaluate current knowl-
such effusions in the clinical setting. In Maria Vittoria hospital, an edge on the management of pericardial effusion. A thorough litera-
urban general hospital in Torino and an Italian referral centre for ture review has been performed without language restriction with
pericardial diseases, the mean annual incidence and prevalence of the MeSH term ‘pericardial effusion’ or ‘pericardial’[All Fields] and
pericardial effusion have been, respectively, 3 and 9% in a 6 ‘effusion’[All Fields]) or ‘pericardial effusion’[All Fields]. After the
years experience of the echo laboratory (2000–05).4 Such data initial identification of 1520 papers, 139 papers were selected for
mainly depend on the epidemiological background (especially detailed review based on novelty or important data leading to
developed vs. developing country, where tuberculosis is a leading the final inclusion of 50 papers in the final reference list.

* Corresponding author. Tel: +39 011 4393391, Fax: +39 011 4393334, Email: massimo_imazio@yahoo.it
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2012. For permissions please email: journals.permissions@oup.com
Management of pericardial effusion 1187

Initial evaluation and but, in any case, terminate to mediastinal, tracheobronchial, or iux-
taesophageal lymph nodes. On the ventral surface, the lymphatics
pathophysiological issues of the parietal pericardium connect to lymphatics in the pericardial
When a pericardial effusion is detected, the first step is to evaluate fat and areolar tissue. On the lateral and posterior surfaces, the
its size and haemodynamic importance, as well as the possible as- lymphatics of the parietal pericardium anastomose with lymphatics
sociation with concomitant diseases. Echocardiography is the first of the reflected mediastinal pleura (Supplementary material online,
diagnostic tool for this assessment as also acknowledged by the Reference C). Lymphatic drainage of the pericardium to the medi-
AHA/ACC guidelines on the use of echocardiography, that gave astinal and tracheobronchial lymph nodes and interactions with
a class I indication for the use of echocardiography in any case pleural lymphatics (Supplementary material online, Reference D)
of suspected pericardial disease.10 provide the anatomical basis for pathological involvement of the
Pericardial effusion may be classified based on its onset (acute, pericardium in specific diseases (i.e. pleuro-pulmonary diseases
subacute vs. chronic when dating .3 months), distribution (cir- such as pulmonary tuberculosis and lung cancer).
cumferential or loculated), haemodynamic impact (none, cardiac Any pathological process usually causes an inflammatory
tamponade, effusive-constrictive), composition (exudates, transu- process with the possible increased production of pericardial

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date, blood, rarely air, or gas from bacterial infections), and espe- fluid (exudate). An alternative mechanism of the formation of peri-
cially by its size as mild, moderate, and large (Table 1) based on a cardial fluid may be the decreased reabsorption due to increased
simple semiquantitative echocardiographic assessment (Figure 1) systemic venous pressure generally as a result of congestive
that has been demonstrated useful also to estimate the risk of heart failure or pulmonary hypertension (transudate). If pericardial
specific aetiology and complications during follow-up.4,7,9,11,12 fluid is free to move within the pericardial sac following the gravity
The normal pericardial sac contains 10 –50 mL of pericardial forces, it usually starts accumulating posteriorly to the left ventricle
fluid acting as a lubrificant between the pericardial layers. Surpris- when the patient is laying on his/her left side for echocardiographic
ingly, little is known about the formation and removal of pericardial evaluation (mild effusion detected initially as posterior), then cir-
fluid, because of the paucity of comprehensive studies, especially cumferentially in the case of moderate to large pericardial effu-
in human subjects, and methodological difficulties to distinguish sions. A mild pericardial effusion may also be detected close to
between the dynamics of normal pericardial fluid and those of a the right atrium because this is the cardiac chamber with the
pathological effusion (Supplementary material online, Reference lowest pressures within the cardiac cycle and thus pericardial
A). Nevertheless, normal pericardial fluid is generally considered fluid accumulation is easier in this position (Figure 2). An isolated
an ultrafiltrate of plasma (Supplementary material online, Refer- mild anterior pericardial fluid is unusual on echocardiography
ence B). The arrangement of lymphatic vessels is complex and without previous pericardial scarring as following surgery or
has been described in human cadavers (Supplementary material chronic pericarditis, and should be regarded as fat rather than peri-
online, References C and D). The lymphatic vessels include differ- cardial fluid.13 Computed tomography (CT) or cardiac magnetic
ent pathways according to ventral, lateral, and posterior surfaces, resonance (CMR) may confirm the finding in specific cases14
(Figure 3). On the contrary after pericardial scarring (i.e. after
cardiac surgery or chronic pericarditis, or bacterial infections),
pericardial fluid may not have a uniform distribution within the
Table 1 Classification of pericardial effusion
pericardial space and may give rise to loculated effusions that
Onset Acute (,1 week) should be evaluated with multiple cardiac views.14,15
Subacute (.1 week but ,3 months) The pressure– volume curve of the normal pericardium is a
Chronic (.3 months) J-shaped curve: after an initial short shallow portion that allows
Size Mild (,10 mm) the pericardium to stretch slightly in response to physiological
Moderate (10– 20 mm)
events, such as changes in posture or volume status, with
Large (.20 mm)
minimal pressure increase, then the pericardium does not allow
Distribution Circumferential
Loculated further sudden increases of the volume without a marked increase
Haemodynamic Without cardiac tamponade in the intrapericardial pressure. Thus a sudden increase of pericar-
effect With cardiac tamponade dial volume of 100–200 mL, as in haemopericardium, may elevate
Effusive-constrictive pericardial pressure till 20 –30 mmHg with acute cardiac tampon-
Composition/type Transudate ade (acute or surgical cardiac tamponade). On the contrary a
Exudate slowly accumulating pericardial fluid may allow pericardial disten-
Hydropericardium (transudate, plasma
tion till the accumulation of 1–2 L of pericardial fluid without
ultrafiltrate)
Haemopericardium (blood in pericardial the development of cardiac tamponade (Figure 4) till advanced
space) stages often because of intercurrent events (chronic cardiac tam-
Chylopericardium (chylous pericardial fluid) ponade or medical cardiac tamponade).1,3,16
Pyopericardium (purulent pericardial effusion)
Pneumopericardium (air in the pericardium)
Aetiology
No precise definition is available for acute and subacute pericardial effusion,
while the definition of chronic as .3 months is more clearly defined. A wide variety of aetiologic agents may be responsible of pericar-
dial effusions, since all known causes of pericardial disease may
1188 M. Imazio and Y. Adler

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Figure 1 (A) The semiquantitative assessment of the pericardial effusion size in a case of idiopathic chronic pericardial effusion. A large peri-
cardial effusion of .30 mm in diastole is shown in parasternal long-axis view. (B) Acute pleuropericarditis with ST segment elevation and sinus
tachycardia on ECG strip. A large pericardial effusion .20 mm with concomitant pleural effusion is also evident posteriorly to the aorta. Pe,
pericardial effusion; pl, pleural effusion; Ao, aorta.

Figure 2 Presentation of a mild (A) vs. moderate to large pericardial effusions (B) on echocardiography. Mild pericardial effusion is evident
adjacent to the right atrium in four-chambers view and only posterior in parasternal long-axis view (A). As fluid accumulates, the effusion
becomes circumferential (B). Pe, pericardial effusion; RA, right atrium; Ao, aorta.

be causative agents (Table 2). The more common causes of renal failure), myopericardial diseases (especially pericarditis, but
pericardial effusions include infections (viral, bacterial, especially also myocarditis, heart failure), aortic diseases, especially aortic dis-
tuberculosis), cancer, connective tissue diseases, pericardial in- section extending into the pericardium, and selected drugs (i.e.
jury syndromes (post-myocardial infarction effusions, post- minoxidil). Hydropericardium, a non-inflammatory transudative
pericardiotomy syndromes, post-traumatic pericarditis either pericardial effusion, may occur not only in heart failure, but also
iatrogenic or not), metabolic causes (especially hypothyroidism, advanced hypoalbuminaemia, such as in cirrhosis and nephrotic
Management of pericardial effusion 1189

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Figure 3 Differential diagnosis of pericardial effusion vs. epicardial fat. (A) Echocardiographic view. Anterior pericardial echo-free space.
No effusion was evident adjacent to the right atrium in four-chambers view. (B) Epicardial fat and thickened pericardium with contrast enhance-
ment on CT scan.

Figure 4 Pressure/volume curve of the pericardium with fast accumulating pericardial fluid leading to cardiac tamponade with a smaller
volume (A) compared with the slowly accumulating pericardial fluid reaching cardiac tamponade only after larger volumes (B).

syndrome, when Starling forces promote the accumulation of a At present, the largest cohort of patients with moderate (echo-
plasma ultrafiltrate across the pericardium as well as other mem- free space of 10–20 mm during diastole) and large pericardial effu-
branes (e.g. pleura and peritoneum). sions (echo-free space .20 mm) comes from Spain and includes
In the last 20 years, five major surveys have been published on 322 cases (mean age 56 years, 52% males). Cases were collected
the characteristics of moderate to large pericardial effusions retrospectively from 1990 to 93 and then prospectively from
(Table 3).17 – 21 Obviously, the relative frequency of different 1994 to 96 in a 637-bed university general hospital in Barcelona.
causes depends on the local epidemiology (especially the preva- The authors adopted a three-stage protocol including a basic
lence of tuberculosis), the hospital setting, and the diagnostic evaluation for all (stage I including clinical history, physical examin-
protocol that has been adopted. Many cases still remain idiopathic ation, electrocardiography, chest X-ray, echocardiography, evalu-
in developed countries (up to 50%), while other common causes ation for tuberculosis, measurement of serum antinuclear
include especially cancer (10– 25%), pericarditis and infectious antibodies and thyroid hormones, and other targeted studies
causes (15–30%), iatrogenic causes (15 –20%), and connective according to specific presentation), followed by stage II with peri-
tissue disease (5–15%), whereas tuberculosis is the dominant cardiocentesis and pericardial fluid analysis for those with cardiac
cause in developing countries (.60%), where tuberculosis is tamponade, suspicion of purulent pericarditis, or chronic large
endemic.22 In the setting of pericarditis with pericardial effusion, pericardial effusions. Stage III (surgical biopsy of the pericardium)
the prevalence of malignant or infectious aetiologies ranges from was limited to those with persistent or recurring tamponade
15 to 50% depending on published series.12,17 – 21 after pericardiocentesis, and when the effusion lasted for .3
1190 M. Imazio and Y. Adler

iatrogenic perforations, the evolution is dramatic and only small

Table 2 Causes of pericardial effusion amounts of blood are responsible of a quick rise of intrapericardial
pressure and overt cardiac tamponade in minutes. On the contrary
Infectious a slowly accumulating pericardial fluid allows the collection of a
Viral (most common: Echovirus and Coxsackievirus (usual), Influenza, large effusion in days to weeks before a significant increase in peri-
EBV, CMV, Adenovirus, Varicella, Rubella, Mumps, HBV, HCV, HIV,
cardial pressure becomes responsible of symptoms and signs.3
Parvovirus B19 and Human Herpes Virus 6 (increasing reports)
Classical symptoms include dyspnoea on exertion progressing to
Bacterial [most common: tuberculous (4 –5%), Coxiella burnetii, other
bacterial rare may include Pneumo-, Meningo-, Gonococcosis, orthopnoea, chest pain, and/or fullness. Additional occasional
Haemophilus, Staphylococci, Chlamydia, Mycoplasma, Legionella, symptoms due to local compression may include nausea (dia-
Leptospira, and Listeria] phragm), dysphagia (oesophagus), hoarseness (recurrent laryngeal
Fungal (rare: Histoplasma more likely in immunocompetent patients, nerve), and hiccups (phrenic nerve). Non-specific symptoms
Aspergillosis, Blastomycosis, Candida more likely in include also cough, weakness, fatigue, anorexia and palpitations
immunosuppressed host)
and reflect the compressive effect of the pericardial fluid on con-
Parasitic (very rare: echinococcus, toxoplasma)
................................................................................ tiguous anatomic structures or reduced blood pressure and sec-
ondary sinus tachycardia.23

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Non-infectious
Autoimmune and autoinflammatory The classical findings of cardiac tamponade have been described
Systemic inflammatory diseases (more common in systemic lupus by the thoracic surgeon Beck in 1935.24 Beck identified a triad in-
erythematosus, Sjögren syndrome, rheumatoid arthritis, systemic cluding hypotension, increased jugular venous pressure, and a small
sclerosis, systemic vasculitides, Behçet syndrome, Sarcoidosis, and quiet heart. This triad was classically identified in ‘surgical tam-
Familial Mediterranean Fever) ponade’ with acute cardiac tamponade due to intrapericardial
Pericardial injury syndromes (post-myocardial infarction, haemorrhage because of trauma, myocardial or aortic rupture.
post-pericardiotomy syndrome, post-traumatic)
The Beck triad may be lacking in patients with ‘medical tamponade’
Autoreactive
with slowly accumulating pericardial fluid. Hypotension is absolute
Cancer
or relative. Acute cardiac tamponade is usually associated with low
Primary tumours (rare, especially pericardial mesothelioma)
blood pressure (,90 mmHg) but may be only slightly reduced in
Secondary metastatic tumours (lung, breast cancer, lymphomas, and
subacute, chronic tamponade. Hypertensive patients may have
melanoma)
normal to mildly elevated blood pressure concomitant to cardiac
Metabolic (Uraemia, Myxedema)
tamponade.25 Fever is a non-specific sign that may be associated
Trauma
with pericarditis either infectious or immune-mediated (i.e. system-
Direct injury (penetrating thoracic injury, oesophageal perforation, and
iatrogenic) ic inflammatory diseases).
Indirect injury (non-penetrating thoracic injury, and radiation injury) On physical examination classical signs include neck vein disten-
Mediastinal radiation, recent, or remote tion with elevated jugular venous pressure at bedside examination,
Drugs and toxins (rare): Procainamide, hydralazine, isoniazid, and pulsus paradoxus, and diminished heart sounds on cardiac auscul-
phenytoin (lupus-like syndrome), Penicillins (hypersensitivity tation. Pericardial friction rubs are rarely reported, they can be
pericarditis with eosinophilia), Doxorubicin and daunorubicin usually detected in patients with concomitant pericarditis. Rubs
(often associated with a cardiomyopathy, may cause a which occur during the maximal movement of the heart within
pericardiopathy). Minoxidil. Immunosuppressive therapies (e.g.
its pericardial sac, are said to be generated by friction between
methotrexate, cyclosporine)
the two inflamed layers of the pericardium. However, this com-
Haemodynamic (heart failure, pulmonary hypertension, and
hypoalbuminaemia) monly offered explanation for its mechanism may be an oversimpli-
fication as patients with a pericardial effusion may also have an
audible friction rub, and there is no precise correlation between
pericardial rubs and size of the effusion, although pericardial rubs
may be easier to hear in patients without a pericardial effusion,
weeks after admission and without an aetiologic diagnosis. The but this finding is not universal and is not well-documented
most common diagnoses included: acute idiopathic pericarditis (Supplementary material online, Reference E). In a report of 100
(20%), iatrogenic effusions (16%), cancer (13%), and chronic patients with acute pericarditis, a pericardial rub was present in
idiopathic pericardial effusion (9%). In 60% of cases, the cause of 85% of cases without an effusion (Supplementary material online,
pericardial effusion was a known medical condition.18 Reference F). This prevalence is considerably higher than the
35% incidence of friction rubs reported in another series (Supple-
mentary material online, Reference G).
Clinical presentation Pulsus paradoxus has been described for the first time by Kuss-
The clinical presentation of pericardial effusion is varied according maul in 1873 as a palpable reduction of radial pulse on inspiration
to the speed of pericardial fluid accumulation as mentioned in the in patients with cardiac tamponade.26 The so-called paradox was
introduction, and the aetiology of the effusion with possible symp- the ‘waxing and waning’ of the peripheral pulse, in contrast to
toms that may be related to the causative disease. The rate of peri- the unvarying strength of the apical cardiac impulse. Pulsus para-
cardial fluid accumulation is critical for the clinical presentation. If doxus is classically defined as an inspiratory reduction of at least
pericardial fluid is quickly accumulating such as for wounds or 10 mmHg of the systolic blood pressure (Figure 5). It can be
Management of pericardial effusion 1191

Table 3 Aetiologic diagnosis of moderate to large pericardial effusions according to major published series

Feature Corey et al.17 Sagrista-Sauleda et al.18 Levy et al.19 Reuter et al.20 Ma et al.21
...............................................................................................................................................................................
Patients 57 322 204 233 140
Study years 1993 1990– 96 1998–2002 1995– 2001 2007– 09
Country USA Spain France South Africa China
Effusion size .5 mm .10 mm NR NR Moderate to largea
Cardiac NR 37 NR NR NR
tamponade
Evaluation Subxiphoid TB, ANA, TSH, BCx, TSH, ANA, Q HIV, sputum, TB, BCx, Pericardiocen-tesis
pericardiotomy pericardiocen-tesis, and fever, viral rectal, and blood chemistry,
biopsy throat swabs and serology
Idiopathic (%) 7 29 48 14 9
Cancer (%) 23 13 15 9 39

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Infections (%) 27 2 16 72 29
Connective tissue 12 5 10 5 6
diseases (%)
Metabolic (%) 24 6 11 0 0
Iatrogenic (%) 0 16 0 0 9

A selection of the most frequent aetiological diagnoses is reported (thus overall sum in columns may be ,100%).
NR, not reported; TB, aetiology search for tuberculosis; BCx, blood cultures.
a
All effusions requiring pericardiocentesis.

In the absence of cardiac tamponade reported symptoms and

signs are non-specific and may include: shortness of breath, dys-
pnoea on exertion, fever, chills, chest pain, paroxysmal nocturnal
dyspnoea, orthoponea, cough, and oedema.23 All these symptoms,
and signs may be secondary to the underlying cause of the effusion
(i.e. systemic disease and pericarditis) or the initial mechanical
interference of pericardial fluid with cardiac function or surround-
ing anatomical structures.

Diagnosis
The diagnosis of pericardial effusion is generally performed by
echocardiography, that also allows the semiquantitative assessment
of the pericardial effusion size and its haemodynamic effects as out-
lined in the paragraph on the initial approach to pericardial effu-
Figure 5 The femoral artery pressure curve showing pulsus sion. The diagnosis of cardiac tamponade is essentially a clinical
paradoxus during cardiac tamponade. A systolic blood pressure diagnosis requiring echocardiographic confirmation of the initial
decline is .10 mmHg during inspiration. diagnostic suspicion. In most patients, cardiac tamponade should
be diagnosed by a clinical examination that shows elevated system-
ic venous pressure, tachycardia, dyspnoea, and paradoxical arterial
pulse. Systemic blood pressure may be normal, decreased, or even
easily detected recording the systolic pressure at which Korotkoff elevated. The diagnosis is confirmed by an echocardiographic dem-
sounds are first audible and the systolic pressure at which they are onstration of moderately large or large circumferential pericardial
audible through the whole respiratory cycle. Pulsus paradoxus is effusion and in most instances, of right atrial compression, abnor-
due to exaggerated ventricular interdependence occurring in mal respiratory variation in right and left ventricular dimensions,
cardiac tamponade when overall volume of cardiac chambers and in tricuspid and mitral valve flow velocities usually associated
becomes fixed and any change in the volume of one side of the with inferior vena cava plethora (Table 4 and Figure 6) (Supplemen-
heart causes the opposite changes in the other side (i.e. inspiratory tary material online, Reference H).27
increase of venous return and right chambers with decreased left However, a more complex task is the evaluation of the aeti-
chambers volume and reduced systemic blood pressure). ology. Different diagnostic protocols have been proposed.4,8,17 – 21
1192 M. Imazio and Y. Adler

Nevertheless, the diagnostic work-up should be guided by the glucose can separate exudates from transudates, but are not dir-
epidemiology and the clinical presentation to avoid performing ectly diagnostic (class IIb). Nevertheless, purulent effusions with
an extensive and blinded testing. As already remarked, developing positive cultures have significantly lower fluid glucose levels than
countries have a high rate of pericardial effusions correlated to tu- non-infectious effusions. White cell count is highest in inflamma-
berculosis (.60, and .80% with HIV infection)28,29 that should be tory and infectious diseases, and lowest in myxedema. Technical
ruled out in such context, as well as in immigrants and HIV-infected advances in instrumentation, introduction of pericardioscopy and
patients. Non-idiopathic and non-viral aetiologies (especially bac- contemporary pathology, virology, and molecular biology techni-
terial and neoplastic) are associated with an increased risk of ques have improved the diagnostic value of epicardial/pericardial
cardiac tamponade and large effusion, and pericardiocentesis is biopsy. Pericardioscopy performed through air instead of fluid,
mandatory when cardiac tamponade or such aetiologies are made it possible to inspect large areas of pericardial surface,
suspected.4,6,7 select the biopsy site, and take numerous samples. Targeted peri-
Analyses of pericardial effusion can establish the diagnosis of in- cardial/epicardial biopsy during pericardioscopy was particularly
fectious and neoplastic pericardial effusions. Cytology and tumour useful in the diagnosis of neoplastic pericarditis. No major compli-
markers [carcinoembryonic antigen (CEA), alfafeto protein, carbo- cations were reported with the use of flexible pericardioscopies

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hydrate antigens CA 125, CA 72-4, CA 15-3, CA 19-9, etc.) should (Supplementary material online, References I and J). Such techniques
be performed in suspected malignant disease. In suspected tuber- and approaches are warranted in skilled tertiary referral centres for
culosis acid-fast bacilli staining, mycobacterium culture or radio- selected cases, when a specific diagnosis, that may require a targeted
metric growth detection (e.g. BACTEC-460), adenosine therapy (i.e. neoplastic pericardial effusion), is suspected and cannot
deaminase (ADA), interferon (IFN)-gamma, pericardial lysozyme, be diagnosed by traditional diagnostic means.
and as well as PCR analyses for tuberculosis should be performed In the 2004 ESC guidelines, a specific definition is provided
(indication class I, level of evidence B). Differentiation of tubercu- for autoreactive pericarditis/pericardial effusion. The diagnosis of
lous and neoplastic effusion is virtually absolute with low levels of autoreactive pericarditis is established using the following criteria:
ADA and high levels of CEA. In addition, high ADA levels may (i) increased number of lymphocytes and mononuclear cells
predict the evolution towards pericardial constriction. In suspected .5000/mm3 (autoreactive lymphocytic), or the presence of anti-
bacterial infections, at least three cultures of pericardial fluid for bodies against heart muscle tissue (antisarcolemmal) in the pericar-
aerobes and anaerobes as well as the blood cultures are manda- dial fluid (autoreactive antibody mediated); (ii) signs of myocarditis
tory (indication class I, level of evidence B). PCR analyses for car- on epicardial/endomyocardial biopsies by .14 cells/mm2; (iii) ex-
diotropic viruses have been suggested (indication class IIa, level of clusion of active viral infection both in pericardial effusion and
evidence B), but are rarely used in clinical practice. Analyses of the endomyocardial/ epimyocardial biopsies (no virus isolation, no
pericardial fluid specific gravity (.1015), protein level (.3.0 g/dL), IgM titer against cardiotropic viruses in pericardial effusion, and
fluid/serum ratio .0.5, LDH .200 mg/dL, serum/fluid .0.6, and negative PCR for major cardiotropic viruses); (iv) tuberculosis,
Borrelia burgdorferi, Chlamydia pneumoniae, and other bacterial
infection excluded by PCR and/or cultures; (v) neoplastic infiltration
absent in pericardial effusion and biopsy samples; (vi) exclusion of sys-
Table 4 Major echocardiographic signs of cardiac temic, metabolic disorders, and uraemia. This is essentially a diagnosis
tamponade (Supplementary material online, of exclusion for pericardial effusions with an autoimmune patho-
Reference H) genesis not related to a known systemic inflammatory disease,
and that may be efficiently treated by corticosteroids.
Sign Sensitivity Specificity
................................................................................ A standard recommended approach for the analysis of pericar-
Large pericardial effusion with swinging n.a. n.a. dial fluid is reported in Table 5.
heart Among specific causes of pericardial effusion, tuberculosis is es-
Diastolic collapse of right atrium (RA) 50– 100% 33– 100% pecially important to be recognized, because it is a dangerous
Duration of RA inversion by the RA .90% 100% disease with a high mortality if untreated, and a high risk of evolu-
inversion time index (duration of tion towards constrictive pericarditis (30–50% of cases). A previ-
inversion/cardiac cycle length); ous history of tuberculosis, an origin from an area, where
for values .0.34
tuberculosis is endemic (i.e. Africa and India), a subacute course,
Diastolic collapse of right ventricle (RV) 48– 100% 72– 100%
low grade fever, weight loss, night sweats, a moderate to large peri-
Variations in E velocities during n.a. n.a.
respiration across the mitral valve,
cardial effusion are all features associated with a high risk of a tu-
tricuspid valve, and pulmonary berculous cause of the effusion. A definite diagnosis of tuberculous
outflow that are greater than 25, 50, effusion requires the demonstration of tuberculosis bacilli in peri-
and 30% cardial fluid or tissue. However, the diagnosis is probable if tuber-
Inferior vena cava (IVC) pletora 97% 40% culosis is shown in patients with the diagnosis of tuberculosis
(dilatation .20 mm and ,50% elsewhere in the body (i.e. pulmonary), or with a lymphocytic peri-
reduction in the diameter of IVC
with respiratory phases)
cardial exudate with elevated ADA levels. The empiric response to
antituberculosis therapy as ex-iuvantibus diagnosis may be accept-
n.a, not available. able only in countries, where tuberculosis is endemic, but not in
Western Europe and North America.4,28
Management of pericardial effusion 1193

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Figure 6 Mitral valve flows respiratory changes .25% (A) and inferior vena cava plethora (B; dilatation .20 mm and ,50% reduction
in inferior vena cava diameter) in case of cardiac tamponade.

diseases because of its widespread availability, portability, and

limited costs, CT and CMR provide a larger field of view, allowing
Table 5 Routine analyses to be performed
the detection of loculated pericardial effusion, pericardial thicken-
on pericardial fluid
ing and masses, as well as associated chest abnormalities. Cardiac
Analysis Test Aetiology magnetic resonance may also provide a combined morphological
or feature and functional evaluation. For both CT and CMR, the pericardium
................................................................................ is ideal for imaging studies, because of a high natural contrast
General Specific gravity. 1015, protein Exudate between pericardial layers separated by pericardial fluid, and con-
chemistry level .3 g/dL, protein fluid/
serum ratio .0.5,
tiguous fat tissue in the mediastinal and subepicardial space. Com-
LDH .200 mg/dL, fluid/serum puted tomography density measurements and the analysis of CMR
ratio .0.6a signals may enable the initial characterization of pericardial fluid
Glucose, blood cell count better than echocardiography. With inflamed pericardium, the
Cytology Cytology (higher volumes of Cancer patient usually has the combination of effusion and pericardial
fluid, centrifugation, and thickening. On CT, generally, pericardial effusions are of low
rapid analysis improve
diagnostic yield)
density in the range of 0–20 Hounsfield units (HU). When the ef-
fusion contains higher amounts of protein, such as in bacterial
Biomarkers Tumour markers (i.e. CEA Cancer
.5 ng/mL or CYFRA 21-1 infections, or when it is haemorrhagic, its density may rise to
.100 ng/mL) 50 HU and more. Inflamed pericardium may also show contrast
Adenosine deaminase .40 U/ TBC enhancement. In CT imaging of the pericardium, difficulty may be
L, IFN-gamma encountered in differentiating fluid from thickened pericardial
Polymerase chain PCR for specific infectious TBC tissue. Cardiac magnetic resonance is superior to CT in differenti-
reaction (PCR) agents (i.e. TBC)
ating fluid, especially highly proteinaceous exudative effusions, from
Microbiology Acid-fast bacilli staining, TBC
thickened pericardium. On the contrary, CT may detect even
mycobacterium cultures, Other bacteria
aerobic, and anaerobic minimal amounts of pericardial calcium, whereas CMR may miss
cultures significant deposits. Computed tomography requires less time
than echocardiography and CMR. However, CT requires the use
LDH, lactate dehydrogenase; TBC, tuberculosis. of intravenously administered iodinated contrast materials and ion-
a
These chemical features have been especially validated for pleural fluid and not
izing radiation. Moreover, if performed without ECG gating, CT
pericardial fluid, although generally used also for pericardial effusion.
may lead to cardiac motion artefacts, that limit the evaluation of
pericardial thickness. However, the use of more recent and
updated CT scanners with a greater spatial and temporal reso-
The presence of elevated inflammatory markers and other lution and more sophisticated algorithms for image reconstruction
criteria for pericarditis (chest pain, pericardial rubs, and ECG may allow a significant reduction in CT imaging artefacts. Cardiac
changes) suggests pericarditis and management should follow the magnetic resonance has a superior ability to characterize pericar-
triage and management recommended for pericarditis.30 dial effusions and masses with the use of a combination
Integrated cardiovascular imaging, including echocardiography, of T1-weighted, T2-weighted, and gradient-recalled echo cine
CT, and CMR may provide valuable aid in the search for the sequences without the use of either iodinated contrast material
cause of pericardial effusions.31 – 36 Although echocardiography or ionizing radiation. However, a possible disadvantage of CMR
remains the primary diagnostic tool for the study of pericardial with ECG gating is that arrhythmias, often associated with
1194 M. Imazio and Y. Adler

Figure 7 Evidence of acute pericarditis with mild pericardial effusion on cardiac magnetic resonance (A). The pericardium is thickened

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and contrast enhancement is evident on the inflamed pericardium (B, see red arrows).

myopericardial diseases, may cause artefacts. Another disadvantage

of CMR is related to its limited availability and higher costs. Use of Table 6 Empiric anti-inflammatory therapy
i.v. injected gadolinium may be useful for pericarditis detection, for inflammatory pericardial effusions
because gadolinium has been reported to enhance inflamed peri-
cardium (Figure 7), as well as for the detection of concomitant Drug Attack Dose Treatment Level of
myocardial involvement in myopericarditis.4,7,14,34 – 37 length evidencea
.................................................................................
Acetylsalicylic acid 750– 1000 mg t.i.d. 1– 2 weeks B
Ibuprofen 600 mg t.i.d. 1– 2 weeks B
Therapy Indomethacin 50 mg t.i.d. 1– 2 weeks C
The therapy of pericardial effusion should be targeted at the aeti- Prednisone or 0.2–0.5 mg/kg/day First episode: B
steroid at 2 weeks
ology as much as possible.37 – 41 In 60% of cases, the effusion is
equivalent dose Recurrence:
associated with a known disease,18 and the essential treatment is 4 weeks
that of the underlying disease. When pericardial effusion is associated Colchicine 0.5 mg b.i.d First episode: B
with pericarditis, management should follow that of pericarditis.30,37 (≥70 kg) 3 months
Nevertheless, when diagnosis is still unclear or idiopathic, and 0.5 mg once Recurrence: A
inflammatory markers are elevated, a trial of aspirin or a non- (,70 kg) 6 months
steroidal anti-inflammatory drug (NSAID) can be prescribed also
to evaluate the response (Table 6). A viral or idiopathic form is t.i.d., three times daily; b.i.d.,: twice daily; tapering may be considered in case of
normalization of markers of inflammation and significant response to therapy
often responsive to such empiric therapy. For the management (symptoms, regression or reduction of pericardial effusion). A low tapering is
of recurrent inflammatory cases, the first step is considering especially required for corticosteroids (i.e. decrease prednisone 2.5 mg every 2–4
the combination of aspirin or a NSAID plus colchicine,42 while weeks).
a
A in case of multiple randomized trials or meta-analysis, B for a single-randomized
corticosteroids at low to moderate doses may be considered for trial or non-randomized studies, C for consensus opinion of experts.
specific indications (i.e. systemic inflammatory diseases and preg-
nancy),43 and in case of intolerance, contraindications, or failure
of aspirin/NSAID; other therapies are based on less solid evidence:
less toxic and less expensive drugs (e.g. azathioprine or methotrex- Other non-steroidal agents may increase the risk of thinning the
ate) should be preferred, tailoring the therapy for the individual infarction zone. Corticosteroid therapy can be used for refractory
patient and the physician experience.44 symptoms only, but could delay myocardial infarction healing (class
In the 2004 ESC guidelines, ibuprofen is proposed as the favour- IIa indication, level of evidence B). Post-infarction pericardial effu-
ite first choice for empiric anti-inflammatory therapy of pericardi- sion .10 mm may be associated with haemopericardium, and up
tis, due to rare side effects, favourable effect on the coronary flow, to two-thirds of these patients may develop tamponade/free wall
and the large dose range.7 However, other approaches have been rupture. In this setting, urgent surgical treatment is life saving.
published, and aspirin is used as first favourite choice in several However, if the immediate surgery is not available or contraindi-
clinical trials in the setting of acute and recurrent pericardi- cated, pericardiocentesis, and intrapericardial fibrin-glue instillation
tis.4,37,38,42 For patients who already are taking or need aspirin, could provide an alternative immediate treatment, as proposed in
such drug is the best anti-inflammatory choice.37 In the setting of the 2004 ESC guidelines.7
post-myocardial infarction pericarditis, ibuprofen, which increases In the setting of autoreactive pericardial effusion, growing evi-
the coronary flow, is the preferred agent of choice according to dence supports the possible use of intrapericardial therapies to
2004 ESC guidelines.7 Aspirin has been also successfully applied. reduce side effects related to the oral use of corticosteroids
Management of pericardial effusion 1195

(Supplementary material online, Reference K). Systemic corticos- weeks (e.g. 6–8 weeks), especially when there are signs of right-
teroids offer an effective treatment option for autoreactive peri- sided collapse, in order to prevent the possible progression of
carditis; however, their use is limited by adverse effects and they the effusion towards tamponade following additional events (e.g.
are an independent risk factor for pericarditis recurrence. In a re- pericarditis, bleeding following chest trauma).47
cently published systematic review (Supplementary material online, Unfortunately, there are no proven effective medical therapies
Reference L), one case series and three open-label trials evaluating to reduce an isolated effusion; in the absence of inflammation,
intrapericardial triamcinolone for the management of autoreactive NSAID as well as colchicine and corticosteroids are generally
pericarditis were reviewed. Included studies were limited by small not efficacious.42 Pericardiocentesis alone may be necessary for
sample sizes (n ¼ 2 –84), lack of control groups, short durations of the resolution of large effusions but recurrences are also
follow-up (24 h–12 months), use of adjuvant agents, lack of patient common and pericardiectomy or less invasive options (i.e. pericar-
demographic data, subjective report of symptom relief, and lack dial window) should be considered whenever fluid reaccumulates,
of consistent dose of intrapericardial triamcinolone. Despite becomes loculated, or biopsy material is required.37 The feasibility
these limitations, available data suggest symptom resolution and of pericardiocentesis is high (.90%) in patients with anterior effu-
reduced pericarditis recurrence with the administration of intra- sion, while the rate of success is ,60% with small, posteriorly

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pericardial triamcinolone to patients with autoreactive pericarditis located effusions. Pericardiocentesis with echocardiography guid-
(Supplementary material online, Reference L). ance is feasible in .95% of cases. The most serious complications
When a pericardial effusion becomes symptomatic without of pericardiocentesis are laceration and perforation of the myocar-
evidence of inflammation or when empiric anti-inflammatory dium and the coronary vessels. In addition, patients can experience
drugs are not successful, drainage of the effusion should be consid- air embolism, pneumothorax, arrhythmias (usually vasovagal brady-
ered. Pericardiocentesis with prolonged pericardial drainage till cardia), and puncture of the peritoneal cavity or abdominal viscera.
,30 mL/24 h is recommended to promote adherence of pericar- Internal mammary artery fistulas, acute pulmonary oedema, and
dial layers and prevent further accumulation of fluid, although purulent pericarditis were rarely reported. The safety was improved
evidence to support this indication is based on case reports, retro- with echocardiographic or fluoroscopic guidance. Recent large
spective studies, and expert opinion. If pericardiocentesis is not echocardiographic series reported an incidence of major complica-
feasible or fails, the creation of a so-called pericardial window tions of 1–1.6%. In a large series of fluoroscopy-guided percutan-
should be considered either by conventional heart surgery or eous pericardiocenteses, cardiac perforations occurred in ,1%,
video-assisted thoracoscopy. Balloon pericardiotomy is an alterna- serious arrhythmias in 0.6%, arterial bleeding in 1.1%, pneumothorax
tive to surgical creation of a pericardial window, which has been in 0.6%, infection in 0.3%, and a major vagal reaction in 0.3%.6,7 The
shown successful especially in the setting of neoplastic pericardial need for intervention in all cases remains controversial and requires
disease. The technique involves inserting a deflated single catheter the understanding of the possible benefit/risk ratio (i.e. possible
or double balloon catheters into the pericardial space using a sub- trigger of recurrences).48
xiphoid approach under fluoroscopic or echocardiographic guid- Special considerations should be done for the management of
ance. Although successful in preventing recurrence in .80% of neoplastic pericardial effusions (Supplementary material online,
cases, stretching of the pericardium is often painful so appropriate References L and M –Q). Malignant pericardial effusion and
analgesia is recommended.37,38 cardiac tamponade are known complications of many advanced
The 2004 ESC guidelines gave a class IIa recommendation to malignancies, such as breast cancer, lung cancer, lymphomas, and
pericardiectomy for frequent and highly symptomatic recurrences leukaemias. There are many treatment options available, ranging
resistant to medical treatment. Other reported indications include from simple drainage to thoracic surgery. It is essential that treating
repeated recurrences with cardiac tamponade, and evidence of physicians choose a treatment plan in the context of the cancer
serious steroid toxicity.7 Although surgical experiences are not stage, the patient’s prognosis, the success rates and risks of the
always concordant, pericardiectomy is generally considered as a various modalities, and local availability and expertise. Given the
therapeutic option of doubtful efficacy in recurrent idiopathic peri- poor prognosis of most patients presenting with malignant pericar-
carditis or pericardial effusion and should be considered only in ex- dial effusions, reducing symptoms and improving the quality of life
ceptional cases. Chronic permanent constriction remains the are the primary goals of treatment. Management of these patients
major indication for such intervention.37 However, incessant peri- requires multidisciplinary approaches with cooperation between
carditis, as distinguished from recurrent intermittent pericarditis, cardiologists, cardiac surgeons, oncologists, radiotherapists, and
may respond favourably to surgical removal, especially in the pres- palliative care physicians.38 Immediate relief of symptoms may be
ence of recurrent pericardial effusion.45 An idiopathic chronic peri- obtained with percutaneous drainage or with a surgical approach.
cardial effusion is defined as a collection of pericardial fluid that For long-term prevention of recurrences, various approaches have
persists for .3 months and has no apparent cause; large effusions been proposed: extended drainage, pericardial window (either sur-
have a risk of progression to cardiac tamponade (up to one-third, gical or percutaneous balloon pericardiostomy), sclerosing local
according to a Spanish study). On this basis some authors have therapy, local and/or systemic chemotherapy, or radiation
advocated the need for pericardiectomy for such cases, whenever therapy. The outcomes of various therapeutic approaches vary
a large effusion recurs after pericardiocentesis.46 Since drainage is for different tumour types. Lymphoma and leukaemias can be suc-
relatively safe and easy in some cases with guided pericardiocen- cessfully treated with systemic chemotherapy; for solid tumours,
tesis, drainage has been recommended for large subacute effusions, percutaneous drainage and the use of systemic and/or local scler-
that do not respond to empiric therapy, and are stable after several osing and antineoplastic therapy seems to offer the best chance of
1196 M. Imazio and Y. Adler

success. The use of ‘pure’ sclerosing agents has been replaced by complications either early or intermediate (cardiac tamponade,
agents with both sclerosing and antineoplastic activity (bleomycin recurrences) or late (constrictive pericarditis).49 Idiopathic pericar-
or thiotepa), which seems to be quite effective in breast cancer, dial effusion and pericarditis have an overall good prognosis with a
at least when associated with systemic chemotherapy. Local chemo- very low risk of complications especially if the effusion is mild to
therapy with platinum, mitoxantrone, and other agents may lead to moderate. In contrast with these observations, a recently published
good local control of the disease, but the addition of systemic prospective study has shown that even with mild pericardial effu-
chemotherapy is probably relevant to improve survival. The ration- sion the overall prognosis may be worse than in age- and sex-
ale of local instillation of antineoplastic agents is to cure the metas- matched controls.50
tases, rather than simply prevent effusion by mechanical means. Large idiopathic chronic effusion (.3 months) have a 30 –35%
Intrapericardial treatment tailored to the type of cancer indicates risk of progression to cardiac tamponade.46 Also subacute (4–6
that cisplatin is more effective in secondary lung cancer, whereas weeks) large effusions not responsive to conventional therapy
thiotepa seems to be effective in breast cancer.7 Surgical or percu- and with echocardiographic signs of right chambers collapse may
taneous pericardiostomy and radiation therapy may be useful in re- have an increased risk of progression according to some authors
curring effusions or cases not responsing to other treatments who recommend preventive drainage in such cases.47
(Supplementary material online, References P and Q).40

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Idiopathic pericarditis has a very low documented risk of con-
strictive pericarditis despite even several recurrences: here the risk
is related to the aetiology and not the number of recurrences.49
Prognosis and follow-up The follow-up of pericardial effusion is mainly based on the
The prognosis of pericardial effusion is essentially related to the evaluation of symptoms and the echocardiographic size of the ef-
aetiology, and, thus, it is important to identify specific aetiology fusion, as well as additional features such as inflammatory markers
that requires targeted therapies. The size of the effusion is corre- (i.e. C-reactive protein). There are no specific recommendations
lated to the prognosis, because moderate to large effusions are from pericardial diseases guidelines. A mild idiopathic effusion
more common for specific aetiologies, such as bacterial, neoplastic (,10 mm) is usually asymptomatic, has generally a good prognosis
or related to a systemic inflammatory disease.4,12,30 Bacterial aeti- and does not require specific monitoring. Moderate to large effu-
ologies as well as post-radiation pericardial diseases, pericardial sions (.10 mm) may worsen and especially severe effusions may
injury syndromes have an increased risk of developing evolve towards cardiac tamponade in up to one-third of cases as

Figure 8 A simplified algorithm for pericardial effusion triage and management. CRP, C-reactive protein.
Management of pericardial effusion 1197

already mentioned. We usually recommend to tailor the follow-up 1997 Guidelines for the Clinical Application of Echocardiography). Circulation
2003;108:1146 – 1162.
to the aetiology, adopted therapies (usually a control after 1– 2
11. Weitzman LB, Tinker WP, Kronzon I, Cohen ML, Glassman E, Spencer FC. The
weeks and then after 1 month and 6 months), and monitoring incidence and natural history of pericardial effusion after cardiac surgery—an
the possible evolution towards worsening pericardial effusion, echocardiographic study. Circulation 1984;69:506 –511.
cardiac tamponade, and constrictive pericarditis. For idiopathic 12. Imazio M, Cecchi E, Demichelis B, Ierna S, Demarie D, Ghisio A, Pomari F,
Coda L, Belli R, Trinchero R. Indicators of poor prognosis of acute pericarditis.
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Relatively, few data have been published on the management of raphy 2008;25:321 – 327.
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