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Overview of pericardial disease

Overview of pericardial disease
Author:
Brian D Hoit, MD
Section Editor:
Martin M LeWinter, MD
Deputy Editor:
Susan B Yeon, MD, JD
Literature review current through: Jan 2024.
This topic last updated: Nov 27, 2023.

INTRODUCTION — The pericardium is a fibroelastic sac surrounding the heart that contains a small physiologic amount of fluid (15 to 50 mL). Pericardial diseases are relatively common in clinical practice as either isolated disease or as a manifestation of a systemic disorder. An overview of clinical syndromes associated with pericardial disease is presented here.

CLASSIFICATION OF PERICARDIAL SYNDROMES — Pericardial syndromes are classified according to clinical features, time course, and etiology (table 1 and table 2). The main syndromes are [1]:

Acute, recurrent, incessant, and chronic pericarditis – (See "Acute pericarditis: Clinical presentation and diagnosis" and "Recurrent pericarditis".)

Pericardial effusion – (See "Pericardial effusion: Approach to diagnosis".)

With hemodynamic compromise (cardiac tamponade). (See "Cardiac tamponade".)

Without hemodynamic compromise. (See "Pericardial effusion: Approach to diagnosis", section on 'Hemodynamic effects'.)

Constrictive pericarditis – (See "Constrictive pericarditis: Clinical features and causes" and "Constrictive pericarditis: Diagnostic evaluation".)

There is overlap among clinical syndromes. For example, some patients presenting with acute, recurrent, or chronic pericarditis have pericardial effusion. Also, some patients presenting with pericardial effusion have constrictive pericarditis, and thus have effusive-constrictive pericarditis. (See 'Effusive-constrictive pericarditis' below.)

ETIOLOGY — The etiology of pericardial disease can be classified into the following categories (table 1) [2,3]:

Idiopathic (presumed to be viral or immune-mediated [4,5]), which typically presents as acute pericarditis. (See "Acute pericarditis: Clinical presentation and diagnosis".)

Infectious – Nearly any infectious organism can infect the pericardium. While most types of pericardial infection present with acute pericarditis and/or pericardial effusion, some pericardial bacterial or fungal infections present with purulent pericarditis, defined as infection with macroscopically or microscopically purulent pericardial fluid. (See "Purulent pericarditis".)

Viral – Includes coxsackievirus (types A and B), echovirus, adenovirus, Epstein-Barr virus, cytomegalovirus, herpes, influenza, varicella, rubella, human immunodeficiency virus (HIV), hepatitis B, mumps, parvovirus B19, vaccina (smallpox vaccine), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

Bacterial – Includes Mycobacterium tuberculosis (see "Tuberculous pericarditis"), Staphylococcus, Streptococcus, Haemophilus, Neisseria (N. gonorrhoeae or N. meningitidis), Chlamydia (C. psittaci or C. trachomatis), Legionella, Pneumococcus, Salmonella, Borrelia burgdorferi, Mycoplasma, Actinomyces, Nocardia, Tropheryma whipplei, Treponema, Rickettsia.

Fungal – Includes Histoplasma, Aspergillus, Blastomyces, Coccidioides, Candida. (See "Candida infections of the abdomen and thorax", section on 'Pericarditis'.)

Parasitic – Includes Echinococcus, amebic, Toxoplasma.

Autoimmune and autoinflammatory

Systemic inflammatory diseases (eg, systemic lupus erythematosus, rheumatoid arthritis). (See "Pericardial involvement in systemic autoimmune diseases".)

Autoinflammatory conditions (eg, familial Mediterranean fever, tumor necrosis factor associated periodic syndrome [TRAPS], IgG4-related disease). (See "Clinical manifestations and diagnosis of familial Mediterranean fever", section on 'Chest pain' and "Tumor necrosis factor receptor-1 associated periodic syndrome (TRAPS)", section on 'Clinical manifestations' and "Clinical manifestations and diagnosis of IgG4-related disease", section on 'Clinical features'.)

Post-cardiac injury syndrome, which includes (see "Post-cardiac injury syndromes"):

-Post-myocardial infarction

-Postpericardiotomy

-Posttraumatic (including iatrogenic)

Other – Includes granulomatosis with polyangiitis, polyarteritis nodosa, sarcoidosis, inflammatory bowel disease (Crohn, ulcerative colitis), giant cell arteritis, Behçet syndrome, rheumatic fever. (See "Granulomatosis with polyangiitis and microscopic polyangiitis: Clinical manifestations and diagnosis" and "Clinical manifestations and diagnosis of polyarteritis nodosa in adults" and "Overview of extrapulmonary manifestations of sarcoidosis", section on 'Cardiovascular' and "Clinical manifestations, diagnosis, and prognosis of Crohn disease in adults" and "Clinical manifestations, diagnosis, and prognosis of ulcerative colitis in adults" and "Whipple's disease" and "Clinical manifestations of giant cell arteritis" and "Clinical manifestations and diagnosis of Behçet syndrome" and "Acute rheumatic fever: Clinical manifestations and diagnosis", section on 'Carditis'.)

Neoplasm – Including lung and breast cancer, Hodgkin lymphoma, and mesothelioma. (See "Pericardial disease associated with cancer: Clinical presentation and diagnosis".)

Trauma – Blunt or penetrating (including iatrogenic injury). (See "Initial evaluation and management of blunt cardiac injury" and "Initial evaluation and management of penetrating thoracic trauma in adults", section on 'Cardiac injury' and "Post-cardiac injury syndromes".)

Metabolic (uremia, dialysis-associated, hypothyroidism, ovarian hyperstimulation syndrome). (See "Overview of the management of chronic kidney disease in adults", section on 'Pericarditis' and "Clinical manifestations of hypothyroidism", section on 'Cardiovascular system' and "Pathogenesis, clinical manifestations, and diagnosis of ovarian hyperstimulation syndrome", section on 'Clinical manifestations'.)

Radiation – Most cases are secondary to radiation therapy for Hodgkin lymphoma, breast cancer, or lung cancer. Improved shielding and dose calculation have reduced the incidence of this complication. (See "Cardiotoxicity of radiation therapy for breast cancer and other malignancies".)

Drugs and toxins (table 2)

PERICARDITIS — Pericarditis refers to inflammation of the pericardial sac and is the most common pericardial disorder.

Pericarditis syndromes

Acute pericarditis

Clinical features — Acute pericarditis is a condition (with or without pericardial effusion) lasting less than four to six weeks with at least two of the following criteria (table 3) [1,6] (see "Acute pericarditis: Clinical presentation and diagnosis"):

Typical chest pain (sharp and pleuritic, improved by sitting up and leaning forward).

Pericardial friction rub (a superficial scratchy or squeaking sound best heard with the diaphragm of the stethoscope over the left sternal border) (movie 1).

Characteristic changes on the electrocardiogram (ECG; typically widespread ST-segment elevation) (waveform 1).

New or worsening pericardial effusion.

In resource-abundant countries, the cause of acute pericarditis is often unknown (idiopathic) and is presumed to be caused by a virus or immune response to a virus (table 4). In resource-limited countries, the most common cause of acute pericarditis is tuberculosis. (See "Tuberculous pericarditis".)

Prognosis — While most patients with acute idiopathic or viral pericarditis have a good long-term prognosis, a minority of patients develop recurrent or incessant disease and are at risk for developing constrictive pericarditis. (See 'Recurrent pericarditis' below and 'Incessant and chronic pericarditis' below and 'Risk of constrictive pericarditis after acute pericarditis' below.)

Recurrent pericarditis — Recurrent pericarditis is identified as recurrence of symptoms of acute pericarditis after a symptom-free interval of least four to six weeks [7,8]. Four to six weeks has been established as the minimum required symptom-free interval as it represents the typical duration of antiinflammatory therapy (including taper). The recurrence rate for idiopathic acute pericarditis may be as high as 37 percent in patients not treated with colchicine and 15 percent for those treated with colchicine [9]. (See "Acute pericarditis: Treatment and prognosis", section on 'Colchicine'.)

Incessant and chronic pericarditis — Pericarditis is categorized as incessant when symptoms and signs persist for greater than four to six weeks up to three months without a sustained remission [7]. This includes recurrence of symptoms after a symptom-free interval of less than four to six weeks after the acute episode. Such recurrences often occur during attempted drug weaning, particularly following glucocorticoid therapy; they are less common following nonsteroidal antiinflammatory drug (NSAID) use.

Chronic pericarditis is defined as occurring when symptoms persist for greater than three months [7].

Cholesterol pericarditis is a complication of chronic pericardial effusion exacerbated by cholesterol crystals. Causes include tuberculous pericarditis , rheumatoid pericarditis, and pericardial trauma, a less common cause. (See "Tuberculous pericarditis" and "Pericardial involvement in systemic autoimmune diseases", section on 'Rheumatoid arthritis' and "Post-cardiac injury syndromes".)

Incessant pericarditis and chronic pericarditis are associated with an increased risk of developing constrictive pericarditis. (See 'Constrictive pericarditis' below.)

Myopericarditis — While the terms myopericarditis and perimyocarditis are often used interchangeably, the terms represent two different disease processes with distinct approaches to diagnosis and treatment.

"Myopericarditis" refers to cases of confirmed acute pericarditis with elevated troponin but without left ventricular systolic dysfunction. (See "Myopericarditis".)

"Perimyocarditis" refers to cases presenting as acute pericarditis with elevated troponin and left ventricular ejection fraction less than 55 percent. The diagnostic approach and management for perimyocarditis is the same as for myocarditis. (See "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Clinical manifestations' and "Treatment and prognosis of myocarditis in adults".)

Management of pericarditis

General measures and treatment of cause — Management of pericarditis includes effective communication with the patient about the disease course and therapy directed at the disease process or cause (if known) (algorithm 1):

For inflammatory conditions – Most patients with acute or recurrent pericarditis are treated with antiinflammatory agents (table 5), including those with the following clinical presentations:

Acute or recurrent pericarditis which is idiopathic (presumed immune reaction to viral infection). However, when an ongoing viral infection is confirmed, glucocorticoid therapy is avoided [1].

Management of acute pericarditis during pregnancy is modified to take into consideration the impact of medical therapies on the fetus. (See "Management of pericardial effusion and acute pericarditis during pregnancy", section on 'Management'.)

Acute pericarditis caused by radiation therapy. (See "Pericardial disease associated with cancer: Clinical presentation and diagnosis", section on 'Radiation'.)

Post-cardiac injury syndromes (post-myocardial infarction syndrome, postpericardiotomy syndrome, posttraumatic pericarditis). (See "Post-cardiac injury syndromes", section on 'Treatment'.)

The role of prophylactic colchicine following cardiac surgery to reduce the risk of postpericardiotomy syndrome is discussed separately. (See "Post-cardiac injury syndromes", section on 'Colchicine'.)

Patients with systemic autoimmune disease with asymptomatic pericardial involvement are generally treated with standard therapy for their autoimmune condition. Those who develop symptomatic acute pericarditis are generally treated with antiinflammatory therapy (table 5). (See "Pericardial involvement in systemic autoimmune diseases", section on 'Clinical presentation, diagnosis, and treatment'.)

For uremia - Management of uremic pericarditis involves initiation or intensification of dialysis. Dialysis alone may improve chest pain associated with pericarditis and decrease the size of the pericardial effusion, particularly in patients recently initiating dialysis. When pharmacologic therapy is required, treatment is similar to that for patients without chronic kidney disease. (See "Acute pericarditis: Treatment and prognosis", section on 'Treatment in patients with chronic kidney disease'.)

For infection – Management involves treatment with the appropriate antimicrobial agent. Purulent pericarditis requires urgent management, as discussed below. (See 'Urgent conditions' below.)

Pericardiectomy — Pericardiectomy is an option for patients with recurrent pericarditis who have persistent symptoms after failure of medical regimens (table 5) including NSAID or aspirin, colchicine, and glucocorticoid therapy. In this setting, the potential benefits and risks of immune therapy (eg, interleukin-1 inhibitor [rilonacept or anakinra]) and of pericardiectomy (as an alternative to drug therapy) are discussed with the patient. (See "Recurrent pericarditis", section on 'Treatment'.)

PERICARDIAL EFFUSION — A pericardial effusion is present when accumulated fluid within the sac exceeds the small physiologic amount (15 to 50 mL). Pericardial effusions are caused by a wide range of diseases (table 1 and table 6). (See "Pericardial effusion: Approach to diagnosis".)

Urgent conditions

Cardiac tamponade – Cardiac tamponade requires urgent diagnosis and management. It is caused by pericardial fluid accumulating under pressure, impairing cardiac filling and reducing stroke volume. Tamponade is suspected based upon the patient's history (which may include a cause of pericardial disease), symptoms (eg, fatigue, dyspnea, syncope, presyncope), and signs. Nearly all patients with cardiac tamponade have at least one of the following findings: sinus tachycardia, elevated jugular venous pressure (which may not be present in severely hypovolemic patients), pulsus paradoxus, and hypotension. (See "Cardiac tamponade".)

With cardiac tamponade, the pericardial effusion is usually moderate or large (movie 2) but may be surprisingly small if the effusion has accumulated rapidly. The speed of pericardial fluid accumulation affects the size of pericardial effusion that causes cardiac tamponade (figure 1).

Purulent pericarditis – Purulent pericarditis (defined as infection with macroscopically or microscopically purulent pericardial fluid) requires urgent diagnosis and management. It typically presents with high fever and tachycardia with or without chest pain, often in the setting of predisposing conditions. (See "Purulent pericarditis".)

Purulent pericarditis may be caused by bacterial (including tuberculous) and fungal infection. It is treated with urgent pericardial fluid removal (pericardiocentesis when feasible and/or surgical pericardial fluid drainage with window to prevent hemodynamic compromise) and antimicrobial therapy. (See "Purulent pericarditis", section on 'Treatment' and "Candida infections of the abdomen and thorax", section on 'Pericarditis' and "Tuberculous pericarditis", section on 'Treatment'.)

Other clinical presentations — Many patients with pericardial effusion without tamponade have no symptoms or signs directly caused by the pericardial effusion, although they may have symptoms related to the underlying cause of pericardial disease (eg, fever in the setting of infectious or immune-mediated pericarditis). Thus, pericardial effusions are often discovered incidentally during evaluation for other cardiopulmonary and noncardiopulmonary diseases. (See "Pericardial effusion: Approach to diagnosis", section on 'When to suspect pericardial effusion'.)

Treatment of chylopericardium including dietary therapy is discussed separately. (See "Chylopericardium and cholesterol pericarditis", section on 'Treatment'.)

Diagnostic evaluation — Most pericardial effusions are identified by transthoracic echocardiogram (TTE), which also enables assessment of the hemodynamic effects of the effusion (determination of whether it is causing cardiac tamponade) and provides an estimate of its size. (See "Pericardial effusion: Approach to diagnosis", section on 'Echocardiography' and "Echocardiographic evaluation of the pericardium".)

In some cases, the likely cause of the pericardial effusion will be evident from the clinical context (eg, malignant pericardial disease in a patient with lung cancer). If the cause is not apparent, evaluation of the pericardial fluid (with or without biopsy) may suggest an etiology (table 6). (See "Pericardial effusion: Approach to diagnosis", section on 'Pericardial fluid analysis and biopsy'.)

Management of pericardial effusion

Indications for drainage – Urgent pericardial fluid removal is required for patients with cardiac tamponade and for patients with purulent pericarditis (algorithm 2). (See "Cardiac tamponade" and "Purulent pericarditis".)

Patients who do not require immediate pericardial fluid drainage are monitored; some may undergo pericardial fluid sampling for diagnostic purposes. (See "Pericardial effusion: Approach to diagnosis", section on 'Pericardial fluid analysis and biopsy'.)

Choice of procedure – When pericardial fluid drainage is indicated, the choice of procedure is based largely upon whether the pericardial effusion is accessible to percutaneous drainage and whether there is a critical cardiac or aortic bleeding site that requires surgical management (algorithm 2) [1]. In patients with cardiac tamponade, invasive hemodynamic monitoring during the pericardial drainage procedure enables definitive confirmation of cardiac tamponade. (See "Pericardial effusion: Approach to management", section on 'Choice of pericardial drainage procedure'.)

Monitoring and treatment of cause – Patients in whom the initial approach is observation (or who have undergone pericardiocentesis) should undergo serial clinical and echocardiographic evaluation, avoid volume depletion, and receive treatment for the underlying cause of the pericardial effusion, if known. (See "Pericardial effusion: Approach to management", section on 'General management'.)

Prevention and treatment of recurrent effusion – For patients deemed at high risk for recurrent pericardial effusion (including those with malignant pericardial effusion, purulent pericarditis, or cholesterol pericarditis), initial management with pericardial fluid removal may be combined with or followed by one or more measures to prevent or treat recurrent pericardial effusion, such as prolonged catheter drainage, repeated pericardiocentesis, surgical pericardiotomy (pericardial window), or pericardiectomy (for cholesterol pericarditis) along with treatment of the underlying cause of the effusion (eg, chemotherapy for malignancy). (See "Pericardial effusion: Approach to management", section on 'Management of recurrent pericardial effusion' and "Pericardial disease associated with cancer: Management", section on 'Prevention and treatment of recurrent malignant pericardial effusion' and "Chylopericardium and cholesterol pericarditis", section on 'Cholesterol pericarditis'.)

CONSTRICTIVE PERICARDITIS

Clinical presentation and diagnosis — Constrictive pericarditis is a clinical syndrome in which an inelastic thickened pericardium restricts cardiac filling [1,6,10]. Constrictive pericarditis should be suspected in any patient with symptoms and signs consistent with the diagnosis (such as dyspnea on exertion, peripheral edema, and unexplained elevation of jugular venous pressure with prominent y descent (figure 2)), particularly if there is a history of a predisposing condition such as malignancy, prior cardiac surgery, prior radiation therapy, or prior purulent pericarditis. Patients with constrictive pericarditis typically present months to years after an initial insult involving the pericardium. (See "Constrictive pericarditis: Diagnostic evaluation", section on 'When to suspect constrictive pericarditis'.)

Risk of constrictive pericarditis after acute pericarditis — The risk of developing constrictive pericarditis after acute pericarditis varies depending on the cause of acute pericarditis, with low risk (0.76/1000 person-years) in patients with idiopathic/viral cause, higher risk in patients with pericardial injury syndrome or systemic autoimmune disorders (4.4/1000 person-years) or neoplasm (6.33/1000 person-years), and highest risk (52.74/1000 person-years) with purulent pericarditis (including tuberculous pericarditis, 31.65/1000 person-years), as discussed separately [11]. (See "Constrictive pericarditis: Clinical features and causes", section on 'Incidence and causes'.)

The cause of acute pericarditis that precedes constrictive pericarditis varies widely depending on the population studied, with idiopathic or posttreatment (eg, postoperative or postradiation) causes being more common in resource-abundant countries and infectious etiologies (tuberculosis) being more prominent in resource-limited countries. (See "Constrictive pericarditis: Clinical features and causes", section on 'Incidence and causes'.)

Transient constrictive pericarditis — In a minority of cases of constrictive pericarditis, the constriction resolves spontaneously or with medical therapy, with most such cases resolving within two to six months with antiinflammatory therapy (table 5 and algorithm 3). Cases of transient (subacute) constrictive pericarditis commonly present as effusive-constrictive pericarditis. (See "Constrictive pericarditis: Clinical features and causes", section on 'Transient constrictive pericarditis'.)

Chronic constrictive pericarditis — Most constrictive pericarditis has a chronic course, with constriction persisting for greater than three to six months. Chronic constrictive pericarditis which is manifested by anasarca, atrial fibrillation, hepatic dysfunction, and/or pericardial calcification. Pericardial effusion is rarely a prominent feature of chronic constrictive pericarditis. (See "Constrictive pericarditis: Clinical features and causes", section on 'Constrictive pericarditis'.)

Effusive-constrictive pericarditis — Effusive-constrictive pericarditis is a clinical syndrome caused by pericardial effusion (often with cardiac tamponade) and concurrent constrictive pericarditis. This syndrome overlaps with transient constrictive pericarditis and is diagnosed by hemodynamic evaluation during pericardial fluid removal by failure of the right atrial pressure to fall by 50 percent or to <10 mmHg after pericardial fluid removal [1]. (See "Constrictive pericarditis: Clinical features and causes", section on 'Effusive-constrictive pericarditis'.)

This condition is treated with pericardial fluid drainage (generally pericardiocentesis) followed by medical therapy for transient constrictive pericarditis. If chronic constrictive pericarditis develops, it is usually treated with pericardiectomy. (See 'Management of constrictive pericarditis' below.)

Diagnosis of constrictive pericarditis — The diagnosis of constrictive pericarditis is often made by echocardiography, with additional evaluation by cardiovascular magnetic resonance (CMR) imaging and/or cardiac computed tomography (CT) and occasional need for invasive cardiac catheterization (algorithm 4). (See "Constrictive pericarditis: Diagnostic evaluation".)

On echocardiography, respirophasic ventricular septal shift, plus either or both of hepatic vein diastolic flow reversal ratio ≥79 percent and medial e' velocity ≥9 cm/s is generally sufficient to confirm a diagnosis of constrictive pericarditis (algorithm 4).

Although the presence of increased pericardial thickness (best seen on cardiac CT or CMR imaging) suggests the presence of constrictive pericarditis, this finding is not sufficient to establish a diagnosis of constrictive pericarditis, and absence of pericardial thickening does not exclude the presence of constrictive pericarditis. (See "Constrictive pericarditis: Diagnostic evaluation", section on 'Additional testing'.)

Management of constrictive pericarditis

For early disease – The presence of chest pain, elevated erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP), pericardial effusion, and pericardial delayed hyperenhancement on CMR suggests a subacute process that may respond to antiinflammatory therapy. Doses of antiinflammatory agents are the same as those used for acute pericarditis, but the duration of therapy is generally longer for constrictive pericarditis (table 5 and algorithm 3). (See "Constrictive pericarditis: Management and prognosis", section on 'Treatment of early (subacute) disease'.)

For chronic constriction – Pericardiectomy is the only definitive treatment for patients with late (chronic) constrictive pericarditis (algorithm 3), but the procedure is associated with significant operative risk. Pericardiectomy involves removal of as much of the constricting parietal and epicardial (visceral) layers as possible, including layers over the right atrium, superior vena cava, inferior vena cava, and the inferior part of the right ventricle adjacent to the diaphragm, while preserving the bilateral phrenic nerves. Diuretic therapy is used only as a temporizing measure and for patients who are not candidates for surgery. (See "Constrictive pericarditis: Management and prognosis", section on 'Treatment of late (chronic) disease'.)

Pericardiectomy is reserved for patients who meet all of the following criteria:

Symptoms and signs have persisted despite at least 4 to 12 months of antiinflammatory therapy (algorithm 3).

Symptoms are moderate to severe (New York Heart Association functional class III or IV (table 7)).

Constrictive pericarditis has not progressed to "end-stage." Manifestations of end-stage disease can include cachexia, markedly reduced resting cardiac output (cardiac index ≤1.2 L/m2 per min), hypoalbuminemia due to protein-losing enteropathy, and/or congestive hepatopathy including cardiac cirrhosis. (See "Congestive hepatopathy".)

There is no concomitant restrictive cardiomyopathy (eg, due to radiation-induced injury). (See "Restrictive cardiomyopathies".)

There are no other comorbid conditions that would place the patient at high risk (eg, end-stage kidney disease or ventricular systolic dysfunction).

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pericardial disease".)

SUMMARY AND RECOMMENDATIONS

Classification – Pericardial syndromes are classified according to clinical features, time course, and etiology (table 1 and table 2).

Acute and recurrent pericarditis - Acute pericarditis is a condition lasting less than four to six weeks with at least two of four diagnostic features (table 3). While most patients with acute idiopathic or viral pericarditis have a good long-term prognosis, a minority of patients develop recurrent, incessant, or chronic disease and are at risk for developing constrictive pericarditis. (See 'Acute pericarditis' above.)

Management of acute or recurrent pericarditis includes therapy directed at the disease process or cause (if known) (algorithm 1). Most patients with acute or recurrent pericarditis are treated with antiinflammatory agents (table 5). (See 'Management of pericarditis' above.)

Pericardial effusion

Urgent conditions – The following conditions require urgent diagnosis and pericardial fluid removal (algorithm 2):

-Cardiac tamponade (pericardial fluid accumulating under pressure and impairing cardiac filling) presents with symptoms such as fatigue, dyspnea, and syncope and signs such as sinus tachycardia, elevated jugular venous pressure, pulsus paradoxus, and hypotension. The size of the pericardial effusion is commonly moderate or large but may be relatively small if the fluid has accumulated rapidly (figure 1). (See "Cardiac tamponade".)

-Purulent pericarditis (defined as infection with macroscopically or microscopically purulent pericardial fluid) typically presents with high fever and tachycardia with or without chest pain, often in the setting of predisposing conditions. It is caused by bacterial (including tuberculous) or fungal infection and is treated with urgent pericardial fluid removal and antimicrobial therapy (See "Purulent pericarditis".)

Nonurgent conditions – Patients who do not require immediate pericardial fluid drainage are monitored; some may undergo pericardial fluid sampling for diagnostic purposes (algorithm 2). (See "Pericardial effusion: Approach to diagnosis", section on 'Pericardial fluid analysis and biopsy'.)

Pericardial drainage – When pericardial fluid drainage is indicated, this is usually performed by percutaneous drainage unless the fluid is inaccessible or there is a critical cardiac or aortic bleeding site that requires surgical management (algorithm 2) [1].

Reaccumulation – For patients deemed at high risk for recurrent pericardial effusion (including those with malignant pericardial effusion or purulent pericarditis), initial management with pericardial fluid removal may be combined with or followed by one or more measures to prevent or treat recurrent pericardial effusion, as discussed separately. (See "Pericardial effusion: Approach to management" and "Pericardial disease associated with cancer: Management", section on 'Prevention and treatment of recurrent malignant pericardial effusion'.)

Constrictive pericarditis – Constrictive pericarditis is a clinical syndrome in which an inelastic thickened pericardium restricts cardiac filling. Patients with constrictive pericarditis typically present months to years after an initial insult involving the pericardium. (See "Constrictive pericarditis: Clinical features and causes".)

Diagnosis is often made by echocardiography with additional cardiac testing as needed (algorithm 4). (See "Constrictive pericarditis: Diagnostic evaluation".)

A minority of cases of constrictive pericarditis are transient with resolution within two to six months spontaneously or with medical therapy (table 5 and algorithm 3). Most constrictive pericarditis has a chronic course for which pericardiectomy is the only definitive treatment. (See "Constrictive pericarditis: Management and prognosis".)

  1. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC)Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J 2015; 36:2921.
  2. Spodick DH. Pericardial disease. In: Heart Disease: A Textbook of Cardiovascular Medicine, Braunwald E, Zipes D, Libby P (Eds), Saunders, New York 2001. p.183.
  3. Troughton RW, Asher CR, Klein AL. Pericarditis. Lancet 2004; 363:717.
  4. Caforio AL, Brucato A, Doria A, et al. Anti-heart and anti-intercalated disk autoantibodies: evidence for autoimmunity in idiopathic recurrent acute pericarditis. Heart 2010; 96:779.
  5. Maestroni S, Di Corato PR, Cumetti D, et al. Recurrent pericarditis: autoimmune or autoinflammatory? Autoimmun Rev 2012; 12:60.
  6. Chiabrando JG, Bonaventura A, Vecchié A, et al. Management of Acute and Recurrent Pericarditis: JACC State-of-the-Art Review. J Am Coll Cardiol 2020; 75:76.
  7. Andreis A, Imazio M, Casula M, et al. Recurrent pericarditis: an update on diagnosis and management. Intern Emerg Med 2021; 16:551.
  8. Soler-Soler J, Sagristà-Sauleda J, Permanyer-Miralda G. Relapsing pericarditis. Heart 2004; 90:1364.
  9. Alabed S, Cabello JB, Irving GJ, et al. Colchicine for pericarditis. Cochrane Database Syst Rev 2014; :CD010652.
  10. Welch TD. Constrictive pericarditis: diagnosis, management and clinical outcomes. Heart 2018; 104:725.
  11. Imazio M, Brucato A, Maestroni S, et al. Risk of constrictive pericarditis after acute pericarditis. Circulation 2011; 124:1270.
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