Pericarditis

Diagnostic approach

• ABCDE survey
• Targeted cardiac evaluation
• 12-lead ECG
• TTE
• CBC with differential
• ESR
• CRP
• Troponin T/I

Diagnostic criteria

Characteristic pleuritic chest pain PLUS ≥ 1 additional finding:

• Pericardial friction rub
• Diffuse ST elevation and/or PR depression on ECG
• Elevated inflammatory markers
• New or worsening pericardial effusion
• Pericardial inflammation on cardiac imaging (cardiac MRI or CT)

Red flag features

• Fever > 38°C
• Pulsus paradoxus
• Features of constrictive pericarditis (e.g., pericardial knock)
• Signs of cardiac tamponade (e.g., Beck triad)
• Pericardial effusion > 20 mm on TTE
• Immunosuppression
• Anticoagulant therapy
• Elevated troponin
• Recurrent pericarditis or incessant pericarditis
• Posttraumatic pericarditis

Management checklist

• Patient with cardiac tamponade: urgent therapeutic pericardiocentesis
• Treatable etiology identified: targeted therapy
• Idiopathic, viral, or postcardiac injury pericarditis
  • High-dose aspirin (off-label) OR NSAID (e.g., off-label )
  • PLUS colchicine (off-label)
• Consider acid suppression medication if using high-dose aspirin or NSAIDS.
• Consult cardiology for red flag features.

Pericarditis is inflammation of the pericardium and can be classified as acute, incessant, recurrent, or chronic. Pericarditis results from various infectious and noninfectious etiologies, with idiopathic and viral causes being the most common in high-income countries. In low-income countries, tuberculosis, often in the setting of HIV, is the most common cause of pericarditis. Clinical features typically include retrosternal pleuritic chest pain, low-grade fever, and a pericardial friction rub. Features of complications, such as clinical features of cardiac tamponade or signs of constrictive pericarditis, may also be present. Diffuse ST-segment elevations or PR depressions on ECG, elevated inflammatory markers, and characteristic findings on cardiac imaging help establish the diagnosis. Treatment often involves dual anti-inflammatory therapy with an NSAID or high-dose aspirin plus colchicine to improve symptoms and prevent recurrences. When a treatable etiology (e.g., TB pericarditis) is identified, treatment is focused on the underlying cause. Interventional management may include therapeutic pericardiocentesis for pericardial effusion with cardiac tamponade and radical pericardiectomy for refractory chronic or recurrent pericarditis. Purulent pericarditis is caused by bacterial or fungal infection of the pericardium and is characterized by macroscopic or microscopic evidence of pus in the pericardial space. Diagnostic pericardiocentesis with Gram stain and cultures of the pericardial fluid is required for definitive diagnosis. Treatment involves urgent pericardial drainage and intravenous antibiotic therapy.

• Pericarditis: inflammation of the pericardium ^[1]
  • Acute pericarditis: symptoms persist less than 4–6 weeks
  • Incessant pericarditis: symptoms persist more than 4–6 weeks and up to 3 months without full remission, despite treatment
  • Recurrent pericarditis: recurrence of symptoms after completion of treatment and a 4–6 week remission
  • Chronic pericarditis: symptoms persist > 3 months
• Pericarditis-myocarditis overlap syndromes ^[1]
  • Myopericarditis: pericarditis with secondary myocardial involvement; criteria for both are met, without new LV dysfunction
  • Perimyocarditis: Myocarditis with secondary pericardial involvement; criteria for both are met, with new LV dysfunction

• Idiopathic
• Infectious
  • Most commonly viral (e.g., coxsackie B virus) ^[2]
  • M. tuberculosis
  • Bacterial; (e.g., Staphylococcus spp., Streptococcus spp.)
  • Fungal
  • Parasitic (e.g., toxoplasmosis)
• Complications of myocardial infarction , e.g.,:
  • Peri-infarction pericarditis (fibrinous); : within 1–3 days as an immediate reaction
  • Post-cardiac injury syndrome, e.g., Dressler syndrome; : weeks to months after an acute myocardial infarction
• Postoperative (postpericardiotomy syndrome): due to blunt or sharp trauma to the pericardium
• Posttraumatic pericarditis: with or without hemopericardium
• Uremia (e.g., due to acute or chronic renal failure)
• Radiation
  • Exudative pericarditis: develops acutely during or after radiation therapy ^[3]
  • Constrictive pericarditis: develops several years after radiation therapy ^[4]
• Neoplasms (e.g., Hodgkin lymphoma)
• Autoimmune connective tissue diseases (e.g., rheumatoid arthritis, systemic lupus erythematosus, scleroderma)
• Following mRNA vaccination (e.g., COVID-19 vaccination) ^[5][6]

In high-income countries, pericarditis is most often idiopathic or viral; in low-income countries, tuberculosis, frequently in the setting of HIV, is the leading cause. ^[7]

• Pericardial chest pain
  • Pleuritic (caused by inflammation of the parietal pleura)
  • Improves on sitting and leaning forward
  • Can radiate to the neck and shoulders (most commonly to the left side)
• Pericardial friction rub: high-pitched scratching on auscultation
  • Indicates friction between the visceral and parietal pericardial tissue
  • Best heard over the left sternal border during expiration while the patient is sitting up and leaning forward
  • May be faint and/or intermittent and usually disappears if a significant pericardial effusion develops
  • Occurs in atrial and ventricular systole, as well as early diastole
  • Present in 85% of patients with acute pericarditis
• Other: low-grade intermittent fever, tachypnea, dyspnea, nonproductive cough
• Features of complicated pericarditis
  • Clinical features of pericardial effusion: e.g., faint heart sounds, Ewart sign
  • Clinical features of cardiac tamponade: e.g., Beck triad
  • Clinical features of constrictive pericarditis or effusive-constrictive pericarditis: e.g., signs of right heart failure

Pericarditis classically presents with retrosternal pleuritic chest pain that is acute, sharp, and typically aggravated by coughing, swallowing, or deep inspiration. ^[8]

Purulent pericarditis ^[1]

• Definition: infection of the pericardium with macroscopic or microscopic evidence of pus in the pericardial space
• Etiology
  • May occur after thoracic/cardiac procedures, trauma, or result from contiguous or systemic infection
  • Typically caused by Staphylococcus spp., Streptococcus spp., or fungi
• Clinical features
  • Clinical features of sepsis and/or septic shock: e.g., high fever, tachycardia, hypotension
  • Dyspnea
  • Clinical features of pericarditis: e.g., pleuritic chest pain, pericardial friction rub
  • Clinical features of pericardial effusion (cardiac tamponade may occur)
• Diagnosis
  • ECG features of pericarditis
  • Elevated inflammatory markers
  • Transthoracic echocardiography (TTE): to identify pericardial effusion and assess for tamponade physiology
  • Urgent pericardiocentesis: to obtain sample for pericardial fluid analysis including Gram stain and culture ^[1]
  • Blood cultures
• Management
  • Urgent pericardial drainage
    • Therapeutic pericardiocentesis and/or pericardial window
    • Intrapericardial fibrinolysis for loculated effusions
  • Empiric broad-spectrum intravenous antibiotic therapy (e.g., vancomycin, ceftriaxone)
    • Tailor antibiotic choice based on the likely mechanism of infection (e.g., include coverage of anerobes in the setting of esophageal rupture).
    • Adjust antibiotics to culture results and sensitivities.
    • Minimum duration: 3 weeks ^[1]
  • Pericardiectomy for persistent infection despite adequate antibiotics and drainage, or for subsequent constrictive pericarditis

Constrictive pericarditis ^[1][7]

Definitions ^[1][7]

• Constrictive pericarditis: loss of pericardial elasticity resulting in impaired ventricular filling and heart failure
• Subacute (transient) constrictive pericarditis: reversible; caused by active pericardial inflammation
• Chronic constrictive pericarditis: irreversible; characterized by scarring, fibrosis, and calcifications

Etiology ^[7]

Constrictive pericarditis may complicate pericarditis from any cause (see "Etiology of pericarditis").

• Tuberculosis (TB) is the most common cause in endemic areas.
• In non-TB endemic areas, constrictive pericarditis is most commonly idiopathic or due to cardiac surgery or mediastinal radiation.

Constrictive pericarditis can develop during or following active pericarditis, but the preceding episode may be remote or clinically unrecognized. ^[9]

Clinical features ^[8]

Constrictive pericarditis classically presents with clinical features of right heart failure.

• Signs of fluid overload (i.e., backward failure)
  • Jugular vein distention: ↑ jugular venous pressure with prominent x descents and y descents
  • Kussmaul sign
  • Congestive hepatopathy: hepatomegaly, painful liver capsule distention, hepatojugular reflux
  • Peripheral edema or anasarca, ascites with abdominal discomfort
• Symptoms and signs of reduced cardiac output (i.e., forward failure)
  • Fatigue, dyspnea on exertion
  • Tachycardia
  • Pericardial knock: sudden cessation of ventricular filling during early diastole that is heard best at the left sternal border
  • Pulsus paradoxus: decrease in systolic blood pressure by at least 10 mm Hg during inspiration; occurs in ∼ ⅓ of patients with constrictive pericarditis ^[8]

Diagnosis ^[1][7]

Suspect constrictive pericarditis in patients who present with clinical features of right heart failure and preserved biventricular function on focused cardiac ultrasound.

Approach ^[7]

• Perform a noninvasive hemodynamic assessment with transthoracic echocardiography (TTE).
• Obtain a cardiac MRI to assess for pericardial inflammation and provide supportive evidence, especially if TTE is inconclusive.
• Consider cardiac CT to identify pericardial calcification and for preoperative assessment.
• If noninvasive imaging is nondiagnostic, obtain invasive hemodynamic assessment with right heart catheterization.

Laboratory studies ^[10]

• Inflammatory markers: may be elevated in subacute constrictive pericarditis
• BNP: typically normal or only mildly elevated
• Liver chemistries: may show evidence of congestive hepatopathy

ECG features of constrictive pericarditis ^[7]

• Usually nonspecific
• Low QRS voltage
• Atrial fibrillation may occur.

Noninvasive imaging ^[1][7]

• TTE features of constrictive pericarditis ^[7]
  • ↑ Pericardial thickness may be seen.
  • Ventricular interdependence with respiration
    • Inspiratory leftward shift of the interventricular septum
    • ↑ tricuspid inflow velocity with inspiration
    • ↓ mitral inflow velocity with inspiration
  • Elevated diastolic filling pressures
    • E-wave predominant mitral inflow pattern
    • Dilated inferior vena cava
    • Expiratory hepatic venous diastolic flow reversal
  • Preserved myocardial relaxation: elevated medial e′ tissue Doppler velocity
• Cardiac MRI
  • Supports the diagnosis of constrictive pericarditis when TTE is inconclusive
  • Evaluates for active pericardial inflammation, which suggests subacute constrictive pericarditis
• Cardiac CT
  • Detects pericardial calcifications, which are typically seen in chronic constrictive pericarditis
  • Used for preoperative assessment when pericardiectomy is being considered
• Chest x-ray: may show thickened pericardial contour and pericardial calcifications

Signs of active inflammation on cardiac MRI suggest subacute constrictive pericarditis, while pericardial calcifications on cardiac CT suggest chronic constrictive pericarditis. ^[1][7]

Right heart catheterization ^[1][7]

• Indication: Noninvasive imaging is nondiagnostic.
• Findings: demonstrate constrictive hemodynamics and help differentiate constrictive pericarditis from restrictive cardiomyopathy
  • ↑ Right atrial pressure with rapid x descents and y descents
  • Equalization of pressures: similar end-diastolic pressures in the left and right ventricles
  • Square root sign: dip-and-plateau waveform
    • Rapid early diastolic filling followed by an abrupt halt in ventricular filling, producing a plateau in late diastole
    • The pressure tracing resembles the square root symbol.
  • Ventricular interdependence with respiration

Differential diagnosis ^[1][7]

• Restrictive cardiomyopathy (RCM)
• Cardiac tamponade
• Effusive-constrictive pericarditis
• Other causes of right heart failure: e.g., pulmonary hypertension, severe tricuspid regurgitation
• See "Differential diagnosis of restrictive cardiomyopathy" for a comparison of RCM, constrictive pericarditis, and cardiac tamponade.

Treatment ^[1][7]

• Trial of anti-inflammatory therapy: indicated in subacute constrictive pericarditis ^[7]
  • First-line: NSAIDs and colchicine for ≥ 3 months, slowly tapering NSAIDs ^[7]
  • Second-line: Consider adding anti–IL-1 therapy or corticosteroids.
  • See "Treatment of pericarditis" for details on medication regimens and dosing.
• Radical pericardiectomy: indicated for chronic constrictive pericarditis and refractory subacute constrictive pericarditis
• Disposition and supportive care
  • Consider hospital admission for symptomatic patients.
  • Diuretics (e.g., loop diuretics) may be used as a temporizing measure to improve peripheral edema and anasarca.

Effusive-constrictive pericarditis ^[1][7]

• Definition: constrictive pericarditis with concurrent pericardial effusion
• Etiology: may complicate pericarditis of any cause (see "Etiology of pericarditis")
  • Usually occurs as a manifestation of subacute constrictive pericarditis
  • TB is the most common cause in endemic areas.
  • In non-TB endemic areas, most commonly idiopathic
• Clinical features: may present with clinical features of constrictive pericarditis, clinical features of pericardial effusion (including cardiac tamponade), or both
• Diagnosis: Typically diagnosed when constrictive pericardial physiology is uncovered after drainage of a pericardial effusion. ^[1][7]
  • Pericardiocentesis
  • TTE
  • Pericardial fluid analysis
  • See "Diagnosis" in "Pericardial effusion and cardiac tamponade" and in "Constrictive pericarditis" for additional workup.
• Treatment ^[1][7]
  • Therapeutic pericardiocentesis followed by trial of anti-inflammatory therapy
  • Pericardiectomy for refractory cases
  • See "Treatment of pericardial effusion and cardiac tamponade" and "Treatment" in "Constrictive pericarditis" for details.

Approach ^[1][7]

• Obtain ECG, inflammatory markers, and TTE to determine if diagnostic criteria are met.
• Check cardiac biomarkers to evaluate for concurrent myocarditis.
• Consider advanced cardiac imaging (e.g., cardiac MRI) if the diagnosis is inconclusive.
• Consider diagnostic pericardiocentesis and additional laboratory studies to evaluate for specific causes.

Rule out other causes of acute chest pain.^[11]

Diagnostic criteria for pericarditis ^[7]

• Characteristic retrosternal pleuritic chest pain; or equivalent clinical presentation must be present. ^[1][7]
• Plus 1 of the following for a possible diagnosis; ≥ 2 findings for a definite diagnosis:
  • Pericardial friction rub
  • Diffuse ST elevation and/or PR depression on ECG
  • Elevated inflammatory markers
  • New or worsening pericardial effusion
  • Pericardial inflammation on cardiac imaging (e.g., cardiac MRI or CT)

Patients who meet criteria for pericarditis and have evidence of myocardial injury (e.g., elevated cardiac enzymes) are diagnosed with myopericarditis if left ventricular systolic function is preserved or perimyocarditis if there is new left ventricular systolic dysfunction. ^[1]

Laboratory studies ^[1][7]

• Initial studies: indicated in all patients
  • Inflammatory markers: ↑ CRP, ↑ ESR, leukocytosis
  • Cardiac biomarkers: Elevated troponin and/or CK-MB suggest concurrent myocarditis or an alternative diagnosis (e.g., acute coronary syndrome).
• Additional studies: Consider based on the suspected etiology.
  • Uremic pericarditis: BUN, creatinine, electrolytes
  • Purulent pericarditis: blood cultures (2 sets)
  • Tuberculous pericarditis: interferon-γ release assay, HIV test
  • Autoimmune pericarditis: ANA, rheumatoid factor

ECG features of pericarditis ^[8]

Not all patients go through all stages, and manifestations may vary. In particular, pericarditis due to uremia may not involve characteristic ECG changes. ^[12]

• Stage 1: diffuse ST elevations; , ST depression in aVR and V1, PR segment depression
• Stage 2: ST segment normalizes in ∼ 1 week.
• Stage 3: inverted T waves
• Stage 4: ECG returns to normal baseline (as prior to onset of pericarditis) after weeks to months.

Consider the differential diagnosis of ST elevation on ECG: In contrast to myocardial infarction, pericarditis is characterized by a diffuse distribution of ST elevation on ECG.

Imaging ^[1][7][13]

The goal of imaging is to assess for pericardial effusion, identify features of pericardial inflammation, and rule out alternative etiologies.

• Transthoracic echocardiography (TTE)
  • Indications: initial imaging of choice in all patients with suspected pericarditis
  • Findings are often normal, but may show any of the following:
    • Pericardial thickening
    • Ultrasound findings of pericardial effusion with or without TTE features of cardiac tamponade
    • TTE features of constrictive pericarditis
    • Left ventricular systolic dysfunction suggesting concurrent myocarditis (i.e., perimyocarditis)
  • See "Focused cardiac ultrasound" for bedside assessment of the pericardium, pericardial space, and left ventricular function.
• Cardiac MRI (cMRI)
  • Indications: diagnostic uncertainty, lack of response to first-line therapy, complicated, subacute, recurrent, or chronic pericarditis
  • Findings: signs of pericardial inflammation, thickening, constriction, effusion, and/or myocarditis ^[1]
• Cardiac CT with IV contrast
  • Indications: alternative second-line imaging if cardiac MRI is contraindicated or unavailable
  • Findings: signs of pericardial inflammation, thickening, effusion, and/or calcification
• Chest x-ray: usually normal; may show an enlarged cardiac silhouette if a large pericardial effusion is present

TTE is often normal in patients with pericarditis, but is needed to assess for pericardial effusion or constriction, cardiac tamponade, and myocardial involvement. ^[7]

Cardiac tamponade can occur with relatively small pericardial effusions if pericardial fluid accumulation is rapid. ^[14]

Diagnostic pericardiocentesis ^[1][7]

• Indications: suspected purulent pericarditis, tuberculous pericarditis, or malignant pericarditis
• Testing: pericardial fluid analysis

Treat the underlying cause when a treatable etiology (e.g., TB pericarditis, uremic pericarditis) is identified.

Approach ^[1][7]

• Perform urgent therapeutic pericardiocentesis in patients with impending or established pericardial tamponade.
• For idiopathic, viral, or post-cardiac injury pericarditis, start anti-inflammatory pharmacotherapy.
• Consult cardiology and consider hospitalization for patients with high-risk features of pericarditis.
• Provide supportive care and monitor for treatment response, recurrence, and complications.
• Refer to a specialized pericardial center for complicated or recurrent pericarditis or consideration of advanced therapies.

In patients with concurrent myocarditis, management is guided by the predominant involvement: myopericarditis is treated as pericarditis, whereas perimyocarditis follows the treatment of myocarditis. ^[1]

Pharmacotherapy ^[1][7]

Anti-inflammatory pharmacotherapy is the mainstay of treatment for idiopathic, viral, and post-cardiac injury pericarditis.

• First-line: for acute pericarditis and first recurrence
  • High-dose aspirin or NSAID therapy: Taper weekly after symptoms resolve and inflammatory markers normalize.
    • Aspirin (off-label) : preferred in patients with other indications for aspirin ^[7]
    • Ibuprofen (off-label) ^[7]
    • Indomethacin (off-label) ^[7]
  • PLUS colchicine (off-label) : Continue for 3 months for acute pericarditis or 6–12 months for recurrent pericarditis. ^[7]
• Adjunctive therapy: Consider in addition to first-line therapy for refractory pericarditis or multiple recurrences; specialist consultation is advised.
  • Glucocorticoids (e.g., prednisone): preferred for noninflammatory phenotype (normal or low inflammatory markers)
  • Interleukin-1 receptor antagonists (e.g., anakinra, rilonacept): preferred for inflammatory phenotype (elevated inflammatory markers, active inflammation on cMRI)

Invasive management ^[1][7]

• Pericardial fluid drainage
  • Therapeutic pericardiocentesis: indicated for impending or established pericardial tamponade
  • Surgical pericardiotomy (pericardial window): considered for recurrent, persistent, or loculated symptomatic pericardial effusions
  • See "Treatment of pericardial effusion and cardiac tamponade" for details.
• Radical pericardiectomy: considered at high-volume surgical centers for refractory chronic or recurrent pericarditis

Management of underlying causes ^[1][7]

• Early infarct-associated pericarditis: supportive care (e.g., acetaminophen). See "Complications" in "Myocardial infarction." ^[15]
• Purulent pericarditis: pericardial drainage and antibiotics. See "Management" in "Purulent pericarditis."
• Tuberculous pericarditis: antituberculosis therapy. See "Treatment" in "Pericardial tuberculosis."
• Uremic pericarditis: Consider dialysis. ^[16]
• Neoplastic pericarditis: treatment of the underlying malignancy; extended drainage (3–6 days) for malignant pericardial effusions ^[1]
• Autoimmune or connective tissue disease: disease-specific therapy, e.g., treatment of rheumatoid arthritis, treatment of systemic lupus erythematosus

Supportive care and monitoring ^[1][7]

• Consider acid suppression medication for gastric protection if using high-dose aspirin or NSAIDS.
• Avoid elevated heart rates. ^[7]
  • Restrict physical activity for ≥ 1 month until clinical remission. ^[7]
  • Consider beta blockers in patients with persistent symptoms and a resting heart rate > 75 beats/min. ^[1]
• Monitor symptoms and inflammatory markers (CRP, ESR) to assess treatment response.
• Consider serial imaging (e.g., TTE, cMRI) in patients with pericardial effusion, myocardial involvement, and/or complicated or refractory disease.

Disposition ^[1][7]

• Consider hospitalization for patients with high-risk features of pericarditis. ^[1]
  • Fever > 38°C
  • Pulsus paradoxus
  • Features of constrictive pericarditis (e.g., pericardial knock)
  • Signs of cardiac tamponade (e.g., Beck triad)
  • Pericardial effusion > 20 mm on echocardiogram
  • Immunosuppression
  • Anticoagulant therapy
  • Elevated troponin
  • Recurrent pericarditis or incessant pericarditis
  • Posttraumatic pericarditis
  • Concurrent myocarditis (i.e., myopericarditis or perimyocarditis)
  • Lack of response to aspirin or NSAID therapy after ≥ 1 week
• Clinically stable patients without high-risk features can usually be treated in the outpatient setting; review after 1 week to assess treatment response.

• Pericardial effusion
• Cardiac tamponade
• Constrictive pericarditis
• Effusive-constrictive pericarditis

We list the most important complications. The selection is not exhaustive.

Pericarditis in children ^[1][17][18]

Epidemiology

• ♂ > ♀ ^[17]
• Accounts for up to 5% of pediatric ED presentations with chest pain in children without prior heart disease. ^[18]

Etiology

• Similar to the etiology of pericarditis in adults ^[1][17]
• Postpericardiotomy syndrome is the most common cause in children. ^[1]

Clinical features ^[1][18]

• Similar to clinical features of pericarditis in adults
• Fever and pleuropulmonary involvement (e.g., pleural effusion) are more common in children. ^[19]

Diagnosis ^[1][17][18]

• Diagnosis of pericarditis is the same as for adults.
• Findings are similar to those in adults; exceptions include: ^[19]
  • CRP is more likely to be elevated.
  • ANA is less likely to be positive.

Treatment ^[1][17][18]

• Treatment of pericarditis is similar in children and adults.
• Consult cardiology to guide management, e.g.:
  • Determining disposition (e.g., hospital admission, outpatient management)
  • Pharmacological therapy
    • First-line: for acute pericarditis and first recurrence
      • NSAIDs (e.g., ibuprofen, indomethacin) PLUS colchicine
      • Aspirin and, when possible, corticosteroids are avoided because of the risk of adverse effects.
    • Adjunctive: Add anti–IL-1 therapy (e.g., anakinra) for refractory pericarditis or multiple recurrences.

Avoid aspirin and corticosteroids when managing pericarditis in children. ^[1]

Recurrence occurs in up to 35% of children and adults. ^[17][18]