Pericarditis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Homa Najafi, M.D.[2]

Pericarditis is a condition in which the sac-like covering surrounding the heart (the pericardium) becomes inflamed. Symptoms of pericarditis include chest pain which increases with deep breathing and lying flat.

The pericardium is a double-walled sac that contains the heart and the roots of the great vessels. Morphologically, it is a conical-shaped, double-walled fibro-serous membrane. It rests posteriorly to the sternum at the level of second to sixth costal cartilages and T5-T8 vertebrae.

Pericarditis may be classified according to duration of the disease and recurrence into acute, Incessant, recurrent and chronic. Moreover, pericarditis can be classified based on the etiology in two groups of infectious and non-infectious causes.

Pericarditis is inflammation of the pericardium, which is the double-walled sac that contains the heart and the roots of the great vessels. There can be an accompanying accumulation of fluid that can be either serous (free flowing fluid) or fibrinous (an exudate, which is a thick fluid composed of proteins, fibrin strands, inflammatory cells, cell breakdown products, and sometimes bacteria). Vascular congestion of the pericardium is also present. The underlying myocardium may or may not be inflamed as well. If the myocardium is involved in the inflammatory process, it is called myopericarditis, and CK and troponin levels may be elevated. Cardiotropic viruses usually spread to the myocardium and pericardium hematogenously and cause acute inflammation with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. Most patients with viral pericarditis recover completely with few developing recurrences. Some patients develop constrictive pericarditis which could be disabling. Bacterial pericarditis results from contiguous spread of infection within the chest, either de novo or after surgery or trauma, spread from infective endocarditis, hematogenous, or direct inoculation as a result of penetrating injury or cardiothoracic surgery.

The causes of pericarditis can be divided into infectious and non-infectious ones. Infectious causes include bacterial, viral, fungal and, parasitic. While, non-infectious causes include autoimmune, neoplastic, metabolic, traumatic and iatrogenic, and drug-related. Acute myocardial infarction, Addisonian crisis, aortic dissection and rupture, blunt or penetrating chest trauma, esophageal perforation, gastric perforation, and myocardial rupture are life threatening causes of pericarditis. Common causes of pericarditis include viral, bacterial organisms, neoplasms, autoimmune and renal failure.

Pericarditis must be differentiated from diseases presenting with chest pain, shortness of breath and tachypnea which include myocardial infarction, pulmonary embolism, congestive heart failure, pneumonia, vasculitis, and chronic obstructive pulmonary disease (COPD). Manifestation of the pericarditis can help in differentiation from myocardial infarction. Moreover, other differential diagnosis include aortic stenosis, coronary artery vasospasm, esophageal rupture, esophageal spasm, esophagitis,acute gastritis, gastroesophageal reflux disease, and peptic ulcer disease should be considered.  

The incidence of acute pericarditis is approximately 27.7 per 100,000 individuals annually. The recurrence of disease is seen in almost 30% of patients after first episode. The mortality rate of acute pericarditis is approximately 1.1% in developed countries. Patients of all age groups may develop acute pericarditis. Although it commonly affects men in 20 to 50 years of age. Pericarditis in developed countries is most commonly due to malignancy or viral infection. It usually follows respiratory infections, most commonly echovirus or coxsackie virus. In children, it is most commonly caused by adenovirus or coxsackie virus. In developing countries pericarditis is usually secondary to tuberculosis or HIV infection. Tuberculous pericarditis, caused by Mycobacterium tuberculosis, is found in approximately 1% of all autopsied cases of TB and in 1% to 2% of instances of pulmonary TB.

There is insufficient evidence to recommend routine screening for pericarditis.  

Pericarditis is often self-limited and most people recover in 2 weeks to 3 months. However, the condition can be complicated by significant fluid buildup around the heart (a pericardial effusion or cardiac tamponade) and may require urgent intervention including pericardiocentesis. If scarring of the sac around the heart (the pericardium) occurs, then this is called constrictive pericarditis which may require surgical stripping of the scar.

Patients with pericarditis commonly present with chest pain that changes with position, cough, fever, breathlessness, and fatigue are the other common symptoms. Less common symptoms include palpitations, hiccup, odynophagia, faint, dizziness, and abdominal pain which is seen mostly in children.

A careful physical examination must be performed to exclude the presence of cardiac tamponade, a dangerous complication of pericarditis. If cardiac tamponade is present, then pulsus paradoxus, hypotension, an elevated jugular venous pressure and peripheral edema may be present.

Non-specific markers of inflammation are generally elevated in pericarditis. These include the leukocyte count, C-reactive protein, and ESR. The cardiac troponin is elevated if there is an injury to the underlying myocardium, a condition termed as myopericarditis. Diagnostic pericardiocentesis and biopsy help in identifying an underlying infectious or malignant process.Non-specific markers of inflammation are generally elevated in pericarditis. These include the leukocyte count, C-reactive protein, and ESR. The cardiac troponin is elevated if there is an injury to the underlying myocardium, a condition termed as myopericarditis. Diagnostic pericardiocentesis and biopsy help in identifying an underlying infectious or malignant process.

In the presence of a large effusion or tamponade, there may be diminished voltage and electrical alternans (alternation of QRS complex amplitude or axis between beats).

A flask-shaped, enlarged cardiac silhouette will be observed on chest x-ray in pericarditis complicated with pericardial effusion or tamponade. A mass may also be seen when malignancy is the cause. Calcification of pericardium may be noted in constrictive pericarditis.

Echocardiography is generally performed to assess for the presence of a pericardial effusion and to assess and monitor its size. Echocardiography is critical in confirming the clinical suspicion cardiac tamponade.

On CT, pericardial fluid adds to the thickness of pericardium as both have the similar signal intensities. In pericarditis, pericardium can generate an intermediate signal intensity and may enhance after gadolinium administration. In pericardial effusion, hemorrhagic effusions can be differentiated from a transudate or an exudate based on signal characteristics (high signal on T1-weighted images) or density (high-density clot on CT). CT is superior to MRI in the visualization of pericardial calcification which is often seen in the patient with pericardial constriction. CT imaging also helps in detecting the presence of tumors and the extent of metastasis of the neoplasm.

On MRI, normal pericardium appears as a thin dark band that is bordered by a bright band on both sides on T1 weighted spin imaging. These surrounding bright bands are associated with the surrounding epicardial and pericardial fat. Following the administration of gadolinium, pericardium may appear thick and inflamed in the setting of pericarditis. Lower intensity signal is observed in constrictive pericarditis than in acute pericarditis. Comprehensive visualization of the LV endocardium and the physiologic consequences of abnormal pericardial thickening can also be obtained without exposure to ionizing radiation.

Echocardiography guided pericardiocentesis may be helpful in the diagnosis of the pericarditis etiology. Pericardial fluid aspiration for cytology and immunohistochemistry analysis should be done in pericarditis with effusion. Pericardiocentesis should be done in patients with high susceptibility of neoplastic pericarditis which cytology analysis for malignancy was negative.

The management of pericarditis depends on whether the patient has an uncomplicated vs. complicated disease course. Uncomplicated pericarditis is generally treated with non-steroidal anti-inflammatory drugs, such as Ibuprofen in cases of either viral or idiopathic pericarditis, and Aspirin in cases of post-MI pericarditis. Pericarditis complicated with either effusion or cardiac tamponade is generally treated with urgent pericardiocentesis in the case of cardiac tamponade, antibiotics in the case of purulent pericardial effusion, and either steroids or colchicine among patients with recurrent or refractory disease.

Percutaneous pericardiocentesis is a procedure where fluid is aspirated from the pericardium (the sac enveloping the heart) using a needle via a percutaneous approach. Pericardiocentesis can provide a diagnostic sampling of pericardial fluid and can be used as a therapeutic maneuver to evacuate pericardial fluid and lower the pericardial pressure.

Creation of a pericardial window is a cardiac surgical procedure in which an opening is made in the pericardium to drain fluid that has accumulated around the heart by creating a fistula or “window” from the pericardial space to the peritoneal cavity. Flow of fluid into the peritoneal cavity prevents the accumulation of fluid around the heart (a pericardial effusion), which might cause compression and impaired filling of the heart (cardiac tamponade), a dangerous complication. The procedure is performed for both diagnostic and therapeutic purposes. The creation of a pericardial window is usually performed by a cardiac surgeon or thoracic surgeon who makes an incision, commonly sub-xiphoid, and cuts a small hole in the pericardium. This surgery is performed with local anesthesia. An incision is made either below the sternum, or alternately between the ribs of the left chest. The resection can be with scissors, cautery, a stapling device, or a harmonic scalpel, with no one technique demonstrably better than another. It is best to have a combination of techniques available to resect the pericardium adequately. The surgeon may place a catheter in the pericardial window so that fluid can continue to drain for a short period of time after the surgery. Chest tubes are removed in 2-3 days once the drainage is less than 200cc/24hrs.

Pericardiectomy is the surgical removal of part or most of the pericardium. This operation is performed to relieve constrictive pericarditis or to remove a pericardium that is calcified and fibrous. Constrictive pericarditis is a progressive disease without spontaneous reversal of pericardial thickening. Some patients can be medically managed for several years. Edema can be controlled with diuretics and slowing the heart rate can maximize the diastolic filling time. Many patients eventually develop significant debility from impaired cardiac output and elevated right and left sided filling pressures. The definitive treatment for constrictive pericarditis is pericardiectomy which is also known as pericardial stripping. This is a surgical procedure where the entire pericardium is peeled away from the heart. Due to the significant risks involved with pericardial stripping, many patients are treated medically, with judicious use of diuretics.

Template:WH Template:WS

Template:Infobox Anatomy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor(s)-in-Chief: Rim Halaby

The pericardium is a double-walled sac that contains the heart and the roots of the great vessels. Morphologically, it is a conical-shaped, double-walled fibro-serous membrane. It rests posteriorly to the sternum at the level of second to sixth costal cartilages and T5-T8 vertebrae.

• The pericardium is made up of two layers:
  • Fibrous pericardium
    • Hard protective external layer
    • Attached to sternum anteriorly by sterno-pericardial ligaments and fused with the central tendon of the diaphragm and great vessels to allow mobility of the pericardial sac against sudden cardiac overfilling
  • Serous pericardium
    • Smooth internal layer made up of 2 components:
      • Parietal: reflects onto fibrous pericardium
      • Visceral: reflects onto heart and great vessels and forms the epicardium, the external layer of the heart wall
• Pericardial cavity: Potential space between parietal and visceral layers. It contains a serous fluid film that occupies the cavity and functions as lubricant against friction by all chest movements.^[1][2][3]

• There are two small chambers or sinuses located where the visceral and parietal pericardia are continuous with one another within the pericardial cavity.
• Transverse sinus:
  • Located posterior to the pulmonary trunk and ascending aorta at the level between the superior vena cava and aortic arch
  • Formed after dorsal mesocardium rupture embryonically
  • Functional role is to allow the unhindered expansion of great arteries posteriorly during cardiac systole
  • Utilized surgically to pass surgical clamps or place ligatures around great arteries.
• Oblique sinus:
  • A blind recess (cul-de-sac) posterior to the left atrium between superior vena cava, right and left pulmonary veins inferior to the transverse sinus
  • Formed embryonically by the incorporation of the pulmonary vein tributaries into the left atrium
  • Functional role believed to be the expansion of the left atrium upon normal collapse of the thorax^[4][5][6]

• Pericarditis is an inflammatory condition of the pericardium.
• Pericardial effusion is fluid accumulation in the pericardial sac.
• Constrictive pericarditis occurs when there is a scar encasing, the heart that chronically constricts the filling of the heart.
• Cardiac tamponade is a medical emergency in which fluid in the pericardial sac acutely restricts the filling of the heart. This requires surgical drainage or pericardiocentesis.

• 
  The phrenic nerve and its relations with the vagus nerve.
• 
  Thoracic portion of the sympathetic trunk.
• 
  Liver with the septum transversum. Human embryo 3 mm long.
• 
  The thymus of a full-time fetus, exposed in situ.

de:Herzbeutel it:Pericardio la:Pericardium ms:Perikardium nl:Pericard nn:Hjartepose fi:Perikardium

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Homa Najafi, M.D.[2]

Pericarditis may be classified according to duration of the disease and recurrence into acute, Incessant, recurrent and chronic. Moreover, pericarditis can be classified based on the etiology in two groups of infectious and non-infectious causes.

• Pericarditis may be classified according to duration of the disease and recurrence into four groups:^[1][2][3][4]
  • Acute
  • Incessant
  • Recurrent
  • Chronic

• Moreover, pericarditis can be classified based on the etiology in two groups:^[1][2][3][5]
  • Infectious:
    • Viral
    • Bacterial
    • Fungal
    • Parasitic
  • Non-infectious:
    • Autoimmune
    • Neoplastic
    • Metabolic
    • Traumatic and iatrogenic
    • Drug-related

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S., Cafer Zorkun, M.D., Ph.D. [2], Rim Halaby Homa Najafi, M.D.[3]

Pericarditis is inflammation of the pericardium, which is the double-walled sac that contains the heart and the roots of the great vessels. There can be an accompanying accumulation of fluid that can be either serous (free flowing fluid) or fibrinous (an exudate, which is a thick fluid composed of proteins, fibrin strands, inflammatory cells, cell breakdown products, and sometimes bacteria). Vascular congestion of the pericardium is also present. The underlying myocardium may or may not be inflamed as well. If the myocardium is involved in the inflammatory process, it is called myopericarditis, and CK and troponin levels may be elevated. Cardiotropic viruses usually spread to the myocardium and pericardium hematogenously and cause acute inflammation with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. Most patients with viral pericarditis recover completely with few developing recurrences. Some patients develop constrictive pericarditis which could be disabling. Bacterial pericarditis results from contiguous spread of infection within the chest, either de novo or after surgery or trauma, spread from infective endocarditis, hematogenous, or direct inoculation as a result of penetrating injury or cardiothoracic surgery.

• The pericardium is made up of two layers:^[1][2][3]
  • Fibrous pericardium:
    • Hard protective external layer
    • Attached to sternum anteriorly by sterno–pericardial ligaments and fused with the central tendon of the diaphragm and great vessels to allow mobility of the pericardial sac against sudden cardiac overfilling
  • Serous pericardium:
    • Smooth internal layer made up of 2 components:
      • Parietal: reflects onto fibrous pericardium
      • Visceral: reflects onto heart and great vessels and forms the epicardium, the external layer of the heart wall
• Pericardial cavity: Potential space between parietal and visceral layers. It contains a serous fluid film that occupies the cavity and functions as lubricant against friction by all chest movements.

• There are two small chambers or sinuses located where the visceral and parietal pericardium are continuous with one another within the pericardial cavity.^[4][5][6]
• Transverse sinus:
  • Located posterior to the pulmonary trunk and ascending aorta at the level between the superior vena cava and aortic arch
  • Formed after dorsal myocardium ruptured embryonically
  • Functional role is to allow the unhindered expansion of great arteries posteriorly during cardiac systole
  • Utilized surgically to pass surgical clamps or place ligatures around great arteries.
• Oblique sinus:
  • A blind recess (cul-de-sac) posterior to the left atrium between superior vena cava, right and left pulmonary veins inferior to the transverse sinus
  • Formed embryonically by the incorporation of the pulmonary vein tributaries into the left atrium
  • Functional role believed to be the expansion of the left atrium upon normal collapse of the thorax

• Pericarditis is an inflammatory condition of the pericardium.
• Pericardial effusion is fluid accumulation in the pericardial sac.
• Constrictive pericarditis occurs when there is a scar encasing, the heart that chronically constricts the filling of the heart.
• Cardiac tamponade is a medical emergency in which fluid in the pericardial sac acutely restricts the filling of the heart. This requires surgical drainage or pericardiocentesis.

• 
  The phrenic nerve and its relations with the vagus nerve.
• 
  Thoracic portion of the sympathetic trunk.
• 
  Liver with the septum transversum. Human embryo 3 mm long.
• 
  The thymus of a full-time fetus, exposed in situ.

• Cardiotropic viruses usually spread to the myocardium and pericardium hematogenously and cause acute inflammation with infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. This may cause pericardial effusion and fibrinous change of the pericardium. The pericardium may also develop a serous or hemorrhagic effusion. Most patients with viral pericarditis recover completely with few developing recurrences. Some patients develop constrictive pericarditis which could be disabling.^[7][8][9]

• Bacterial pericarditis results from:^{[10][11][12][13][14]}

1. Contiguous spread of infection within the chest, either de novo or after surgery or trauma.
2. Spread from infective endocarditis
3. Hematogenous spread of infection
4. Direct inoculation as a result of penetrating injury or cardiothoracic surgery

• Tuberculous pericarditis develops from lymphatic spread of peritracheal, peribronchial or mediastinal lymph nodes or by contiguous spread from a focus of infection in the lung or pleura. There are four pathologic stages observed:^[15][16][17]

• Stage 1: Presence of diffuse fibrin deposition, granulomas and abundant mycobacterium.

• Stage 2: Development of serous or serosanguineous pericardial effusion with a predominantly lymphocytic exudate with monocytes and foam cells.

• Stage 3: Absorption of effusion with the organization of granulomatous caseation and thickening of pericardium secondary to deposition of fibrin and collagen.

• Stage 4: Development of constrictive pericarditis. The pericardial space is obliterated by dense adhesions with marked thickening of the parietal layer and replacement of granulomas by fibrous tissue.

These types of granulomatous pericarditis also occur with fungal infections, rheumatoid arthritis (RA), and sarcoidosis.

• Pericarditis in renal failure is thought to result from inflammation of the visceral and parietal layers of the pericardium by metabolic toxins such as urea, creatinine, uric acid, methylguanidine, guanidinoacetate, parathyroid hormone, beta2-microglobulin, and others. It may be associated with hemorrhagic or serous effusion.

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2] Ahmed Zaghw, M.D. [3] Homa Najafi, M.D.[4]

The causes of pericarditis can be divided into infectious and non-infectious ones. Infectious causes include bacterial, viral, fungal and, parasitic. While, non-infectious causes include autoimmune, neoplastic, metabolic, traumatic and iatrogenic, and drug-related. Acute myocardial infarction, Addisonian crisis, aortic dissection and rupture, blunt or penetrating chest trauma, esophageal perforation, gastric perforation, and myocardial rupture are life threatening causes of pericarditis. Common causes of pericarditis include viral, bacterial organisms, neoplasms, autoimmune and renal failure.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated and include:^[1][2][3][4]

• Acute myocardial infarction
• Addisonian crisis
• Aortic dissection
• Aortic rupture
• Blunt or penetrating chest trauma
• Esophogeal perforation
• Gastric perforation
• Myocardial rupture

• Acute myocardial infarction
• Cardiac catheterization
• Staphylococcus aureus (MSSA, MRSA)
• Streptococcus pneumoniae
• Neisseria meningitidis
• Enterobacteriaceae
• Tuberculosis
• Histoplasmosis
• Coxsackie B virus
• Echovirus
• HIV
• Adenovirus
• Influenza
• Neoplasm
• Renal Failure
• Sulfa drugs
• Aminosalicylic acid
• Amiodarone
• Systemic lupus erythematosus
• Rheumatoid arthritis
• Idiopathic

• 5-Fluorouracil
• Actinomycosis
• Acute myocardial infarction
• Acute rheumatic fever
• Addisonian crisis
• Adenovirus
• Amebiasis
• Aminosalicylic acid
• Amiodarone
• Amyloidosis
• Angioma
• Ankylosing spondylitis
• Anticoagulants
• Aortic dissection
• Aortic rupture
• Asbestosis
• Behcet’s disease
• Benign obstruction of thoracic duct
• Blunt or penetrating chest trauma
• Borrelia
• Breast cancer
• Bromocriptine
• Carcinoid
• Cardiac catheterization
• Cardiopulmonary resuscitation
• Cathether ablation for arrhythmias
• Certolizumab pegol
• Chlamydia psittaci
• Cholesterol pericarditis
• Chylopericardium
• Coccidioidomycosis
• Collagen vascular disease
• Coronary artery bypass grafting
• Coxsackie B virus
• Cromolyn sodium
• Cyclophosphamide
• Cyclosporine
• Cytarabine
• Cytomegalovirus
• Dantrolene
• Daunorubicin
• Dermatomyositis
• Dialysis
• Dissecting aortic aneurysm
• Doxorubicin
• Dressler’s syndrome
• EBV
• Echinococcosis
• ECHO virus
• Endocarditis
• Esophageal rupture
• Esophogeal perforation
• Familial mediterranean fever
• Fibroma
• Francisella
• Gastric perforation
• Gaucher disease
• Heart surgery
• Herpes viruses
• Histoplasmosis
• HIV
• Hydantoin
• Hydralazine
• Hypothyroidism
• Idiopathic
• Infectious mononucleosis
• Inflammatory bowel disease
• Influenza virus
• Isoniazid
• Jacobs arthropathy-camptodactyly syndrome
• Kaposi’s sarcoma
• Kawasaki disease
• Leiomyoma
• Legionella
• Leukemia
• Lipoma
• Lung cancer
• Lymphoma
• Melanoma
• Meningococci
• Mesalazine
• Mesothelioma
• Methyldopa
• Methysergide
• Minoxidil
• Mixed connective tissue disease
• Mulibrey nanism syndrome
• Mumps virus
• Mycoplasma
• Myocardial rupture
• Myocarditis
• Myxedema
• Neisseria gonorrhoeae
• Neoplasia that has spread to the pericardium,
• Ovarian cancer
• Pacemaker syndrome
• Pancreatic-pericardial fistula
• Penicillin
• Percutaneous coronary intervention
• Pergolide
• Phenylbutazone
• Pneumococci
• Pneumonia
• Polyarteritis nodosa
• Polymyositis
• Polytetrafluoroethylene inhalation
• Postpericardiotomy syndrome
• Practolol
• Procainamide
• Radiation therapy
• Recurrent hereditary polyserositis
• Rhabdomyosarcoma
• Reiter’s syndrome
• Renal failure
• Reserpine
• Rheumatoid arthritis
• Rickettsia
• Sarcoidosis
• Sarcoma
• Scleroderma
• Serum sickness
• Silicosis
• Sipple syndrome
• Staphylococci
• Streptococci
• Streptokinase
• Streptomycin
• Sulfa drugs
• Systemic lupus erythematosus
• TAVI
• Temporal arteritis
• Teratoma
• Thiazides
• Thiouracil
• Thoracic surgery
• Thorax trauma
• Thrombolytics
• Tocainide
• Toxoplasmosis
• Treponema pallidum
• Tuberculosis
• Ureaplasma
• Uremia
• Vaccines (smallpox, yellow fever)
• Valvuloplasty
• Varicella virus
• Wegener’s granulomatosis
• Whipple’s Disease

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [3] Homa Najafi, M.D.[4]

Pericarditis must be differentiated from diseases presenting with chest pain, shortness of breath and tachypnea which include myocardial infarction, pulmonary embolism, congestive heart failure, pneumonia, vasculitis, and chronic obstructive pulmonary disease (COPD). Manifestation of the pericarditis can help in differentiation from myocardial infarction. Moreover, other differential diagnosis include aortic stenosis, coronary artery vasospasm, esophageal rupture, esophageal spasm, esophagitis,acute gastritis, gastroesophageal reflux disease, and peptic ulcer disease should be considered.

• Pericarditis must be differentiated from diseases presenting with chest pain, shortness of breath and tachypnea.
  • For a full discussion of the differential diagnosis of chest pain click here
  • For an expert algorithm that aids in the diagnosis of the cause of chest pain click here
• Pericarditis must be differentiated from myocardial infarction as an important cause of chest pain.The differentiating features include:^[1]

The differentials include the following:^{[2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21]}

Pericarditis also resembles the following disorders and needs to be differentiated from them:

Template:WH Template:WS

​

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. Homa Najafi, M.D.[2]

The incidence of acute pericarditis is approximately 27.7 per 100,000 individuals annually. The recurrence of disease is seen in almost 30% of patients after first episode. The mortality rate of acute pericarditis is approximately 1.1% in developed countries. Patients of all age groups may develop acute pericarditis. Although it commonly affects men in 20 to 50 years of age. Pericarditis in developed countries is most commonly due to malignancy or viral infection. It usually follows respiratory infections, most commonly echovirus or coxsackie virus. In children, it is most commonly caused by adenovirus or coxsackie virus. In developing countries pericarditis is usually secondary to tuberculosis or HIV infection. Tuberculous pericarditis, caused by Mycobacterium tuberculosis, is found in approximately 1% of all autopsied cases of TB and in 1% to 2% of instances of pulmonary TB.

• The incidence of acute pericarditis is approximately 27.7 per 100,000 individuals annually.^[1][2][3][4]
• The incidence of hospitalization for acute pericarditis was estimated to be 3.32 cases per 100,000 individuals annually.
• The recurrence of pericarditis is seen in almost 30% of patients after first episode of disease.

• The mortality rate of acute pericarditis is approximately 1.1% in developed countries.^[2]

• Patients of all age groups may develop acute pericarditis. Although it commonly affects people in 20 to 50 years of age.^[5]

• There is no racial predilection to acute pericarditis.

• Men are more commonly affected by acute pericarditis than women.

• Pericarditis in developed countries is most commonly due to malignancy or viral infection.^[6][7][8]
• It usually follows respiratory infections, most commonly echovirus or coxsackie virus.
• In children, it is most commonly caused by adenovirus or coxsackie virus.
• The incidence and prevalence of viral pericarditis vary with season and region.

• In developing countries pericarditis is usually secondary to tuberculosis or HIV infection.^{[9][10][11][12]}
• Tuberculous pericarditis, caused by Mycobacterium tuberculosis, is found in approximately 1% of all autopsied cases of TB and in 1% to 2% of instances of pulmonary TB. It accounted for 69.5% (162 of 233) of cases referred for diagnostic pericardiocentesis in a study in Western Cape Province of South Africa, while the same accounts for 4% of cases in developed countries.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. Homa Najafi, M.D.[2]

Pericarditis can lead to the development of pericardial effusion, cardiac tamponade and constrictive pericarditis. Cardiac tamponade, or compression of the heart by fluid in the pericardial sac, reduces the ability of the heart to pump blood. It is a medical emergency that requires urgent pericardiocentesis or a pericardial window. The prognosis depends on the complications of pericarditis, the underlying etiology, and the associated co-morbidities. Pericarditis secondary to malignancy, MI, autoimmune disease and renal failure carries a poor prognosis.

Pericarditis is inflammation of the pericardium, the double-walled sac that contains the heart and the roots of the great vessels. There can be an accompanying accumulation of fluid that can be either serous (free flowing fluid) or fibrinous (an exudate, which is a thick fluid composed of proteins, fibrin strands, inflammatory cells, cell breakdown products, and sometimes bacteria), which leads to development of pericardial effusion and cardiac tamponade. Vascular congestion of the pericardium is also present. The underlying myocardium may or may not be inflamed as well. If the myocardium is involved in the inflammatory process, it is called myopericarditis, and the CK and troponin levels may be elevated. Subsequent scarring of the pericardium may lead to constrictive pericarditis.

Common complications of pericarditis include:^[1]

• Pericardial Effusion
  • Many forms of pericarditis can be complicated by significant fluid buildup around the heart, which is known as a pericardial effusion.
• Pericardial Tamponade
  • If the fluid accumulates too rapidly or is too large, then cardiac tamponade, a condition in which the heart is compressed by the fluid and cannot pump enough blood forward, may occur. Cardiac tamponade may require urgent intervention including pericardiocentesis or a pericardial window. This complication is more common in patients with specific underlying etiologies such as malignancy, tuberculosis, or purulent pericarditis. It rarely occurs in idiopathic pericarditis.
• Constrictive Pericarditis
  • If scarring of the sac around the heart (pericardium) occurs, then this is called constrictive pericarditis which may require surgical stripping of the scar (pericardiectomy).

The prognosis associated with pericarditis depends on the underlying cause and associated condition(s).^[2][3][4][5]

• Idiopathic Pericarditis:
  • Idiopathic pericarditis is often self-limited and most patients recover in 2 weeks to 3 months. Idiopathic or viral pericarditis is associated with a favorable long-term prognosis with few developing recurrences. Approximately 15-30% of patients with idiopathic acute pericarditis who are not treated with colchicine will develop recurrent pericarditis.
• Post MI Pericarditis or Dressler’s Syndrome:
  • Post MI pericarditis is usually associated with larger infarcts, and therefore these patients have a poorer long term prognosis.
• Tuberculous Pericarditis:
  • The mortality rate associated with tuberculous pericarditis in the preantibiotic era was 80-90%. The mortality is 17-34% if the tuberculous pericarditis is associated with HIV.
• Traumatic Pericardial Injury:
  • In penetrating injuries, pericardial effusion and tamponade may develop rapidly. Early detection and early treatment of cardiac tamponade is associated with a good prognosis. Minor perforations, isolated right ventricular wounds, and a systolic blood pressure more than 50 mm Hg are all associated with better outcomes.
• Malignant Pericarditis:
  • Pericarditis associated with malignancy is associated with poorer outcomes and a more complicated course.
• Autoimmune Disease:
  • Pericarditis associated with scleroderma and rheumatic fever is associated with worse outcomes.
• Renal Failure:
  • Pericarditis associated with renal failure is associated with significant morbidity and may result in hemorrhagic pericarditis.

Template:WS Template:WH

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2] Ahmed Zaghw, M.D. [3] Homa Najafi, M.D.[4] Hafiz M. Ahmed, M.D.[5]

The management of pericarditis depends on whether the patient has an uncomplicated or complicated disease course. Uncomplicated pericarditis is treated with an NSAID or aspirin combined with colchicine. Aspirin is preferred when concomitant ischemic heart disease is present. For recurrent or incessant pericarditis failing first-line therapy, treatment is guided by phenotype: anti-IL-1 agents (anakinra, rilonacept, goflikicept) are preferred for the inflammatory phenotype, while low-dose corticosteroids are preferred for the noninflammatory phenotype. Cardiac tamponade requires urgent pericardiocentesis. Purulent pericarditis requires antibiotics and drainage.

Patients with uncomplicated acute pericarditis can generally be treated and followed up in an outpatient clinic. First-line therapy consists of dual anti-inflammatory treatment with a non-steroidal anti-inflammatory drug (or aspirin) combined with colchicine. Aspirin is the preferred agent when concomitant ischemic heart disease is present. Patients should be observed for gastrointestinal side effects, and a proton-pump inhibitor should be co-prescribed for gastric protection. If the underlying cause of pericarditis is something other than viral or idiopathic, the specific etiology should be treated.^[1]

• NSAIDs are a mainstay of therapy for uncomplicated pericarditis (viral or idiopathic pericarditis), used in combination with colchicine as dual first-line therapy. The goal of therapy is to reduce pain and inflammation. The preferred NSAID is ibuprofen, dosed at 600 to 800 mg three times daily for days to weeks as needed. Indomethacin 25 to 50 mg three times daily is another option. In order to minimize recurrence, a slow tapering of the NSAID dose guided by symptom resolution and normalization of C-reactive protein (CRP) is recommended rather than abrupt discontinuation. In patients with relative contraindications to NSAIDs (such as heart failure, chronic kidney disease, peptic ulcer disease, bleeding diathesis, or concurrent use of anticoagulants, ACE inhibitors, ARBs, or calcineurin inhibitors), NSAIDs should be prescribed at the lowest effective dose for the shortest duration, and alternatives such as high-dose aspirin should be considered. A proton-pump inhibitor should be co-prescribed for gastric protection. The gastroprotection recommendation is based on several studies that have evaluated factors placing patients at increased risk of gastroduodenal toxicity from NSAIDs.^[1][2][3][4]

• The American College of Gastroenterology identified the five most important risk factors for gastroduodenal toxicity:^[5]

• Age 60 years (relative risk [RR] 5.52)
• History of an adverse gastroduodenal event (RR 4.76)
• High-dosage NSAIDs (more than twice normal; RR 10.1)
• Concurrent use of glucocorticoids (RR 4.4)
• Concurrent use of anticoagulants (RR 12.7).

Note: Patients with several risk factors are at the highest risk of NSAID-induced gastroduodenal toxicity.

Aspirin at 500 to 1,000 mg three times daily is a first-line therapy for acute pericarditis, equivalent to ibuprofen. It is the preferred agent when the patient has concomitant ischemic heart disease or is already receiving aspirin for another clinical indication. As with other NSAIDs, a proton-pump inhibitor should be co-prescribed.^[1][6]

In pericarditis following acute myocardial infarction, NSAIDs other than aspirin should be avoided since they can impair scar formation.

Failure to respond to NSAIDs within one week (as indicated by persistence of fever, a worsening of symptoms such as chest pain, the development of a new pericardial effusion), likely indicates that the underlying cause may not be viral or idiopathic in nature. These patients may require re-evaluation, observation, and more aggressive therapy as described in the next section.

Colchicine is recommended as adjunctive first-line therapy alongside an NSAID or aspirin for both acute and recurrent pericarditis. The standard dose is 0.6 mg twice daily. For patients weighing less than 70 kg, or those with severe renal or hepatic impairment or gastrointestinal intolerance, the dose should be reduced to 0.6 mg once daily. The recommended duration is 3 months for a first episode and at least 6 months for recurrent pericarditis. Tapering may be considered at the end of the treatment course.

The rate of recurrence after an initial episode is lowered with colchicine therapy by approximately 50% – from 26% to 14% (see Forest plot).^[7]

For example, in a multicenter, double-blind trial, the use of colchicine at a dose of 0.5 mg twice daily for 3 months for patients weighing >70 kg or 0.5 mg once daily for patients weighing ≤70 kg in acute pericarditis, when added to conventional antiinflammatory therapy with aspirin or ibuprofen, significantly reduced the rate of symptom persistence at 72 hours (19.2% vs. 40.0%, P=0.001), the number of recurrences per patient (0.21 vs. 0.52, P = 0.001), the hospitalization rate (5.0% vs. 14.2%, P = 0.02), and the remission rate at 1 week (85.0% vs. 58.3%, P<0.001), as compared with placebo.^[8]

Colchicine is generally well tolerated, though gastrointestinal side effects (nausea, vomiting, diarrhea, abdominal pain) may require dose reduction or discontinuation in approximately 10% of patients. Dose reductions to 0.3 to 0.6 mg daily should be considered when co-prescribing colchicine with potent inhibitors of P-glycoprotein (P-gp) and/or cytochrome P450 3A4 (CYP3A4), such as clarithromycin, cyclosporine, or certain antifungals, to reduce the risk of toxicity. Alternatively, substituting the interacting medication may allow the full colchicine dose to be maintained. Colchicine is contraindicated in patients with severe renal impairment (creatinine clearance less than 30 mL/min).^[1]

Corticosteroids are not recommended as first-line therapy for acute pericarditis. While they provide rapid symptom relief, their use during a first episode has been associated with a higher rate of recurrence in observational studies. When corticosteroids are required (such as in patients who are refractory to or intolerant of NSAIDs and colchicine, or in those with autoimmune disease), they should be prescribed at low to moderate doses (prednisone 0.2 to 0.5 mg/kg/day), maintained until clinical remission, and then slowly tapered over several months. Higher doses (such as prednisone 1.0 mg/kg/day) should be avoided due to increased recurrence risk. For patients with recurrent or incessant pericarditis and evidence of systemic inflammation, anti-IL-1 agents are now preferred over corticosteroids as escalation therapy (see Anti-IL-1 Therapy section). Corticosteroids remain the preferred escalation option for patients with a noninflammatory phenotype (normal or near-normal CRP, often autoimmune-related). Prophylaxis for pneumocystis pneumonia and osteoporosis should be considered for patients requiring glucocorticoid doses equivalent to more than 20 mg of prednisone daily for 1 month or longer.^[1]

The treatment approach for pericarditis that fails first-line therapy is guided by the presence or absence of an inflammatory phenotype. The inflammatory phenotype, which accounts for approximately 80% to 90% of cases, is characterized by elevated CRP (greater than 1 mg/dL or 10 mg/L), fever, neutrophilic leukocytosis, and pericardial or pleural effusions. The noninflammatory phenotype, seen in approximately 10% to 20% of cases, is characterized by low or near-normal CRP and is often associated with underlying autoimmune conditions. This distinction is clinically important because anti-IL-1 agents are the preferred escalation therapy for the inflammatory phenotype, whereas low-dose corticosteroids are preferred for the noninflammatory phenotype.^[1]

Anti-IL-1 agents represent a major advance in the treatment of recurrent and incessant pericarditis. Multiple randomized trials have demonstrated their efficacy in achieving clinical remission, reducing recurrences, and normalizing inflammatory markers in patients with the inflammatory phenotype (elevated CRP greater than 1 mg/dL or 10 mg/L). These agents are now considered the preferred escalation option over corticosteroids for patients who fail first-line dual therapy with NSAIDs and colchicine and who have evidence of systemic inflammation.

Three anti-IL-1 agents have been studied:

• Anakinra (IL-1 receptor antagonist): 1 to 2 mg/kg/day subcutaneously, up to 100 mg/day in adults, for more than 12 months. In the AIRTRIP trial, recurrence occurred in 18% of patients continuing anakinra compared with 90% of those who discontinued it.
• Rilonacept (IL-1 trap): 320 mg subcutaneous loading dose followed by 160 mg weekly, for more than 12 months. Rilonacept is FDA-approved for the treatment and prevention of recurrent pericarditis. In the RHAPSODY trial, recurrence occurred in 6.7% of patients continuing rilonacept versus 74% of those who discontinued it.
• Goflikicept: 80 mg subcutaneously every 2 weeks, for more than 12 months. This agent is not yet available in the United States.

Before initiating anti-IL-1 therapy, patients should be screened for hepatitis B and C, HIV, and tuberculosis. Once established on an anti-IL-1 agent, other anti-inflammatory medications may be sequentially weaned (typically corticosteroids first, then NSAID, then colchicine), although colchicine may sometimes be continued for potential additive benefit. The optimal duration of anti-IL-1 therapy remains uncertain. Recurrence rates are very low while on treatment, but approximately 50% to 75% of patients experience recurrence upon discontinuation. Long-term extension data support treatment beyond 18 months for sustained disease control.^[1]

Exercise restriction is recommended for at least 1 month following a pericarditis diagnosis or flare. During this period, maximal heart rate should be kept below 100 beats per minute regardless of the type of physical activity, until clinical remission is achieved. The rationale is that increased heart rate enhances the frequency of friction between the pericardial layers, which can perpetuate inflammation. Athletes should follow the same restriction, with return to competitive activity guided by symptom resolution and normalization of CRP and imaging findings.

Patients at high risk of developing complications of pericarditis may require admission to an inpatient service for careful observation and hemodynamic monitoring. High-risk features include:^[1]

• High fever (greater than 38°C / 100.4°F) and leukocytosis
• Subacute onset of symptoms (over days to weeks rather than acute)
• Large pericardial effusion (echo-free space greater than 20 mm) resistant to NSAID treatment
• Development of cardiac tamponade
• Concomitant myocarditis (myopericarditis)
• Immunocompromised status
• History of oral anticoagulation therapy
• Pericarditis secondary to acute trauma
• Failure to respond to seven days of NSAID treatment

• Pericardiocentesis may be required to treat cardiac tamponade. Pericardiocentesis is generally not recommended for pericardial effusion in the absence of tamponade physiology.

• Anti-IL-1 agents (anakinra, rilonacept, or goflikicept) are the preferred escalation therapy for recurrent or incessant pericarditis with an inflammatory phenotype (elevated CRP) that fails first-line dual therapy with NSAIDs and colchicine.
• Corticosteroids may be required in patients with autoimmune disease or those with a noninflammatory phenotype (normal or near-normal CRP) who fail first-line therapy. Anti-IL-1 agents are generally preferred over corticosteroids when systemic inflammation is present.
• Colchicine is a component of first-line dual therapy and should be continued as described above.
• Surgery (radical pericardiectomy on cardiopulmonary bypass) may be required in the presence of refractory recurrent pericarditis or constrictive pericarditis. Partial pericardiectomy is not recommended.^[1]

Pericardiocentesis is an invasive procedure in which the pericardial fluid is drained through a needle. A pericardial window is a surgical procedure to drain fluid form the pericardium. Indications for a pericardiocentesis or a pericardial window include the following:^[3]

• Cardiac tamponade
• Large, persistent, symptomatic pericardial effusion
• For diagnostic purposes, if there is suspected purulent, tuberculosis, or neoplastic pericarditis.

Pericardial effusions are classified by echocardiographic size as follows: trivial (less than 1.0 cm, not visible throughout the cardiac cycle), small (less than 1.0 cm), moderate (1.0 to 1.9 cm), large (2.0 to 2.5 cm), and very large (greater than 2.5 cm). Echocardiographic features suggestive of tamponade physiology include diastolic right ventricular collapse (the most specific finding), right atrial inversion lasting more than one-third of the cardiac cycle, dilated inferior vena cava (greater than 2.1 cm) with minimal respiratory variation (sensitive but not specific), and exaggerated respiratory variation in mitral inflow velocities (greater than 30%) and tricuspid inflow velocities (greater than 60%).

• Recurrent pericarditis is defined as a relapse of symptoms after a symptom-free interval of at least 4 to 6 weeks following the initial episode, with completion of medical therapy. Treatment is guided by the inflammatory phenotype.
• First-line therapy consists of an NSAID (aspirin 500 to 1,000 mg three times daily or ibuprofen 600 to 800 mg three times daily) combined with colchicine 0.6 mg twice daily (or 0.6 mg once daily if less than 70 kg or with severe renal/hepatic impairment) for at least 6 months. NSAIDs are started at high dose and tapered after symptom resolution and CRP normalization.
• For patients who fail first-line dual therapy, the treatment approach depends on the phenotype:

• Inflammatory phenotype (elevated CRP, fever, pericardial inflammation on imaging): Anti-IL-1 agents (anakinra, rilonacept, or goflikicept) are the preferred escalation therapy over corticosteroids.
• Noninflammatory phenotype (normal or near-normal CRP, often autoimmune-related): Low-dose corticosteroids (prednisone 0.2 to 0.5 mg/kg/day) are the preferred escalation therapy, maintained until remission and then slowly tapered over months.

• For patients who fail both anti-IL-1 agents and corticosteroids, azathioprine (starting at 1 mg/kg/day, gradually increased to 2 to 3 mg/kg/day) or intravenous immunoglobulin (IVIG, 400 to 500 mg/kg IV daily for 5 days) may be considered.
• Radical pericardiectomy on cardiopulmonary bypass at a high-volume experienced surgical center is a last-resort option for patients who do not respond to pharmacotherapy, have contraindications to medical therapy, or desire pregnancy. Partial pericardiectomy is not recommended. Anti-inflammatory medications may be continued until surgery and for 3 to 6 months postoperatively if active inflammation persists. Most patients will respond to aggressive medical therapy before surgery is needed.^[1]

Referral to a multidisciplinary Pericardial Diseases Center (PDC) should be considered for patients with recurrent, incessant, or chronic pericarditis; suspected or confirmed constrictive pericarditis; large or complex pericardial effusions requiring drainage; or when advanced therapies such as anti-IL-1 agents or pericardiectomy are being considered. A PDC ideally includes expertise in multimodality imaging (echocardiography, CMR, CT), rheumatology, infectious diseases, genetics, cardiothoracic surgery, and specialty pharmacy.^[1]

1. Bacterial Pericarditis

• 1.1. Empiric antimicrobial therapy^[11][12]

• Preferred regimen: Vancomycin 1 g IV q12h targeting trough levels of 15–20 μg/mL for 28 days AND Ciprofloxacin 400 mg IV q12h for 28 days
• Alternative regimen (1): Vancomycin 1 g IV q12h targeting trough levels of 15–20 μg/mL for 28 days AND Cefepime 2 g IV q12h for 28 days
• Alternative regimen (2): Vancomycin 1 g IV q12h targeting trough levels of 15–20 μg/mL for 14–42 days AND Ceftriaxone 2 g IV q24h for 14–42 days

Note: Pericardiocentesis must be promptly performed. Pericardial drainage combined with effective systemic antibiotic therapy is mandatory (antistaphylococcal agent plus aminoglycoside, followed by tailored antibiotic therapy according to cultures). Frequent irrigation of the pericardial cavity with urokinase or streptokinase may be considered. Open surgical drainage through subxiphoid pericardiotomy is preferable. Pericardiectomy may be required in patients with dense adhesions, loculated and thick purulent effusion, recurrence of tamponade, persistent infection, and progression to constriction.

• 1.2. Specific considerations^{[13][14][15][16]}

• 1.2.1. Purulent pericarditis with contiguous pneumonia

• Preferred regimen: Vancomycin 1 g IV q12h targeting trough levels of 15–20 μg/mL AND (Ceftriaxone 1–2 g IV q12h OR Cefotaxime 2 g IV q6–8h) AND (Ciprofloxacin 400 mg IV q12h OR Levofloxacin 500–750 mg IV q24h)

• 1.2.2. Purulent pericarditis with contiguous head and neck infection

• Preferred regimen: Imipenem 500 mg IV q6–8h OR Ampicillin-Sulbactam 3 g IV q6h

• 1.2.3. Purulent pericarditis secondary to infective endocarditis

• Preferred regimen: Vancomycin 15–20 mg/kg IV q8–12h targeting trough levels of 15–20 μg/mL AND Gentamicin 3 mg/kg/day IV q8–12h

• 1.2.4. Purulent pericarditis after cardiac surgery, pediatric

• Preferred regimen: Vancomycin 15 mg/kg IV q6h targeting trough levels of 15–20 μg/mL AND (Ceftriaxone 100 mg/kg/day IV q12–24h OR Cefotaxime 200–300 mg/kg/day IV q6–8h) AND Gentamicin 6–7.5 mg/kg/day IV q8h

• 1.2.5. Purulent pericarditis with genitourinary infection, pediatric

• Preferred regimen: Vancomycin 15 mg/kg IV q6h targeting trough levels of 15–20 μg/mL AND (Ceftriaxone 100 mg/kg/day IV q12–24h OR Cefotaxime 200–300 mg/kg/day IV q6–8h) AND Gentamicin 6–7.5 mg/kg/day IV q8h

• 1.2.6. Purulent pericarditis in immunocompromised host, pediatric

• Preferred regimen: Vancomycin 15 mg/kg IV q6h targeting trough levels of 15–20 μg/mL AND (Ceftriaxone 100 mg/kg/day IV q12–24h OR Cefotaxime 200–300 mg/kg/day IV q6–8h) AND Gentamicin 6–7.5 mg/kg/day IV q8h

• 1.3. Pathogen-directed antimicrobial therapy^[17]

• 1.3.1. Anaerobes

• Preferred regimen: Clindamycin 600–900 mg IV q8h for 14–42 days OR Metronidazole 7.5 mg/kg IV q6h for 14–42 days OR Ampicillin-Sulbactam 3 g IV q6h for 14–42 days

• 1.3.2. Gram-negative bacilli

• Preferred regimen: Ciprofloxacin 400 mg IV q12h for 14–42 days OR Levofloxacin 500–750 mg IV q24h for 14–42 days OR Cefepime 2 g IV q12h for 14–42 days

• 1.3.3. Legionella pneumophila

• Preferred regimen: Ciprofloxacin 400 mg IV q12h for 14–42 days OR Levofloxacin 500–750 mg IV q24h for 14–42 days OR Azithromycin 500 mg IV q24h for 14–42 days

• 1.3.4. Mycoplasma pneumoniae

• Preferred regimen: Doxycycline 100 mg IV q12h for 14–42 days OR Azithromycin 500 mg IV q24h for 14–42 days

• 1.3.5. Neisseria meningitidis

• Preferred regimen: Penicillin G 5–24 MU/day IM/IV q4–6h for 14–42 days OR Cefotaxime 2 g IV q6–8h for 14–42 days OR Ceftriaxone 2 g IV q24h for 14–42 days

• 1.3.6. Staphylococcus aureus, methicillin-susceptible

• Preferred regimen: Nafcillin 1–2 g IV q4h for 14–42 days OR Oxacillin 1–2 g IV q4h for 14–42 days OR Cefazolin 1–2 g IV q48h for 14–42 days OR Vancomycin 1 g IV q12h targeting trough levels of 15–20 μg/mL for 14–42 days OR Clindamycin 600–900 mg IV q8h for 14–42 days

• 1.3.7. Staphylococcus aureus, methicillin-resistant

• Preferred regimen: Vancomycin 1 g IV q12h targeting trough levels of 15–20 μg/mL for 14–42 days OR Linezolid 600 mg IV q12h for 14–42 days

• 1.3.8. Streptococcus pneumoniae, penicillin-susceptible

• Preferred regimen: Penicillin G 5–24 MU/day IM/IV q4–6h for 14–42 days OR Cefotaxime 2 g IV q6–8h for 14–42 days OR Ciprofloxacin 400 mg IV q12h for 14–42 days OR Levofloxacin 500–750 mg IV q24h for 14–42 days

• 1.3.9. Streptococcus pneumoniae, penicillin-resistant

• Preferred regimen: Ciprofloxacin 400 mg IV q12h for 14–42 days OR Levofloxacin 500–750 mg IV q24h for 14–42 days OR Vancomycin 1 g IV q12h targeting trough levels of 15–20 μg/mL for 14–42 days

2. Tuberculous Pericarditis^[18].

• Preferred regimen: (Isoniazid 5 mg/kg (300 mg) PO qd AND Rifampicin 10 mg/kg (600 mg) PO qd AND Pyrazinamide 1,500 mg PO qd AND Ethambutol 1,200 mg PO qd for 2 months) THEN (Rifampicin 10 mg/kg (600 mg) PO qd AND Pyrazinamide 1,500 mg PO qd for 4 months) AND Prednisolone 1–2 mg/kg/day for 5–7 days with slow taper over 6–8 weeks^[19].
• Pediatric doses: Isoniazid 10–15 mg/kg (300 mg); Rifampin 10–20 mg/kg (600 mg); Pyrazinamide 15–30 mg/kg (2.0 g); Ethambutol 15–20 mg/kg daily (1.0 g).
• Note: Intrapericardial drainage is done if needed. If constriction develops inspite of medical therapy, pericardiectomy is indicated.

3. Viral pericarditis^[18]

• 3.1. CMV pericarditis

• Preferred regimen: Immunoglobulin 1 time per day 4 ml/kg on day 0, 4, and 8; 2 ml/kg on day 12 and 16.

Note: Symptomatic treatment is given to the patients with viral pericarditis while in large effusions and cardiac tamponade pericardiocentesis is necessary. The use of corticosteroid therapy is contraindicated except in patients with secondary tuberculous pericarditis, as an adjunct to tuberculosis treatment. Drainage, if needed is done.

• 3.2. Coxsackie B pericarditis

• Preferred regimen: Interferon alpha or beta 2,5 Mio. IU/m² surface area SC 3 times per week

Note: Symptomatic treatment is given to the patients with viral pericarditis while in large effusions and cardiac tamponade pericardiocentesis is necessary. The use of corticosteroid therapy is contraindicated except in patients with secondary tuberculous pericarditis, as an adjunct to tuberculosis treatment. Drainage, if needed is done.

• 3.3. Adenovirus and parvovirus B19 perimyocarditis

• Preferred regimen: Immunoglobulin 10 g IV at day 1 and 3 for 6–8 hours

Note: Symptomatic treatment is given to the patients with viral pericarditis while in large effusions and cardiac tamponade pericardiocentesis is necessary. The use of corticosteroid therapy is contraindicated except in patients with secondary tuberculous pericarditis, as an adjunct to tuberculosis treatment. Drainage, if needed is done.

4. Fungal Pericarditis^[18]

• Empiric therapy : Fluconazole, Ketoconazole, Itraconazole, Amphotericin B, Liposomal amphotericin B or Amphotericin B lipid complex is indicated.

• 4.1. Histoplasmosis

• Preferred regimen: Nonsteroidal anti-inflammatory drugs given during 2–12 weeks.

Note: Corticosteroids and NSAIDs can support the treatment with antifungal drugs. Pericardiocentesis or surgical treatment is indicated for haemodynamic impairment. Pericardiectomy is indicated in fungal constrictive pericarditis.

• 4.2. Nocardiosis

• Preferred regimen: Sulfonamides are the drugs of choice.

Note: Corticosteroids and NSAIDs can support the treatment with antifungal drugs. Pericardiocentesis or surgical treatment is indicated for haemodynamic impairment. Pericardiectomy is indicated in fungal constrictive pericarditis.

• 4.3. Actinomycosis

• Preferred regimen: Combination of three antibiotics including Penicillin.

Note: Corticosteroids and NSAIDs can support the treatment with antifungal drugs. Pericardiocentesis or surgical treatment is indicated for haemodynamic impairment. Pericardiectomy is indicated in fungal constrictive pericarditis.