Acute Pericarditis LESLIE E. TINGLE, MD; DANIEL MOLINA, MD; and CHARLES W. CALVERT, DO Baylor Family Medicine Residency at Garland, Garland, Texas Although acute pericarditis is most often associated with viral infection, it may also be caused by many diseases, drugs, invasive cardiothoracic procedures, and chest trauma. Diagnosing acute pericarditis is often a process of exclusion. A history of abrupt-onset chest pain, the pres- ence of a pericardial friction rub, and changes on electrocardiography suggest acute pericardi- tis, as do PR-segment depression and upwardly concave ST-segment elevation. Although highly specific for pericarditis, the pericardial friction rub is often absent or transient. Auscultation during end expiration with the patient sitting up and leaning forward increases the likelihood of observing this physical finding. Echocardiography is recommended for most patients to con- firm the diagnosis and to exclude tamponade. Outpatient management of select patients with acute pericarditis is an option. Complications may include pericardial effusion with tampon- ade, recurrence, and chronic constrictive pericarditis. Use of colchicine as an adjunct to con- ventional nonsteroidal anti-inflammatory drug therapy for acute viral pericarditis may hasten symptom resolution and reduce recurrences. (Am Fam Physician 2007;76:1509-14. Copyright © 2007 American Academy of Family Physicians.) cute pericarditis is a common Etiology disease that must be considered Although viral infection is the most com- in the differential diagnosis of mon identifiable cause of acute pericardi- chest pain in adults.1 The clinical tis, the condition may be associated with syndromeA of pericarditis results from inflam- many diseases.4 Nonviral causes of pericar- mation of the pericardium, a fibrous sac that ditis include bacterial infection, MI, chest envelops the heart and the base of the great trauma, and neoplasm. Causes of pericardi- vessels. The pericardium has a visceral and a tis are listed in Table 1.5-7 parietal layer, between which up to 50 mL of Pericardial disease is the most common serous fluid is found in healthy patients.2 Peri- cardiovascular manifestation of AIDS, carditis may present as an indolent process occurring in up to 20 percent of patients with no significant pain, as seen in patients with human immunodeficiency virus infec- with tuberculosis, or it may be heralded by tion/AIDS. Although the incidence of bac- the sudden onset of severe substernal chest terial pericarditis is declining in developed pain in acute idiopathic or viral pericarditis. countries, it has increased among patients Although the incidence of acute pericarditis with AIDS.8,9 Patients with AIDS and other is unknown, up to 5 percent of visits to emer- immunocompromised persons are also gency departments for nonacute myocardial at high risk for tuberculous and fungal infarction (MI) chest pain may be related to pericarditis. pericarditis.3 Recognition of the clinical syn- The mortality rate for untreated tuber- drome is important because it must be distin- culous pericarditis approaches 85 percent. guished from acute coronary syndromes and Tuberculous pericarditis often presents pulmonary embolism. Further, the syndrome with subacute illness that includes fever, a may lead to cardiac tamponade large pericardial effusion, and tamponade. or constrictive pericarditis, or The diagnosis is confirmed by identification Nonviral causes of pericardi- may be associated with under- of Mycobacterium tuberculosis in pericar- tis include bacterial infec- lying conditions (e.g., acquired dial fluid or tissue. Other diagnostic tools tion, myocardial infarction, immunodeficiency syndrome include polymerase chain reaction for DNA chest trauma, and neoplasm. [AIDS], malignancy, MI, colla- of mycobacteria, adenosine deaminase, and gen vascular disease). interferon-γ in pericardial fluid.10 Downloaded from the American Family Physician Web site at www.aafp.org/afp. Copyright © 2007 American Academy of Family Physicians. For the private, noncommercial use of one individual user of the Web site. All other rights reserved. Contact [email protected] for copyright questions and/or permission requests. SORT: KEY RECOMMENDATIONS FOR PRACTICE Evidence Clinical recommendation rating References Echocardiography is recommended for patients with suspected pericardial disease, including C 10, 25 effusion, constriction, or effusive-constrictive process. Pericardiocentesis should be reserved to treat cardiac tamponade and suspected purulent pericarditis. C 10, 25 Colchicine should be considered as an adjunct to nonsteroidal anti-inflammatory drug therapy in B 28, 29 patients with acute viral or idiopathic pericarditis. Corticosteroid therapy alone should be avoided in patients with acute or idiopathic pericarditis. B 29 A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease- oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, see page 1435 or http:// www.aafp.org/afpsort.xml. Pericarditis also can arise as a compli- Table 1. Causes of Pericarditis cation of MI. Post–MI pericarditis may develop two to four days after an acute Idiopathic (nonspecific, probably viral) infarction and results from a reaction Infectious causes between the pericardium and the damaged Viruses: coxsackievirus A and B, hepatitis viruses, human immunodeficiency adjacent myocardium. Dressler’s syndrome virus, influenza, measles virus, mumps virus, varicella virus is a post–MI phenomenon in which peri- Bacteria: gram-positive and gram-negative organisms; rarely, carditis develops weeks to months after an Mycobacterium tuberculosis acute infarction; this syndrome is thought Fungi (most common in immunocompromised patients): Blastomyces to reflect a late autoimmune reaction medi- dermatitidis, Candida species, Histoplasma capsulatum ated by antibodies to circulating myocardial Echinococcus granulosus 2 Noninfectious causes antigens. Acute myocardial infarction* Pathophysiology Aortic dissection The acute inflammatory response in pericar- Renal failure† Malignancy: breast cancer, lung cancer, Hodgkin’s disease, leukemia, ditis can produce either serous or purulent lymphoma by local invasion fluid, or a dense fibrinous material. In viral Radiation therapy (usually for breast or lung cancer) pericarditis, the pericardial fluid is most Chest trauma commonly serous, is of low volume, and Postpericardiotomy resolves spontaneously. Neoplastic, tuber- Cardiac procedures: catheterization, pacemaker placement, ablation culous, and purulent pericarditis may be Autoimmune disorders: mixed connective tissue disorder, associated with large effusions that are exu- hypothyroidism, inflammatory bowel disease, rheumatoid arthritis, dative, hemorrhagic, and leukocyte filled.2,11 scleroderma, spondyloarthropathies, systemic lupus erythematosus, Gradual accumulation of large fluid volumes Wegener’s granulomatosis in the pericardium, even up to 250 mL, may Sarcoidosis not result in significant clinical signs.12 Medications Although pericardial effusion may be absent Dantrolene (Dantrium), doxorubicin (Adriamycin), hydralazine in 60 percent of patients, large pericardial (Apresoline; brand not available in the United States), isoniazid (INH), mesalamine (Rowasa), methysergide (Sansert; brand not available effusions may accumulate rapidly and impede in United States), penicillin, phenytoin (Dilantin), procainamide diastolic filling of the right heart, resulting in (Procanbid), rifampin (Rifadin) cardiac tamponade and death.1,3,11 Cardiac tamponade associated with acute pericardial *—Pericardial effusion may occur on the second to fourth day after acute myocardial infarction as a reaction to underlying necrotic myocardium in up to 25 percent of disease is more common in patients with neo- patients. It can also develop weeks to months after myocardial infarction in patients plastic, tuberculous, and purulent pericarditis with post–myocardial infarction syndrome (i.e., Dressler’s syndrome); in this situation, (60 percent) than in patients with acute viral pericarditis occurs because of a late autoimmune reaction stimulated by the entry of 11,13 necrotic myocardial tissue into the circulation, where it acts as an antigen. pericarditis (14 percent). †—Pericarditis in uremia indicates a need for dialysis; pericarditis may also be associ- Prolonged pericarditis may result in ated with hemodialysis. persistent accumulation of pericardial Information from references 5 through 7. fluid. In this case, the fluid constitutes to form a thick coating that surrounds the 1510 American Family Physician www.aafp.org/afp Volume 76, Number 10 ◆ November 15, 2007 Table 2. Differentiation of Acute Pericarditis from Myocardial Ischemia or Infarction Myocardial ischemia myocardium. The ultimate manifestation Clinical finding Acute pericarditis or infarction 4 may be constrictive pericarditis. Chest pain Character Sharp, stabbing Pressure-like, heavy, Diagnosis squeezing History and pHysicaL EXamination Duration Hours to days Minutes to hours Patients with acute pericarditis commonly Change with position Worse when supine; No report a prodrome of fever, malaise, and improved when myalgias. The cardinal features of acute peri- sitting up or leaning carditis are chest pain, pericardial friction forward rub, and gradual repolarization changes on Change with Worse with inspiration No respiration electrocardiography