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How is Acute Pericarditis Diagnosed and Treated?


 

KEY POINTS

  • Acute pericarditis is a clinical diagnosis.
  • Most cases are idiopathic or viral.
  • A pericardial rub is pathognomic but might not be heard.
  • Electrocardiogram typically reveals diffuse ST-segment elevations.
  • NSAIDs and colchicine constitute first-line medical treatment.
  • Hospitalization is required in high-risk cases.
  • Large effusion or tamponade requires drainage via pericardiocentesis.

Case

A 32-year-old female with no significant past medical history is evaluated for sharp, left-sided chest pain for five days. Her pain is intermittent, worse with deep inspiration and in the supine position. She denies any shortness of breath. Her temperature is 100.8ºF, but otherwise her vital signs are normal. The physical exam and chest radiograph are unremarkable, but an electrocardiogram shows diffuse ST-segment elevations. The initial troponin is mildly elevated at 0.35 ng/ml.

Could this patient have acute pericarditis? If so, how should she be managed?

Background

Pericarditis is the most common pericardial disease encountered by hospitalists. As many as 5% of chest pain cases unattributable to myocardial infarction (MI) are diagnosed with pericarditis.1 In immunocompetent individuals, as many as 90% of acute pericarditis cases are viral or idiopathic in etiology.1,2 Human immunodeficiency virus (HIV) and tuberculosis are common culprits in developing countries and immunocompromised hosts.3 Other specific etiologies of acute pericarditis include autoimmune diseases, neoplasms, chest irradiation, trauma, and metabolic disturbances (e.g. uremia). An etiologic classification of acute pericarditis is shown in Table 2 (p. 16).

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Figure 1. Echocardiographic evidence of right atrial and right ventricular diastolic collapse due to large pericardial effusion suggestive of tamponadeRA: right atrium; RV: right ventricle; LA: left atrium; LV: left ventricle; Eff: pericardial effusion compressing RA and RV.

Pericarditis primarily is a clinical diagnosis. Most patients present with chest pain.4 A pericardial friction rub may or may not be heard (sensitivity 16% to 85%), but when present is nearly 100% specific for pericarditis.2,5 Diffuse ST-segment elevation on electrocardiogram (EKG) is present in 60% to 90% of cases, but it can be difficult to differentiate from ST-segment elevations in acute MI.4,6

Uncomplicated acute pericarditis often is treated successfully as an outpatient.4 However, patients with high-risk features (see Table 1, right) should be hospitalized for identification and treatment of specific underlying etiology and for monitoring of complications, such as tamponade.7

Our patient has features consistent with pericarditis. In the following sections, we will review the diagnosis and treatment of acute pericarditis.

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Table 1. High-risk features of acute pericarditis and criteria for hospitalization

Review of the Data

How is acute pericarditis diagnosed?

Acute pericarditis is a clinical diagnosis supported by EKG and echocardiogram. At least two of the following four criteria must be present for the diagnosis: pleuritic chest pain, pericardial rub, diffuse ST-segment elevation on EKG, and pericardial effusion.8

History. Patients may report fever (46% in one small study of 69 patients) or a recent history of respiratory or gastrointestinal infection (40%).5 Most patients will report pleuritic chest pain. Typically, the pain is improved when sitting up and leaning forward, and gets worse when lying supine.4 Pain might radiate to the trapezius muscle ridge due to the common phrenic nerve innervation of pericardium and trapezius.9 However, pain might be minimal or absent in patients with uremic, neoplastic, tuberculous, or post-irradiation pericarditis.

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Figure 2. EKG in acute pericarditis showing diffuse ST-segment elevations

Physical exam. A pericardial friction rub is nearly 100% specific for a pericarditis diagnosis, but sensitivity can vary (16% to 85%) depending on the frequency of auscultation and underlying etiology.2,5 It is thought to be caused by friction between the parietal and visceral layers of inflamed pericardium. A pericardial rub classically is described as a superficial, high-pitched, scratchy, or squeaking sound best heard with the diaphragm of the stethoscope at the lower left sternal border with the patient leaning forward.

Laboratory data. A complete blood count, metabolic panel, and cardiac enzymes should be checked in all patients with suspected acute pericarditis. Troponin values are elevated in up to one-third of patients, indicating cardiac muscle injury or myopericarditis, but have not been shown to adversely impact hospital length of stay, readmission, or complication rates.5,10 Markers of inflammation (e.g. erythrocyte sedimentation rate or C-reactive protein) are frequently elevated but do not point to a specific underlying etiology. Routine viral cultures and antibody titers are not useful.11

Most cases of pericarditis are presumed idiopathic (viral); however, finding a specific etiology should be considered in patients who do not respond after one week of therapy. Anti-nuclear antibody, complement levels, and rheumatoid factor can serve as screening tests for autoimmune disease. Purified protein derivative or quantiferon testing and HIV testing might be indicated in patients with appropriate risk factors. In cases of suspected tuberculous or neoplastic pericarditis, pericardial fluid analysis and biopsy could be warranted.

Electrocardiography. The EKG is the most useful test in diagnosing acute pericarditis. EKG changes in acute pericarditis can progress over four stages:

  • Stage 1: diffuse ST elevations with or without PR depressions, initially;
  • Stage 2: normalization of ST and PR segments, typically after several days;
  • Stage 3: diffuse T-wave inversions; and
  • Stage 4: normalization of T-waves, typically after weeks or months.

While all four stages are unlikely to be present in a given case, 80% of patients with pericarditis will demonstrate diffuse ST-segment elevations and PR-segment depression (see Figure 2, above).12

Table 3 lists EKG features helpful in differentiating acute pericarditis from acute myocardial infarction.

Chest radiography. Because a pericardial effusion often accompanies pericarditis, a chest radiograph (CXR) should be performed in all suspected cases. The CXR might show enlargement of the cardiac silhouette if more than 250 ml of pericardial fluid is present.3 A CXR also is helpful to diagnose concomitant pulmonary infection, pleural effusion, or mediastinal mass—all findings that could point to an underlying specific etiology of pericarditis and/or pericardial effusion.

Echocardiography. An echocardiogram should be performed in all patients with suspected pericarditis to detect effusion, associated myocardial, or paracardial disease.13 The echocardiogram frequently is normal but could show an effusion in 60%, and tamponade (see Figure 1, p. 15) in 5%, of cases.4

Computed tomography (CT) and cardiac magnetic resonance imaging (CMR).CT or CMR are the imaging modalities of choice when an echocardiogram is inconclusive or in cases of pericarditis complicated by a hemorrhagic or localized effusion, pericardial thickening, or pericardial mass.14 They also help in precise imaging of neighboring structures, such as lungs or mediastinum.

Pericardial fluid analysis and pericardial biopsy. In cases of refractory pericarditis with effusion, pericardial fluid analysis might provide clues to the underlying etiology. Routine chemistry, cell count, gram and acid fast staining, culture, and cytology should be sent. In addition, acid-fast bacillus staining and culture, adenosine deaminase, and interferon-gamma testing should be ordered when tuberculous pericarditis is suspected. A pericardial biopsy may show granulomas or neoplastic cells. Overall, pericardial fluid analysis and biopsy reveal a diagnosis in roughly 20% of cases.11

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Table 2. Specific causes of acute pericarditis

How is acute pericarditis treated?

Most cases of uncomplicated acute pericarditis are viral and respond well to NSAID plus colchicine therapy.2,4 Failure to respond to NSAIDs plus colchicine—evidenced by persistent fever, pericardial chest pain, new pericardial effusion, or worsening of general illness—within a week of treatment should prompt a search for an underlying systemic illness. If found, treatment should be aimed at the causative illness.

Bacterial pericarditis usually requires surgical drainage in addition to treatment with appropriate antibiotics.11 Tuberculous pericarditis is treated with multidrug therapy; when underlying HIV is present, patients should receive highly active anti-retroviral therapy as well. Steroids and immunosuppressants should be considered in addition to NSAIDs and colchicine in autoimmune pericarditis.10 Neoplastic pericarditis may resolve with chemotherapy but it has a high recurrence rate.13 Uremic pericarditis requires intensified dialysis.

Treatment options for uncomplicated idiopathic or viral pericarditis include:

NSAIDs. It is important to adequately dose NSAIDs when treating acute pericarditis. Initial treatment options include ibuprofen (1,600 to 3,200 mg daily), indomethacin (75 to 150 mg daily) or aspirin (2 to 4 gm daily) for one week.11,15 Aspirin is preferred in patients with ischemic heart disease. For patients with symptoms that persist longer than a week, NSAIDS may be continued, but investigation for an underlying etiology is indicated. Concomitant proton-pump-inhibitor therapy should be considered in patients at high risk for peptic ulcer disease to minimize gastric side effects.

Colchicine. Colchicine has a favorable risk-benefit profile as an adjunct treatment for acute and recurrent pericarditis. Patients experience better symptom relief when treated with both colchicine and an NSAID, compared with NSAIDs alone (88% versus 63%). Recurrence rates are lower with combined therapy (11% versus 32%).16 Colchicine treatment (0.6 mg twice daily after a loading dose of up to 2 mg) is recommended for several months to greater than one year.13,16,17

Glucocorticoids. Routine glucocorticoid use should be avoided in the treatment of acute pericarditis, as it has been associated with an increased risk for recurrence (OR 4.3).16,18 Glucocorticoid use should be considered in cases of pericarditis refractory to NSAIDs and colchicine, cases in which NSAIDs and or colchicine are contraindicated, and in autoimmune or connective-tissue-disease-related pericarditis. Prednisone should be dosed up to 1 mg/kg/day for at least one month, depending on symptom resolution, then tapered after either NSAIDs or colchicine have been started.13 Smaller prednisone doses of up to 0.5 mg/kg/day could be as effective, with the added benefit of reduced side effects and recurrences.19

Invasive treatment. Pericardiocentesis and/or pericardiectomy should be considered when pericarditis is complicated by a large effusion or tamponade, constrictive physiology, or recurrent effusion.11 Pericardiocentesis is the least invasive option and helps provide immediate relief in cases of tamponade or large symptomatic effusions. It is the preferred modality for obtaining pericardial fluid for diagnostic analysis. However, effusions can recur and in those cases pericardial window is preferred, as it provides continued outflow of pericardial fluid. Pericardiectomy is recommended in cases of symptomatic constrictive pericarditis unresponsive to medical therapy.15

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Table 3. EKG changes in acute pericarditis and myocardial infarction

Back to the Case

The patient’s presentation—prodrome followed by fever and pleuritic chest pain—is characteristic of acute idiopathic pericarditis. No pericardial rub was heard, but EKG findings were typical. Troponin I elevation suggested underlying myopericarditis. An echocardiogram was unremarkable. Given the likely viral or idiopathic etiology, no further diagnostic tests were ordered to explore the possibility of an underlying systemic illness.

The patient was started on ibuprofen 600 mg every eight hours. She had significant relief of her symptoms within two days. A routine fever workup was negative. She was discharged the following day.

The patient was readmitted three months later with recurrent pleuritic chest pain, which did not improve with resumption of NSAID therapy. Initial troponin I was 0.22 ng/ml, electrocardiogram was unchanged, and an echocardiogram showed small effusion. She was started on ibuprofen 800 mg every eight hours, as well as colchicine 0.6 mg twice daily. Her symptoms resolved the next day and she was discharged with prescriptions for ibuprofen and colchicine. She was instructed to follow up with a primary-care doctor in one week.

At the clinic visit, ibuprofen was tapered but colchicine was continued for another six months. She remained asymptomatic at her six-month clinic follow-up.

Bottom Line

Acute pericarditis is a clinical diagnosis supported by EKG findings. Most cases are idiopathic or viral, and can be treated successfully with NSAIDs and colchicine. For cases that do not respond to initial therapy, or cases that present with high-risk features, a specific etiology should be sought.


Dr. Southern is chief of the division of hospital medicine at Montefiore Medical Center in Bronx, N.Y. Dr. Galhorta is an instructor and Drs. Martin, Korcak, and Stehlihova are assistant professors in the department of medicine at Albert Einstein.

References

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