eMedicine Specialties > Cardiology > Pericardial Disease

Pericarditis, Acute: Differential Diagnoses & Workup

Author: Sean Spangler, MD, Cardiology Fellow, Brooke Army Medical Center
Coauthor(s): Garrett S Lynchard, MD, Consulting Cardiologist, Brooke Army Medical Center, Fort Sam Houston; Philip J Gentlesk, MD, Director, Cardiac Electrophysiology, Section of Cardiovascular Disease, Brooke Army Medical Center
Contributor Information and Disclosures

Updated: Mar 3, 2008

Differential Diagnoses

Aortic Dissection
Myocardial Infarction
Coronary Artery Vasospasm
Myocardial Ischemia
Esophageal Rupture
Peptic Ulcer Disease
Esophageal Spasm
Pulmonary Embolism
Esophagitis
Gastritis, Acute

Other Problems to Be Considered

Chest pain

Workup

Laboratory Studies

  • CBC count with differential may show leukocytosis.
  • Erythrocyte sedimentation rate and C-reactive protein levels are usually elevated.
  • BUN and creatinine levels can be measured to evaluate for uremia.
  • Evaluate cardiac biomarkers for associated myocarditis or myocardial infarction. In a recent study by Imazio and colleagues, an elevated troponin I level was found in 32% of patients with viral or idiopathic pericarditis. In this study, the troponin I level was related to the extent of myocardial inflammation but was not a negative prognostic marker.7
  • Further laboratory work may be clinically indicated.
    • Evaluate blood and/or viral cultures.
    • Perform tuberculin testing with sputum for acid-fast bacilli if the illness exceeds one week in duration.
    • Obtain an antistreptolysin titer.
    • Obtain rheumatoid factor, antinuclear antibody, and anti-DNA values, particularly if the illness is prolonged or severe.
    • Evaluate thyroid function in patients with severe pericardial effusion.

Imaging Studies

  • Chest radiography  
    • A flask-shaped, enlarged cardiac silhouette may be the first indication of a large pericardial effusion.
    • Patients with small effusions (less than a few hundred milliliters) may present with a normal cardiac silhouette.
    • In one study, pleural effusions were seen in 33% of patients. Approximately 75% of the effusions were left-sided only.
  • Echocardiography
    • Echocardiography is recommended in all cases. Any form of pericardial inflammation can induce pericardial effusion.
    • Echocardiography is performed urgently if tamponade is suspected.
    • Echocardiography is particularly helpful if pericardial effusion is suspected on clinical or radiographic grounds, the illness lasts longer than 1 week, or myocarditis or purulent pericarditis is suspected.
    • M-mode demonstrates persistence of the echo-free space between the parietal pericardium and the epicardium during the cardiac cycle.
    • Fluid is distributed from the posterobasal left ventricle apically and anteriorly, then laterally and posteriorly to the left atrium. Fluid adjacent to the right atrium is an early indicator of an effusion. Other causes of echo-free space that must be considered include pleural effusion, pericardial masses, and epicardial fat.
    • To a limited extent, an echocardiogram can characterize the effusion. Thin fibrous strands within the pericardial space can be seen in acute effusive pericarditis. Shaggy exudate may indicate a potentially difficult pericardiocentesis, but this finding is not diagnostic.
    • Echocardiography can also be used to evaluate for chamber size, tamponade, and ventricular dysfunction.
  • Computed tomography
    • Effusions are easily detected through different x-ray coefficients of fluid and the pericardium.
    • Similarly, the nature of the effusion may be surmised, given the different attenuation coefficients for blood, exudate, chyle, and serous fluid.
    • Hemopericardium may be difficult to assess without intravenous contrast because blood has the same radiodensity as myocardium.
  • Magnetic resonance imaging: This is a sensitive technique for detecting pericardial effusion and loculated pericardial effusion and thickening.

Other Tests

  • Electrocardiography
    • Classic acute pericarditis evolves through 4 stages (see Image 1, Image 2, Image 3, and Image 4).
    • Stage 1 accompanies the onset of acute pain and is the hallmark of acute pericarditis. ECG changes include diffuse concave upward ST elevation, except aVR and V1 (usually depressed). T waves are upright in the leads with ST elevation, and the PR segment deviates opposite to P-wave polarity.
    • Stage 2 occurs several days later with the return of the ST segment to baseline, followed by flattening of the T waves.
    • In stage 3, T waves become inverted.
    • Finally, in stage 4, the ECG returns to the prepericarditis baseline weeks to months after the onset. The T-wave inversion may persist indefinitely in the chronic inflammation observed with tuberculosis, uremia, or neoplasm.
    • Electrical alternans, the beat-to-beat variability in QRS voltage caused by excessive cardiac mobility, may be seen with an effusion.

Procedures

  • Cardiac catheterization
    • This is used for tamponade.
    • It can evaluate constrictive pericarditis versus restrictive cardiomyopathy.
  • Pericardiocentesis
    • Blind percutaneous pericardial puncture increases the risk of complication to 5-50% and should be performed only in an emergency. Complications include fatal cardiac laceration.
    • Conversely, pericardiocentesis is relatively safe when guided by echocardiography, especially with large free anterior effusion. One study noted only 3 minor complications in 117 procedures with ultrasound guidance.
    • In a large study, diagnostic pericardiocentesis led to a diagnosis in only 6% of cases, versus 29% diagnosed with therapeutic pericardiocentesis. As such, pericardiocentesis should not be performed unless tamponade or suspected purulent pericarditis is present.
    • If a pericardiocentesis is performed for drainage, an indwelling catheter should be placed in the pericardial space for continued drainage over several days. If the catheter continues to drain a large amount, a more definitive procedure should be performed.
    • The pericardial fluid should be analyzed for red cells, total protein level, lactic acid dehydrogenase level, adenosine deaminase activity, and culture (ordinary and Loewenstein media). Directly investigate for tuberculous bacilli and perform a cytologic study.
  • Pericardial window
    • This procedure, in which only 9 cm2 or less of pericardium is resected, is used for effusive pericarditis therapy.
    • In critically ill patients, a balloon catheter may be used to create a pericardial window.
    • Some studies note the need for repeat operation in nearly 25% of patients who undergo the procedure at 2 years.
  • Pericardiectomy
    • This is used for constrictive pericarditis, effusive pericarditis, or recurrent pericarditis with multiple attacks, steroid dependence, and/or intolerance to other medical management.
    • Studies demonstrate that failure rates are proportional to the amount of pericardium removed (ie, the more pericardium removed, the less likely the procedure will fail). In effusive pericarditis, the higher failure rate associated with a pericardial window or partial pericardiectomy is likely secondary to the continued fluid production from the remaining pericardium, with sealing of the remaining pericardium to the heart.
    • The operative mortality rate was 14% in one series, with a range of 1% for New York Heart Association class 1-2, 10% for class 3, and 46% for class 4. The 5-year survival rate was 80% for class 3-4 and approximately 95% for 1-2.
    • As with pericardiocentesis, studies involving pericardiectomy note a greatly improved diagnostic yield if pericardial biopsy is performed as part of a therapeutic procedure. Diagnostic biopsies yielded 5%, whereas therapeutic biopsies were at 22-54%.

More on Pericarditis, Acute

Overview: Pericarditis, Acute
Differential Diagnoses & Workup: Pericarditis, Acute
Treatment & Medication: Pericarditis, Acute
Follow-up: Pericarditis, Acute
Multimedia: Pericarditis, Acute
References

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Further Reading

Keywords

acute pericarditis, pericardial disease, pericardium, heart disease, cardiac disease, inflamed pericardium, pericardial inflammation, chest pain, pericardial friction rub, heart infection, cardiac infection, pericardial infection, tuberculosis, bacterial heart infection, viral heart infection, rheumatoid arthritis, systemic lupus erythematosus, lupus erythematosus, SLE, scleroderma, sarcoidosis, rheumatic fever, renal failure, kidney failure, hypothyroidism, cholesterol pericarditis, myocardial infarction, Dressler syndrome, cardiac neoplasm, pericardiocentesis

Contributor Information and Disclosures

Author

Sean Spangler, MD, Cardiology Fellow, Brooke Army Medical Center
Sean Spangler, MD is a member of the following medical societies: American College of Cardiology and American College of Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Garrett S Lynchard, MD, Consulting Cardiologist, Brooke Army Medical Center, Fort Sam Houston
Garrett S Lynchard, MD is a member of the following medical societies: American College of Cardiology and American College of Physicians
Disclosure: Nothing to disclose.

Philip J Gentlesk, MD, Director, Cardiac Electrophysiology, Section of Cardiovascular Disease, Brooke Army Medical Center
Philip J Gentlesk, MD is a member of the following medical societies: American College of Cardiology, Christian Medical & Dental Society, and Heart Rhythm Society
Disclosure: Nothing to disclose.

Medical Editor

Hanumant Deshmukh, MD †, Former Chief of Cardiology, Veterans Affairs Medical Center; Former Associate Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Steven J Compton, MD, FACC, FACP, Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals
Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, and Heart Rhythm Society
Disclosure: Nothing to disclose.

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

George A Stouffer III, MD, Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center
George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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