eMedicine Specialties > Cardiology > Pericardial Disease

Pericarditis, Constrictive-Effusive: Differential Diagnoses & Workup

Author: D Dirk Bonnema, MD, Cardiology Fellow, Division of Cardiology, Department of Medicine, Medical University of South Carolina; Research Fellow, Division of Cardiology, Department of Medicine, Medical University of South Carolina
Coauthor(s): Terrence X O'Brien, MD, FACC, Office of Research and Development, Ralph H Johnson Veterans Affairs Medical Center; Professor, Department of Medicine, Division of Cardiology, Medical University of South Carolina
Contributor Information and Disclosures

Updated: Aug 26, 2008

Differential Diagnoses

Breast Cancer
Pericardial Effusion
Cardiac Tamponade
Pericarditis, Acute
Cardiomyopathy, Restrictive
Pericarditis, Constrictive
Hypothyroidism
Pericarditis, Uremic
Myocardial Infarction
Tuberculosis
Penetrating Chest Trauma
Uremia

Other Problems to Be Considered

Postradiation syndromes
Neoplasias (metastatic)
Hematologic neoplasias
Immunocompromised states with infection
Connective tissue disease

Workup

Laboratory Studies

  • Laboratory studies for effusive-constrictive pericarditis include tests of serum CBC with differential, serum chemistries with additions depending on the suspected etiology.
  • The most important laboratory studies are those performed on pericardial fluid (always under the assumption that pericardiocentesis is clinically indicated). Hematocrit and cell count with differential, culture (including tuberculosis), glucose, total protein, enzymes (lactate dehydrogenase, adenosine deaminase), Gram staining, and cytology should always be sent on an initial pericardiocentesis.19
  • Other more specific laboratory testing is determined by the priorities of the differential diagnosis.
    • Suspected tuberculosis pericarditis - Purified protein derivative of tuberculin (PPD), appropriate staining of pericardial fluid
    • Suspected infectious pericarditis - Serum aerobic and anaerobic blood cultures, viral titers, or polymerase chain reaction (PCR) of pericardial fluid
    • Suspected malignancy - Pericardial fluid for tumor markers or carbohydrate antigens (CAs, eg, CA-125)
    • Suspected HIV pericarditis - Serum HIV testing
    • Suspected hypothyroid related pericarditis - Serum thyroid function testing
    • Suspected connective tissue disease - Serum connective tissue serologies

Imaging Studies

  • Chest radiography
    • The chest radiograph may consistently show an enlarged cardiac silhouette when the pericardial effusion is greater than 250 mL. The cardiac silhouette may be flask shaped and the lung fields without evidence of congestion, consistent with the absence of a congestive cardiomyopathy.
    • These findings must be interpreted with caution, as they may also be observed in severe aortic insufficiency, congestive heart failure with severe tricuspid insufficiency, severe volume overload, or mitral regurgitation. However, the distinguishing characteristic is that pulmonary vascular congestion may be present with any of these and congestion is usually absent in pericardial disease.
    • A small effusion may have a normal cardiac silhouette. This does not eliminate the diagnosis of effusive-constrictive pericarditis.
  • Echocardiography
    • Echocardiography is the most efficient way to detect an effusion because it has excellent sensitivity and specificity.15,20
    • Pericardial fluid is easily observed as an echolucent region (echo-free space) between the visceral pericardium (epicardium) and the parietal pericardium.
    • The size of the effusion may be estimated, even if the effusion is localized. For example, small effusions usually must be observed in 2 views, particularly behind the left ventricle. Moderate effusions are visualized circumferentially, and large effusions exceed 1.0 cm in thickness on all views.
    • Evidence for cardiac tamponade may be inferred from the echocardiogram. For example, early diastolic collapse of right ventricular free wall and/or late diastolic collapse of right atrium may be observed (see Cardiac Tamponade). Doppler investigation may demonstrate increased respiratory variation of mitral and tricuspid inflow, consistent with constrictive pericarditis. Other echocardiographic findings consistent with constrictive pericarditis include abnormal septal and posterior wall motion noted in the M-mode by using a parasternal short-axis view, a normal velocity of propagation (V p) in color M-Mode, and a normal or supranormal early relaxation (Ea) on tissue Doppler imaging (see Pericarditis, Constrictive).
    • A pericardial effusion can be distinguished from a pleural effusion with echocardiography (where pericardial effusions are anterior to the descending aorta).
  • CT, PET, and MRI
    • The diagnosis of effusive-constrictive pericarditis cannot be made primarily on the basis of CT or MRI findings. However, CT and MRI may provide excellent images of the pericardium and associated mediastinal structures.
    • CT and MRI can be used to effectively image and confirm a thickened pericardium or detect a pericardial effusion if visualization with echocardiography is suboptimal (see Pericarditis, Constrictive).
    • 18 F-2-deoxyglucose (FDG) positron emission tomography has been reported for the assessment of pericardial inflammation. The clinical use of PET imaging in effusive-constrictive pericarditis remains untested.21
    • Some patients with effusive-constrictive pericarditis may have normal pericardial thickness; therefore, the diagnosis of effusive-constrictive pericarditis must be made hemodynamically.

Other Tests

  • Electrocardiography
    • The ECG may not show any specific findings for effusive-constrictive pericarditis. However, the ECG may show changes in the ST segment, T wave, or PR segment and/or low QRS voltage associated with pericarditis and/or effusion.
    • Nonspecific ST- and T-wave abnormalities may be present.
    • With a large effusion, a cardiac rocking motion may be observed on the ECG as electrical alternans.

Procedures

  • Cardiac catheterization and invasive hemodynamics
    • The diagnosis of effusive-constrictive pericarditis is suspected clinically but definitively established by recording right heart and intrapericardial pressures before and after pericardiocentesis.1
    • Before pericardial fluid is removed, cardiac tamponade (or near tamponade) hemodynamic physiology must be present to make the diagnosis of effusive-constrictive pericarditis. Hemodynamic pressure recordings would indicate elevated and equal (or nearly equal) intrapericardial pressures, right atrial and end-diastolic right and left ventricular pressures. There is usually an inspiratory decreased in right-heart filling pressures. A prominent x descent and absent y descent may also be noted.
    • Pericardiocentesis should decrease intrapericardial pressure to zero but may fail to restore cardiac hemodynamics to normal. This is because the visceral constrictive component of the syndrome causes a persistent elevation and equalization of intracardiac diastolic pressures. This constrictive physiology unveils a biphasic pressure tracing in the right atrium, now with a prominent y descent and dip-and-plateau right ventricular pressure tracings, with absent or minimal respiratory variation.
    • Put another way, persistent constriction after pericardiocentesis suggests a constrictive visceral pericardium and thus the diagnosis of effusive-constrictive pericarditis.
  • Pericardiocentesis as a diagnostic test may have a low yield, yet as a therapeutic procedure its diagnostic benefit is much improved. The risks and benefits of any invasive procedure must be considered before the start of testing (see Pericardiocentesis).
  • Pericardial biopsy
    • Clinical circumstances determine when a biopsy is performed since procedural risk is increased. Factors include how symptomatic the patient is and how likely a finding would change clinical management.
    • Pericardioscopy is a developing technique that allows direct viewing of the epicardium with the possibility for biopsy. This is currently an experimental technique.22

Histologic Findings

Pericardial biopsy samples may be examined for malignancy and inflammation by traditional and immunohistologic means. In advanced laboratories, polymerase chain reaction or in situ hybridization may be used to analyze for microbial DNA or RNA. Combined examination of pericardial fluid and biopsy results provides the greatest yield.

More on Pericarditis, Constrictive-Effusive

Overview: Pericarditis, Constrictive-Effusive
Differential Diagnoses & Workup: Pericarditis, Constrictive-Effusive
Treatment & Medication: Pericarditis, Constrictive-Effusive
Follow-up: Pericarditis, Constrictive-Effusive
References

References

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  2. Little WC, Freeman GL. Pericardial disease. Circulation. Mar 28 2006;113(12):1622-32. [Medline].

  3. Hancock EW. Subacute effusive-constrictive pericarditis. Circulation. Feb 1971;43(2):183-92. [Medline].

  4. Hoit BD. Management of effusive and constrictive pericardial heart disease. Circulation. Jun 25 2002;105(25):2939-42. [Medline].

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  12. Spodick DH. The Pericardium: A Comprehensive Textbook. New York, NY: Marcel Dekker; 1997:260-452.

  13. Shabetai R. Pericardial Disease: Etiology, Pathophysiology, Clinical Recognition, and Treatment. New York, NY: Churchill Livingstone; 1995:1024-35.

  14. Sagrista-Sauleda J, Angel J, Sanchez A, et al. Effusive-constrictive pericarditis. N Engl J Med. 2004;350(5):469-75. [Medline].

  15. Zagol B, Minderman D, Munir A, D'Cruz I. Effusive constrictive pericarditis: 2D, 3D echocardiography and MRI imaging. Echocardiography. Nov 2007;24(10):1110-4. [Medline].

  16. Akhter MW, Nuño IN, Rahimtoola SH. Constrictive pericarditis masquerading as chronic idiopathic pleural effusion: importance of physical examination. Am J Med. Jul 2006;119(7):e1-4. [Medline].

  17. Rafailidis PI, Prapas SN, Kasiakou SK, Costeas XF, Falagas ME. Effusive-constrictive calcific pericarditis associated with Streptococcus salivarius. Case report and review of the literature. Cardiol Rev. May-Jun 2005;13(3):113-7. [Medline].

  18. Fowler NO, Manitsas GT. Infectious pericarditis. Prog Cardiovasc Dis. Nov-Dec 1973;16(3):323-36. [Medline].

  19. Maisch B, Seferovic PM, Ristic AD, Erbel R, Rienmüller R, Adler Y. Guidelines on the diagnosis and management of pericardial diseases executive summary; The Task force on the diagnosis and management of pericardial diseases of the European society of cardiology. Eur Heart J. Apr 2004;25(7):587-610. [Medline].

  20. Feigenbaum H, Armstrong W. Pericardial diseases. In: Feigenbaum's Echocardiography. 6th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2004:260-9.

  21. Ha JW, Lee JD, Ko YG, Yun M, Rim SJ, Chung N. Images in cardiovascular medicine. Assessment of pericardial inflammation in a patient with tuberculous effusive constrictive pericarditis with 18F-2-deoxyglucose positron emission tomography. Circulation. Jan 3 2006;113(1):e4-5. [Medline].

  22. Maisch B, Pankuweit S, Brilla C, et al. Intrapericardial treatment of inflammatory and neoplastic pericarditis guided by pericardioscopy and epicardial biopsy: results from a pilot study. Clin Cardiol. Jan 1999;22(1 Suppl 1):I17-22. [Medline].

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Further Reading

Keywords

constrictive-effusive pericarditis, pericarditis, pericardial effusion, pericardial constriction, transudative pericardial effusion, exudative pericardial effusion, sanguineous pericardial effusion, chylous pericardial effusion, chronic effusive pericarditis, chronic pericardial effusion, visceral pericardial constriction, constrictive pericarditis, subacute pericarditis

Contributor Information and Disclosures

Author

D Dirk Bonnema, MD, Cardiology Fellow, Division of Cardiology, Department of Medicine, Medical University of South Carolina; Research Fellow, Division of Cardiology, Department of Medicine, Medical University of South Carolina
D Dirk Bonnema, MD is a member of the following medical societies: South Carolina Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Terrence X O'Brien, MD, FACC, Office of Research and Development, Ralph H Johnson Veterans Affairs Medical Center; Professor, Department of Medicine, Division of Cardiology, Medical University of South Carolina
Terrence X O'Brien, MD, FACC is a member of the following medical societies: American College of Cardiology, American Heart Association, American Society of Echocardiography, Heart Failure Society of America, and South Carolina Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Eric Vanderbush, MD, Chief, Department of Internal Medicine, Division of Cardiology, Clinical Assistant Professor, Harlem Hospital Center and Columbia University
Eric Vanderbush, MD is a member of the following medical societies: American College of Cardiology and American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Ronald J Oudiz, MD, Director of Pulmonary Hypertension, Associate Professor, Department of Medicine, Division of Cardiology, Harbor-UCLA Medical Center, David Geffen School of Medicine at UCLA
Ronald J Oudiz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Heart Association
Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria

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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