Pediatric Constrictive Pericarditis Workup

  • Author: Brian D Soriano; Chief Editor: Stuart Berger, MD   more...
 
Updated: May 11, 2012
 

Laboratory Studies

CBC count

A CBC count may reveal evidence of dilutional anemia when CHF is also present.

Leukocytosis may be evident if an infectious, bacteriologic, or rheumatologic source is the etiology or if patients are receiving treatment with steroid therapy.

Leukopenia may be present in patients in whom chemotherapeutic agents are administered for malignancy.

Electrolyte, BUN, and creatinine levels

Dilution secondary to CHF may demonstrate hyponatremia or pseudohyponatremia.

Contraction alkalosis (ie, hypochloremia with hypercarbia) may occur when diuretics are aggressively used.

With renal insufficiency, short-term elevation of the BUN levels and long-term elevation of creatinine levels are observed.

ABG

Metabolic acidosis (ie, low pH and low bicarbonate) with or without compensatory respiratory alkalosis (ie, decreased partial pressure of carbon dioxide) is frequently observed with right-sided CHF.

Liver function profile

Passive hepatic congestion from cor pulmonale may cause elevated transaminase levels.

Hypoalbuminemia is the hallmark of a protein-losing enteropathy (PLE) that results from increased central venous pressure in the portal system of patients with hepatomegaly and ascites. In patients in whom PLE is suspected, stool α 1 -antitrypsinase should be measured.

Acute phase reactants

Erythrocyte sedimentation rate and C-reactive protein level may be elevated in postpericardiotomy syndrome.

Brain natriuretic peptide (BNP) [3]

Although elevated levels greater than 600 pg/mL can help differentiate constrictive pericarditis from restrictive cardiomyopathy in adults, no data are available in children.

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Imaging Studies

Two-dimensional echocardiography

A thickened pericardium may be observed. Systemic veins may be dilated. The echocardiogram may reveal diminished intraventricular volumes.

Pericardial effusions are easily depicted with this modality.

Interventricular septal motion may be paradoxic or flat as a sign of ventricular interdependence.

The inspiratory increase in chamber size is larger in patients with constrictive pericarditis than in those with restrictive cardiomyopathy.

Pulsed-wave Doppler echocardiography

Transmitral and transtricuspid early diastolic filling (E wave) is rapid with a shortened deceleration time; no significant change occurs in the atrial-filling phase (A wave).

As opposed to restrictive cardiomyopathy, respiratory variation in the filling phases is more pronounced.

Transmitral peak E velocity has a more pronounced decrease during inspiration in patients with constrictive pericarditis than in healthy persons and patients with restrictive cardiomyopathy.

Peak E and peak A tricuspid velocities are significantly increased during inspiration.

Isovolumetric relaxation time (IVRT) is also affected by respiratory variation in constrictive pericarditis, with an increase of more than 25% during inspiration.

During constriction, the pulmonary venous flow pattern demonstrates systolic and diastolic forward flow, with a marked decrease in diastolic flow on inspiration and an increase on expiration. This measurement may help determine if a pseudonormalized diastolic pattern is present on the mitral inflow tracing.

In the pediatric population, no single Doppler measurement can fully characterize left ventricular diastolic function, and no single measurement is free of confounding factors. Most of the parameters are dependent on load, heart rate, and age. In addition, indices of constriction in adults, such as hepatic vein flow reversal and alterations in pulmonary venous Doppler patterns, are complicated by the fact that such patterns are detected in healthy children.

Tissue Doppler echocardiography (TDE)

TDE is useful in distinguishing constrictive versus restrictive physiology. Early mitral annular velocity is usually reduced in restriction, whereas it is normal in constrictive pericarditis.

Chest radiography

Radiographic findings are usually unremarkable.

Pericardial calcifications are present in 40-50% of patients.

MRI

MRI can reveal pericardial thickening (see image below), right atrial dilation, and a characteristic intraventricular septal "bounce" in early diastole.

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Cardiac CT

Both CT and MRI can detect a thickened pericardium (≥ 4 mm), but this is an insensitive finding. The absence of pericardial thickening does not rule out hemodynamically significant restrictive pericarditis.

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Other Tests

Electrocardiography

ECG usually reveals nonspecific ST-T wave changes. Atrial dysrhythmias are common. QRS complexes may demonstrate low voltage.

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Procedures

Diagnostic cardiac catheterization

Cardiac catheterization can be performed to measure intracardiac pressures. The hallmark finding in patients with chronic constrictive pericarditis is elevation of end-diastolic pressures, which are at equal levels in the right atrium, right ventricle, pulmonary artery, left atrium, and left ventricle.

Loss or reversal of respiratory variation of right atrial pressure is noted. When hemodynamic studies are equivocal, response to bolus fluid administration is recorded.

The intraventricular pressure pulse contour characteristically reveals an early rapid fall in diastolic pressure in the right ventricle, followed by a rapid rise to an elevated diastolic plateau (square root sign). The left ventricular pressure pulse tracing is usually similar.

Pulmonary artery systolic pressure should be less than 50 mm Hg. Higher pressures may suggest other diseases, such as restrictive cardiomyopathy and pulmonary arteriolar hypertension.

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Histologic Findings

Myocardial histologic findings include fibrotic thickening, chronic inflammation, granulomas, and calcification.

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Contributor Information and Disclosures
Author

Brian D Soriano  MD, Assistant Professor of Pediatrics, Cardiology Division, University of Washington School of Medicine; Attending Physician, Pediatric Cardiology and Cardiac Imaging, Seattle Children's Hospital

Brian D Soriano is a member of the following medical societies: American Heart Association, American Medical Association, and American Society of Echocardiography

Disclosure: Nothing to disclose.

Coauthor(s)

Charles I Berul, MD  Professor of Pediatrics and Integrative Systems Biology, George Washington University School of Medicine; Chief, Division of Cardiology, Children's National Medical Center

Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, Pediatric and Congenital Electrophysiology Society, and Society for Pediatric Research

Disclosure: Johnson & Johnson Consulting fee Consulting

Renee E Margossian, MD  Instructor, Department of Cardiology, Children's Hospital, Harvard University; Consulting Staff, Department of Cardiology, Boston Medical Center and Brigham and Women's Hospital

Renee E Margossian, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Society of Echocardiography, and Heart Failure Society of America

Disclosure: Nothing to disclose.

Kurt Pflieger, MD, FAAP  Active Staff, Department of Pediatrics, Lake Pointe Medical Center

Kurt Pflieger, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Christopher Johnsrude, MD, MS  Chief, Division of Pediatric Cardiology, University of Louisville School of Medicine; Director, Congenital Heart Center, Kosair Children's Hospital

Christopher Johnsrude, MD, MS is a member of the following medical societies: American Academy of Pediatrics and American College of Cardiology

Disclosure: St Jude Medical Honoraria Speaking and teaching

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Hugh D Allen, MD  Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine

Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, and Western Society for Pediatric Research

Disclosure: Nothing to disclose.

Gilbert Z Herzberg, MD  Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center

Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD  Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Additional Contributors

The authors would like to thank Kurt Pflieger, MD, FAAP for his significant contributions and original work for this article.

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MRI image of constrictive pericarditis in a 13-year-old and an otherwise structurally normal heart. Infectious workup was negative. (Image courtesy of Tal Geva, M.D.)
Left ventricular volume curve in constrictive pericarditis.
 
 
 
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