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Postpericardiotomy Syndrome

  • Author: M Silvana Horenstein, MD; Chief Editor: Howard S Weber, MD, FSCAI  more...
Updated: Dec 10, 2015


Postpericardiotomy syndrome (PPS) is a febrile illness secondary to an inflammatory reaction involving the pleura and pericardium.[1, 2] It is more common in patients who have undergone surgery that involves opening the pericardium (in the United States, the estimated frequency varies from 2% to 30% of these patients). However, postpericardiotomy syndrome has also been described following myocardial infarction (Dressler syndrome) and as an unusual complication after percutaneous procedures such as coronary stent implantation,[3] after implantation of epicardial pacemaker leads[4] and transvenous pacemaker leads,[5, 6, 7, 8, 9] and following blunt trauma,[10] stab wounds,[11] and heart puncture.[12]

Pericardial effusions often accompany the syndrome and may develop into early or late postoperative cardiac tamponade[13] and even recurrent cardiac tamponade.[14] The syndrome is also characterized by pericardial or pleuritic pain, friction rubs, pleural effusions, pneumonitis, and abnormal ECG and radiography findings (see Workup).

PPS usually occurs as a single episode; however, it can recur years later.[15] It is uncommon in patients younger than 2 years,[16]  but the frequency increases in children and adults to as much as 30%. It is more common after repair of tetralogy of Fallot, repair of atrial and ventricular septal defects,[17] and after cardiac transplantation.[18]

It is essential that clinicians diagnose and adequately treat PPS as well as recognize and treat impending or manifest cardiac tamponade.




Postpericardiotomy syndrome is often associated with the development of antiheart antibodies.[19] Various viral agents, including coxsackie B, adenovirus, and cytomegalovirus, have been present in approximately two thirds of patients with postpericardiotomy syndrome, suggesting an autoimmune response associated with a viral infection. However, a prospective study found no evidence to support a viral etiology for postpericardiotomy syndrome.[20] This study suggested that the use of viral titers in the setting of cardiopulmonary bypass and recent blood transfusions is unreliable.



The precise etiology of postpericardiotomy syndrome is not known. Postpericardiotomy syndrome is postulated to be an autoimmune response involving autoantibodies which target antigens exposed after the percardium has been damaged.[19]

In a study of patients who had developed postpericardiotomy syndrome after transplantation, an increased proportion of activated helper T cells (CD4+/25+) and cytotoxic T cells (Leu-7+/CD8+) was found. This led to conclude that, in this population, postpericardiotomy syndrome was possibly secondary to cell-mediated immunity.[18]



Most cases of postpericardiotomy syndrome resolve within a few weeks. Rarely, symptoms may occur for more than 6 months.

Relapse may occur after tapering anti-inflammatory medications. Relapse is estimated to occur in 10-15% of patients. Most recurrences occur within 6 months of the initial surgery.


Postpericardiotomy syndrome usually manifests as a mild, self-limited inflammatory illness. Life-threatening pericardial tamponade can develop due to a rapidly increasing pericardial effusion. Tamponade occurs in less than 1% of patients with postpericardiotomy syndrome. Elevation of cardiac filling pressures, progressive limitation of ventricular diastolic filling, and reduction of stroke volume and cardiac output characterize cardiac tamponade.  This also correlates with the rapidity of pericardial effusion accumulation, because slow accumulation of even large pericardial effusions may not result in clinical signs and symptoms of tamponade.


Cardiac tamponade is a life-threatening complication of postpericardiotomy syndrome. Emergent pericardiocentesis and drainage of pericardial effusion is necessary. Tamponade occurs in approximately 1% of patients with postpericardiotomy syndrome.

Constrictive pericarditis occurs late postoperatively in fewer than 0.5% of patients but may not be related to postpericardiotomy syndrome. The high prevalence of postpericardiotomy syndrome and quite low prevalence of constriction suggests that a direct association is unlikely. With constriction, the pericardium becomes thickened and adherent to the heart and restricts filling of the ventricles. A pericardiectomy may be required for treatment.

Patients with pain from the inflammatory response may demonstrate splinting during breathing. This can result in hypoxemia. Monitor oxygen saturation by pulse oximetry in patients presenting with these findings.

Coronary artery bypass grafting is an unusual procedure in children. Occlusion of the graft is reported as a rare, but fatal, complication of postpericardiotomy syndrome.

Contributor Information and Disclosures

M Silvana Horenstein, MD Assistant Professor, Department of Pediatrics, University of Texas Medical School at Houston; Medical Doctor Consultant, Legacy Department, Best Doctors, Inc

M Silvana Horenstein, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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 Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, Western Society for Pediatric Research, American College of Cardiology, American Heart Association, American Pediatric Society

Disclosure: Nothing to disclose.

Chief Editor

Howard S Weber, MD, FSCAI Professor of Pediatrics, Section of Pediatric Cardiology, Pennsylvania State University College of Medicine; Director of Interventional Pediatric Cardiology, Penn State Hershey Children's Hospital

Howard S Weber, MD, FSCAI is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, Society for Cardiovascular Angiography and Interventions

Disclosure: Received income in an amount equal to or greater than $250 from: St. Jude Medical.

Additional Contributors

Ira H Gessner, MD Professor Emeritus, Pediatric Cardiology, University of Florida College of Medicine

Ira H Gessner, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, Society for Pediatric Research

Disclosure: Nothing to disclose.


The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous authors Kelly S Skoumal, DO, MS, FAAP; John W Graneto, DO, FACEP, FAAP; and David A Lewis, MD, FAAP, FACC, to the original writing and development of this article.

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Upright chest radiograph in a 3-year-old child with dyspnea and fever reveals a large opacity on the left, with obliteration of the left costophrenic angle and a fluid stripe. These findings indicate a pleural effusion.
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