Ann Thorac Surg 2004;78:1684-1687
© 2004 The Society of Thoracic Surgeons
Original article: cardiovascular
Postpericardiotomy Syndrome After Permanent Pacemaker Implantation in Children and Young Adults
Ilana Zeltser, MDa,*,
Larry A. Rhodes, MDa,
Ronn E. Tanel, MDa,
Victoria L. Vetter, MDa,
J. William Gaynor, MDb,
Thomas L. Spray, MDb,
Mitchell I. Cohen, MDa
a Division of Cardiology, The Children's Hospital of Philadelphia and the University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
b Division of Cardiothoracic Surgery, The Children's Hospital of Philadelphia and the University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
Accepted for publication May 3, 2004.
* Address reprint requests to Dr Zeltser, Division of Cardiology, The Children's Hospital of Philadelphia, 34th and Civic Center Blvd, Philadelphia, PA, USA 19104
zeltser{at}email.chop.edu
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Abstract
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BACKGROUND: Postpericardiotomy syndrome (PPS) occurs in 10% to 50% of pediatric patients after cardiac surgery. The incidence and outcome of PPS after permanent pacemaker implantation in children is not described.
METHODS: A retrospective analysis was performed of all pediatric patients who underwent isolated placement of a pacemaker between January 1984 and December 2002. Patients who underwent congenital heart surgery at the time of pacemaker implantation were excluded. PPS was diagnosed on the basis of clinical symptoms with echocardiographic confirmation of a pericardial effusion.
RESULTS: Four hundred and forty-three pacemakers (237 epicardial, 206 transvenous) were implanted in 370 patients (median age 10 years, range 2 months to 24 years). Eight (2%) episodes of PPS (6 epicardial, 2 transvenous) occurred in 7 patients. The median time from implantation to PPS was 12.5 days (range 8 to 22 days). Six (75%) episodes followed primary pacemaker implantation, two occurred after subsequent lead revision. Three patients were initially treated with medical therapy (1 nonsteroidal agents, 2 steroids), and 1 required subsequent pericardiocentesis. Five patients underwent initial pericardiocentesis followed by medication. One patient had echocardiographic recurrence of a pericardial effusion 3 weeks after a nonsteroidal taper, with resolution after nonsteroidal agents were reinitiated. One patient required a pericardial window for a persistent effusion. No pacemaker was explanted.
CONCLUSIONS: PPS occurred in 2% of children undergoing isolated pacemaker implantation of both epicardial and transvenous systems. PPS is usually managed successfully with medical therapy. Patients with medical treatment failure were successfully treated with pericardiocentesis or the surgical creation of a pericardial window.
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Introduction
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Postpericardiotomy syndrome (PPS) is a well-described phenomenon that frequently occurs after cardiac surgical procedures during which the integrity of the pericardium is compromised, resulting in the accumulation of fluid in the pericardial space [1, 2]. Patients with PPS typically present with fever and chest pain and occasionally, with evidence of cardiovascular compromise if a significant pericardial effusion is present. Often, PPS is managed successfully with medical therapy that includes both antiinflammatory agents and diuretics. The consideration of pericardiocentesis or open drainage is warranted in a patient who fails to respond to medical treatment or who evidences progressive hemodynamic compromise.
Postpericardiotomy syndrome has been reported in 10% to 50% of patients after cardiac surgery [3]. Although anecdotal cases of PPS have been reported after pacemaker implantation in adults [49], the incidence and clinical outcome in children and young adults has not been described.
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Patients and Methods
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After Institutional Review Board approval was obtained, patient charts and the pacemaker database were reviewed to identify all pediatric and young adult patients who underwent isolated pacemaker implantation, including both primary implantation as well as lead revision, between January 1984 and December 2002 at Children's Hospital of Philadelphia. Patients who underwent congenital cardiac surgery at the time of pacemaker implantation were excluded to avoid confounding surgical variables. The diagnosis of PPS required both the presence of clinical symptoms and echocardiographic documentation of a pericardial effusion. Private charts, surgical procedure notes, and the echocardiography database were examined to determine the clinical presentation, management, and follow-up of all patients who presented with and were treated for PPS.
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Results
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Patient Population
Four hundred and forty-three pacemakers (237 epicardial, 206 transvenous) were implanted in 370 patients (median 9.99 years, range 2 months to 24 years). One hundred and twenty-six patients had an isolated primary rhythm disturbance, while the remaining 307 patients had either structural heart disease or a cardiomyopathy. Of those with primary conduction system disturbances, 16 had sinus node dysfunction, 74 had atrioventricular nodal block, 25 had long QT syndrome, and 11 had another form of rhythm disturbance.
Eight episodes of PPS (6 epicardial; 2 transvenous) occurred in 7 patients (median age 9 years, range 8.4 months to 24.5 years), with an overall incidence of 2% (Table 1). Of the 7 patients with PPS, 2 had congenital heart disease and 5 had isolated congenital complete heart block or bradycardia that was associated with prolonged QT syndrome. One of the 2 patients with underlying congenital heart disease underwent placement of an epicardial pacing system 6 years after a Fontan procedure, while the second patient received a transvenous pacemaker 1 week after surgical aortic valve replacement.
Six episodes of PPS followed a primary pacemaker implantation, while two occurred after a subsequent lead revision. In the two instances of PPS that were associated with transvenous pacemaker systems, the first patient had a screw-in ventricular lead, and a tine-tip fixation ventricular lead was placed in the second patient. In this second patient, a transvenous pacemaker was placed 1 week after surgical aortic valve replacement. In this instance, an echocardiogram before the pacemaker was placed showed no evidence of a pericardial effusion. In one patient, PPS was documented after primary pacemaker implantation as well as after a subsequent lead revision.
Diagnosis
The median time interval from pacemaker implantation to PPS diagnosis was 12.5 days (range 8 to 22 days). All patients presented with at least one of the following clinical symptoms: decreased oral intake, lethargy, and respiratory or gastrointestinal distress (Table 2). At the time of presentation, all patients were tachypneic, dyspneic, and were noted to have hepatomegaly on physical examination. Echocardiography documented a moderate-to-large circumferential pericardial effusion (largest dimension of 2 cm) in all 8 patients. One patient presented with diastolic collapse and echocardiographic evidence of cardiac tamponade.
Treatment
Three patients underwent medical therapy; 1 with a nonsteroidal antiinflammatory agent (NSAID), and 2 with corticosteroids (Table 2). Of these, 2 responded successfully, and 1 required pericardiocentesis secondary to failed medical management. Five patients, including the one who presented with tamponade, underwent pericardiocentesis followed by antiinflammatory drug therapy. For the 6 patients that required pericardiocentesis, fluid analysis demonstrated serosanguineous exudates and negative bacterial cultures. One patient developed a recurrent effusion after a rapid taper of NSAID. One patient underwent a pericardial window for a persistent effusion despite medical therapy.
Outcome
Median time to resolution of the effusion was 18 days (range 8 to 43 days) (Table 2). All patients were followed for a minimum of 5 months after their effusion resolved without echocardiographic evidence of recurrence. No pacing system had to be explanted secondary to PPS or infection.
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Comment
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Postpericardiotomy syndrome may occur after any surgical procedure in which the pericardial space is opened or traumatized. It is thought to be due to an autoimmune response provoked by the presence of autologous tissue or blood in the pericardial space. This in turn triggers a cascade of biochemical events that ultimately leads to the production and deposition of immune complexes in the pericardial space, with subsequent pericarditis [1]. Although our patients universally did not present with characteristic complaints of chest pain and fever, they likely represent a variant of PPS where patients present with pericardial effusions that may result in cardiovascular compromise.
In adult studies, PPS is a common complication after open heart surgery and manifests as early as 1 week and as late as 2 months postoperatively, with a recurrence rate up to 50% after initial treatment [13, 10]. Although anecdotal cases of PPS have been reported in adults after permanent pacemaker implantation, the incidence and outcome of PPS has not been described in children after pacemaker implantation. At our institution, we found that PPS occurred in 2% of patients undergoing isolated pacemaker implantation.
The overall low incidence of PPS after pacemaker implantation likely reflects the relative minor degree of pericardial trauma incurred during the procedure. Although this mechanism may account for PPS that follows placement of epicardial systems, the exact mechanism of PPS that follows transvenous pacemaker insertion is less clear. It has been theorized that inadvertent ventricular microperforation during the placement of transvenous systems may compromise the integrity of the pericardial space and incite an immunologic response [4]. This rationale does not account for cases of PPS that occur in the instance where a tine-tip transvenous pacing lead is used and the ventricular myocardium is not disrupted. Despite the uncertain mechanism, it is evident that PPS does occur after transvenous pacemakers have been placed, and clinicians must remain vigilant in assessing patients for this complication.
As this is a retrospective study, we have identified only those patients who presented for medical attention with evidence of clinically significant PPS after a pacemaker had been placed. We did not identify those patients with subclinical pathology so we may be underestimating the true incidence of all PPS after placement of pacemaker systems. Given the relative low incidence of PPS in our study, no statistical analysis could be performed to identify a patient population at-risk of PPS after placement of a pacemaker. Therefore, a clinician must be aware that although not common, PPS can occur after the implantation of a pacemaker system in pediatric and young adult patients with or without underlying congenital heart disease.
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References
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