Ann Thorac Surg 2001;71:1346-1347
© 2001 The Society of Thoracic Surgeons
Case report
Aneurysmal pericardial patch producing right ventricular inflow obstruction
Ger B.W.E. Bennink, MD, PhDa,
Francois J. Hitchcock, MDa,
Mirella Molenschot, MDa,
Paul Hutter, MDa,
Narayanswami Sreeram, MDa
a Department of Cardiology, Wilhelmina Children’s Hospital, Utrecht, The Netherlands
Accepted for publication April 14, 2000.
Address reprint requests to Dr Sreeram, Department of Cardiology, Wilhelmina Children’s Hospital, Post Office Box 85090, 3508 AB Utrecht, The Netherlands
e-mail: nsreeram{at}casema.net
 |
Abstract
|
|---|
A 2-month-old infant presented with acute onset of heart failure, having previously undergone anatomical repair of transposition of the great arteries and ventricular septal defect (VSD). Echocardiography demonstrated aneurysmal dilation of the native pericardial patch used for VSD closure, resulting in right ventricular inflow obstruction. The pericardial patch was excised, and the VSD closed using a GoreTex patch.
|
Introduction
|
|---|
A single stage arterial switch operation and closure of ventricular septal defect (VSD) provides excellent outcome for transposition of the great arteries and VSD [1, 2]. We report a hitherto unrecognized complication following closure of VSD using a native pericardial patch.
A 2-month-old infant presented to his local hospital with acute circulatory collapse, which occurred at home, when he was straining to defecate. He had had a 2-day history of constipation before the acute presentation. He had undergone uncomplicated anatomic repair of transposition of the great arteries with ventricular septal defect on day 10 of life. The VSD was located in the subpulmonary position, without override of the pulmonary valve, and measured 5 mm in maximal diameter. As is our standard practice, a native pericardial patch was used for closure of the VSD, which was accomplished by way of the transatrial route. On arrival at our institution, he was hypotensive (mean arterial blood pressure of 35 mm Hg), with a raised central venous pressure (15 to 20 mm Hg). Echocardiography demonstrated aneurysmal dilation of the pericardial patch. The patch herniated through the tricuspid valve into the right atrium during systole, producing ball valvelike right ventricular inflow obstruction (Fig 1). Emergency reoperation was performed. At direct inspection, the body of the VSD patch had thinned out. The attachments to the margins of the VSD were intact, and there was no obvious left-to-right shunt through the material of the patch. On picking up the patch with the forceps, the patch perforated easily at the point of contact. The pericardial patch was removed, and the VSD closed using a GoreTex patch (W.L. Gore & Associates). The postoperative course was uneventful. Detailed neurologic evaluation before discharge from hospital and at serial follow-up have not demonstrated any neurologic deficit resulting from the period of low cardiac output before reoperation.
View larger version (57K):
[in this window]
[in a new window]
|
Fig 1. (A) Standard echocardiogram showing ballooning of the pericardial patch into the right ventricle (RV) and through the tricuspid valve into the right atrium (RA). The margins of the original VSD are demarcated with arrows. The large arrow shows the position of the right atrioventricular groove (LV = left ventricle). (B) Intraoperative epicardial echocardiogram showing herniation of the patch through the tricuspid valve in systole.
|
|
|
Comment
|
|---|
We report a rare complication following the use of native pericardium for VSD closure. Aneurysmal bulging of pericardial tissue is well recognized following transannular pericardial patch repair of the right ventricular outflow tract in tetralogy of Fallot. This occurs predominantly in the setting where residual distal stenoses in the branch pulmonary arteries are present. Over a 10-year period of routinely using pericardial patches for closure of both isolated VSDs and VSDs associated with complex structural defects, we have not encountered such a problem. Echocardiography performed before discharge from hospital, and follow-up examination including echocardiography 4 weeks after operation in our patient did not demonstrate any abnormalities associated with the VSD patch. The association with constipation is interesting. It may be speculated that straining resulted in acute increase in left ventricular afterload, the development of supranormal left ventricular systolic pressure and, consequently, excessive tension on the patch. However, a gradual aneurysmal dilation occurring over time, with the Valsalva maneuver producing further prolapse and acute right heart obstruction cannot be excluded. The patient had no clinical signs suggestive of Marfan’s syndrome or any other collagen disorder that may have been associated with an inherently decreased tensile strength of native pericardium. Large fresh autologous pericardial patches used to close VSDs may be more susceptible to aneurysm formation due to the large surface area that is exposed to systemic pressure over time. Glutaraldehyde fixation of autologous pericardial patches may make this complication less likely.
|
References
|
|---|
-
Brawn W.J., Mee R.B.B. Early results for anatomic correction of transposition of the great arteries and for double-outlet right ventricle with subpulmonary ventricular septal defect. J Thorac Cardiovasc Surg 1998;95:230-238.[Abstract]
-
Bove E.L., Beekman R.H., Snider A.R., et al. Arterial repair for transposition of the great arteries and large ventricular septal defect in early infancy. Circulation 1988;78(Suppl III):26-31.
This article has been cited by other articles:
|
|
|
|
 
A. Y. Denault, M. Chaput, P. Couture, Y. Hebert, F. Haddad, and J.-C. Tardif
Dynamic right ventricular outflow tract obstruction in cardiac surgery
J. Thorac. Cardiovasc. Surg.,
July 1, 2006;
132(1):
43 - 49.
[Abstract]
[Full Text]
[PDF]
|
|
|
Top
Abstract
Introduction
