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Ann Thorac Surg 1998;65:268
© 1998 The Society of Thoracic Surgeons
Department of Cardiology, Wilhelmina Children’s Hospital, Utrecht, the Netherlands
Accepted for publication September 9, 1997.
Dr Hutter, Department of Cardiology, Wilhelmina Children’s Hospital, 3501 CA Utrecht, the Netherlands.
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A 15-year-old girl known to have multiple congenital abnormalities including midline defects, facial dysmorphy, multiple abnormalities of the vertebrae, vesicourethral reflux, vaginal atresia, and hypophysis functional abnormalities was seen at our department with a double-outlet right ventricle, left ventricular hypoplasia, and side-by-side position of the great arteries. She underwent two modified Blalock-Taussig shunts, followed by a Fontan operation (atriopulmonary connection, using redundant native right atrial tissue to fashion the interatrial baffle) in 1990. Two years later she presented with protein-losing enteropathy, which did not respond to conventional medical treatment and required weekly intravenous albumin supplementation.
In December 1996, cardiac catheterization demonstrated a mean right atrial pressure of between 19 and 20 mm Hg, without distal pulmonary arterial stenoses. Transseptal puncture of the atrial baffle was performed, followed by balloon dilation using a 10-mm-diameter balloon. After fenestration, the systemic arterial oxygen saturation decreased from 94% to 85%, and mean right atrial pressure decreased to 17 mm Hg. Clinical improvement was maintained for approximately a month, after which the protein-losing enteropathy also reappeared with the same severity. The systemic arterial saturation had increased to 90%, suggesting a further restriction of the interatrial fenestration.
Repeat heart catheterization was performed 2 months later for further balloon dilation or placement of a stent across the atrial septum to maintain longer term patency of the interatrial communication. The pulmonary vascular resistance index was 1120 dynes/m2. Cardiac output was low, with absolute pulmonary blood flow measuring 1.0 L · min-1 · m-2 and a pulmonary-to-systemic flow ratio of 0.79. A 12-mm-diameter balloon was positioned across the atrial septal defect and easily inflated several times at very low inflation pressures, with complete abolition of the "waist" formed on the balloon by the margins of the fenestration. During balloon deflation there was immediate elastic recoil of the edges of the defect, and consequently no recorded decrease in systemic arterial saturation. Right atrial angiography demonstrated no change in the size of the interatrial communication.
In view of the very low resistance to dilation offered by the native atrial septum it was thought that stent placement would be unsafe, as uniform expansion of the stent during balloon dilation would result in an unstable stent. The fenestration was therefore enlarged using a 16-mm-diameter balloon. The balloon easily passed the atrial septal defect. When the balloon was deflated, the transcutaneous saturation decreased from 90 to 78%, and the mean right atrial pressure to 12 mm Hg. Within a few minutes after removal of the balloon, there was a rapid decrease of the end-tidal CO2 and severe hypoxia (systemic oxygen saturation of 32%), suggesting that most of the systemic venous blood was bypassing the lungs via the enlarged interatrial communication. Echocardiography demonstrated a large atrial septal defect. The patient was successfully resuscitated by repositioning the 16-mm balloon across the atrial septum and inflating it fully, thereby decreasing the right-to-left atrial shunt. After discussion with her parents, immediate surgical closure of the atrial septal defect was declined. Transcatheter closure with a 17-mm umbrella device proved unsuccessful as the device easily pulled through the defect. The girl was transferred to the intensive care unit with the inflated balloon positioned across the atrial septal defect, where she died in the presence of her family after deflation of the balloon. Postmortem examination was not performed.
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The ideal size of the fenestration appears to be one that results in mild systemic desaturation to around 85%. The correct size of balloon required to produce such an atrial septal defect is unclear. Baffles made of synthetic material such as polytetrafluoroethylene are resistant to balloon dilation, and stent placement may be necessary to maintain patency of the defect. The resistance offered by the polytetrafluoroethylene will also allow nonuniform stent expansion, with a central waist and flaring of either extremity of the stent, and consequently a stable stent position.
When the baffle is made of native atrial tissue, as in our case, balloon dilation or stent implantation should be considered uncontrolled procedures, primarily due to the easy stretchability and subsequent recoil of native atrium. Initial percutaneous fenestration offered only temporary relief, and subsequent increase in transcutaneous oxygen saturation at follow-up suggested partial spontaneous closure. Use of a larger balloon almost certainly resulted in tearing of the atrial septum, and the resultant defect could not be occluded with a 17-mm double-umbrella device. In retrospect, the low cardiac output and low pulmonary blood flow before redilation should also have argued against any sustained benefit from further enlargement of the fenestration. In summary, balloon dilation of native atrial tissue may result in uncontrolled tears, with catastrophic consequences.
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