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Ann Thorac Surg 2000;69:1505-1510
© 2000 The Society of Thoracic Surgeons

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Original articles: Cardiovascular

Neonatal repair of Ebstein’s anomaly: indications, surgical technique, and medium-term follow-up

^a Section of Thoracic and Cardiovascular Surgery, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
^b Section of Pediatric Cardiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA

Address reprint requests to Dr Knott-Craig, Section of Thoracic and Cardiovascular Surgery, University of Oklahoma Health Sciences Center, PO Box 26901, Oklahoma City, OK 73190
e-mail: ckc{at}ouhsc.edu

	Abstract

Top Abstract Introduction Patients and methods Comment References

 
Background. Ebstein’s anomaly in the severely symptomatic neonate is usually fatal. Because the mortality for various surgical interventions has been prohibitively high, the indications for operation in these critically ill neonates are unclear.

Methods. We reviewed our results with biventricular repair of three consecutive severely symptomatic neonates (2.8 to 3.2 kg) at our institution since 1994. Each had associated complex cardiac pathology, including multiple muscular ventricular septal defects (n = 1), pulmonary stenosis with functional pulmonary atresia (n = 1), and anatomic pulmonary atresia (n = 1). Preoperatively, all infants had severe tricuspid regurgitation, Great Ormond Street Ebstein echocardiogram scores greater than 1.3:1 (grade 3 or 4) and cardiothoracic ratio greater than 0.85. Two patients were severely cyanotic. Hepatic and renal insufficiency with diffuse coagulopathy was present preoperatively in two patients. Surgical repair consisted of (1) reconstruction of a competent monocuspid tricuspid valve, (2) right ventriculorrhaphy, (3) subtotal closure of atrial septal defect (ASD), (4) aggressive reduction atrioplasty, and (5) repair of all associated cardiac defects.

Results. There were no early or late deaths. All patients are currently asymptomatic, without medications, and in sinus rhythm. At 5-year follow-up, trivial tricuspid regurgitation is present in 1 and mild regurgitation in 2 patients. On the basis of these results and review of the current literature, we propose new indications for surgical repair in the neonate with Ebstein’s anomaly.

Conclusions. Biventricular repair of Ebstein’s anomaly in the critically ill neonate is feasible and medium-term durability of the repair is excellent. Therefore, conventional management of these patients should be revised and early surgical repair encouraged.

	Introduction

Top Abstract Introduction Patients and methods Comment References

 
Ebstein’s anomaly (EA) is a spectrum of disease characterized by varying degrees of displacement of the septal and posterior leaflets of the tricuspid valve into the cavity of the right ventricle, resulting in tricuspid regurgitation, right ventricular failure, and cyanosis [1–6]. Most patients with EA will reach adolescence before symptoms warrant surgical intervention [7–11] either to correct the tricuspid regurgitation and close the ASD, thereby reducing the cyanosis, or to ablate the supraventricular arrhythmias, which are reported to occur in 10% to 20% in this age group. Danielson and colleagues [7, 12, 13] and other researchers [3, 10, 14–16] have reported excellent surgical results and long-term survival with this group of patients, with more than 90% surviving either tricuspid valve repair or replacement. When EA is diagnosed in the severely symptomatic neonate, however, the condition is almost uniformly fatal [2, 9, 17–20]. Successful repair has not been reported to date, and various palliative procedures have been mostly unsuccessful [10, 17, 20], except for some preliminary success with a procedure that converts the anatomy to a single ventricle physiology, as reported by Starnes and associates [21], and others [11, 22].

	Patients and methods

Top Abstract Introduction Patients and methods Comment References

 
In this report we present the technique and medium-term follow-up of a biventricular repair that was successfully done on three consecutive critical neonates with Ebstein’s anomaly, all of whom had concomitant repairs of additional life-threatening congenital heart defects. These patients represent the primary author and surgeon’s entire experience with neonatal EA at the Children’s Hospital of Oklahoma.

Patient 1
The first patient was a 20-day-old 3.2-kg American Indian neonatal boy with severe EA, multiple large muscular ventricular septal defects, 4/4 tricuspid regurgitation, and intractable congestive heart failure. Cardiothoracic ratio was 0.87. Preoperative echocardiogram revealed a mobile anterior tricuspid leaflet and a giant right atrium. The Great Ormond Street Ebstein (GOSE) echocardiogram score [11, 20] was 1.3 (grade 3). On April 4, 1994, he underwent complete repair of EA and patch closure of multiple muscular ventricular septal defects. The anterior leaflet was large and had a fenestration in it, and both the septal and posterior leaflets were displaced well into the right ventricle. The tricuspid annulus was reduced from 23 to 13 mm. The ASD was subtotally closed. Circulatory arrest time was 59 minutes at 15°C. He was maintained on 5 µg · kg^-1 · min^-2 dopamine for 48 hours, and remained in sinus rhythm throughout the early postoperative period. The postoperative course was uncomplicated and the patient was extubated on postoperative day 2, and discharged on postoperative day 6. The patient is currently 5 years old and is fully active without restrictions. He is in sinus rhythm and takes no medications. Recent echocardiogram showed trivial tricuspid regurgitation and good biventricular function. Preoperative and recent chest roentgenograms are shown in Figure 1.

View larger version (76K): [in this window] [in a new window]   Fig 1. (A) Preoperative chest roentgenogram of neonate undergoing repair of Ebstein’s anomaly associated with multiple ventricular septal defects. (B) Recent postoperative chest roentgenogram of neonate undergoing repair of Ebstein’s anomaly associated with multiple ventricular septal defects.

View larger version (81K): [in this window] [in a new window]   Fig 2. (A) Preoperative four-chamber echocardiographic view of a neonate with Ebstein’s anomaly and functional pulmnoary atresia undergoing repair. (RA = right atrium.) (B) Preoperative chest roentgenogram of severely symptomatic neonate with Ebstein’s anomaly and functional pulmonary atresia.

Surgical technique
The surgical technique in these three patients was very similar and comprised of four components:

Radical reduction atrioplasty
To create more room for the lungs to expand postoperatively and to create a more efficient right atrium, the majority of the right atrial free wall was resected using an elliptical incision. At the inferior aspect of this incision care needs to be taken not to include the distal right coronary artery (RCA) in the resected specimen; the RCA lies in the thin-walled atrialized portion of the right ventricle and, as such, may be confused with the free wall of the right atrium. It is important to differentiate between the true tricuspid annulus that is closely approximated by the RCA and is considerably more anterior (closer to the rightward border of the heart) and the apparent tricuspid annulus that is demarcated by the hinge portions of the posterior and septal leaflets of the tricuspid valve, and lies within the atrialized portion of the right ventricle.

Tricuspid valve repair
The tricuspid valve repair was identical in all 3 patients, and consisted of an effective reduction annuloplasty with the potential to grow, and the construction of a competent monoleaflet tricuspid valve. This is facilitated by a large mobile anterior leaflet, which was present in all our patients. The repair is very similar to that described by Danielson [7] and Augustin [15] and their colleagues. Both sides of a pledgetted 5/0 braided nonabsorbable suture is placed through the apparentannulus at the commissure between the anterior and posterior leaflets and the ends are then both brought through the medial wall of the coronary sinus (true annulus) and tied down over a pledget, effectively dividing the tricuspid valve into a double orifice valve (Fig 3 ); the leftward (cephalad) of these two orifices is calibrated to 13 to 14 mm and the suture appropriately adjusted. Competence of the valve is then tested with iced saline. If satisfactory, the rightward (caudal) orifice is closed in two layers using a continuous nonabsorbable suture (Fig 4). This effectively brings the papillary muscles of the anterior leaflet closer to the new annulus making the newly constructed monoleaflet tricuspid valve more competent, plicates the atrialized portion of the right ventricle, and makes the effective right ventricle more efficient. By suturing the apparent annulus of the tricuspid valve (at the commissure between the anterior and posterior leaflets) to the coronary sinus (the true annulus), and then oversewing the rightward "second orifice," this effectively plicates the atrialized portion of the right ventricle in a vertical plane [14, 16], reducing "dead space" and making this a more effective pumping chamber.

View larger version (51K): [in this window] [in a new window]   Fig 3. Technique of repair in neonates with Ebstein’s anomaly.

View larger version (44K): [in this window] [in a new window]   Fig 4. Technique of repair in neonates with Ebstein’s anomaly.

Subtotal atrial septal defect closure
The usually large ASD is closed either primarily or with a pericardial patch, but a 3- to 4-mm fenestration (Fig 4) is left open to allow some right-to-left shunting during the early postoperative period, should there be right heart failure or pulmonary hypertension. There have been no detectable shunts across the intraatrial septum at recent follow-up.

Creation of a functional right ventricular outflow tract
Because the right ventricle is compromised, it is imperative to create prograde flow into the pulmonary arteries without unduly overloading the right ventricle. This mandates that the RVOT reconstruction approximates the normal RVOT, usually 7 to 8 mm in diameter, and the patch is appropriately tailored to achieve this goal. One needs to resist the temptation to make this patch larger in the hope that it will prevent or delay reoperation, as pulmonary regurgitation is very poorly tolerated in the setting of a dysfunctional right ventricle. If the RVOT is inadvertently oversized, early serious consideration needs to be given to placing a small 8-mm to 10-mm pulmonary homograft in the pulmonary position. Again the homograft needs to be small enough not to create more "dead space" for the right ventricle to overcome.

Perioperative management
Pulmonary vascular resistance needs to be aggressively minimized before and after discontinuing bypass. We have used large tidal volumes (12 to 15 mL/kg) hyperventilation, with minimal positive end-expiratory pressure, prophylactic full muscle relaxation, continuous fentanyl infusion at 8 to 10 µg · kg^-1 · h^-2 for 24 to 48 hours, peritoneal dialysis catheters placed in the operating room before closing the chest to drain postoperative ascites collection, thereby minimizing airway pressure and avoiding pulmonary vasoconstrictors such as epinephrine. We did not have nitric oxide available at the time of these operations, but this may be a valuable adjunct to the perioperative care.

These same measures need to be introduced before operation (from birth). In addition, prostaglandins are needed to maintain ductal patency and adequate dopamine infused to maintain renal and hepatic perfusion, that is, mean blood pressure minus central venous pressure more than 35 mm Hg. Daily echocardiograms will document improving ventricular function and lowering of pulmonary vascular resistance, often evident by the pulmonary valve starting to open against the pressure of ductal flow. At this point, usually 4 to 8 days after birth, repair should optimally be undertaken.

	Comment

Top Abstract Introduction Patients and methods Comment References

 
Ebstein’s anomaly is a rare congenital heart defect reported to occur in 0.2% of live births [9]. The essential morphologic defect involves apical displacement of the tricuspid valve leaflets, which results in gross dilatation of the tricuspid annulus, the presence of a thin-walled chamber separating the tricuspid annulus from the functional right ventricle (atrialized portion of the right ventricle), tricuspid regurgitation, and enlargement of the right heart chambers [1, 2, 4–6]. Mimics of EA need to be differentiated from true EA as the repair and prognosis differ greatly [23].

Most children clinically presenting with EA have signs and symptoms of progressive right heart failure, whereas adults usually present with progressive cyanosis, decreasing exercise tolerance, or arrhythmias [4, 7, 10, 11, 13, 14, 24]. In both instances progressive symptoms warrant surgical intervention. In contradistinction, there is currently no consensus about which neonates with EA would benefit from early surgical intervention. The available data suggest that about 20% to 40% of all neonates diagnosed with EA will not survive 1 month, and less than 50% will survive to 5 years of age [2, 8, 17, 19, 20]. The prognosis for symptomatic neonates is almost uniformly fatal in severe cases [2, 17, 20]. Some mildly symptomatic neonates may, however, be tided over with aggressive intensive care only to succumb in early childhood [11, 25]. Most, however, will die during the neonatal period. Therefore, the dilemma is to identify which neonates need urgent surgical intervention during the neonatal period. This dilemma is compounded by almost uniformly unsuccessful attempts to salvage these critically ill neonates in the past. Recently, there has been some renewed enthusiasm for surgical palliation, sparked by the remarkable experience by Starnes and associates [21] with single ventricle palliation in a small group of such patients.

The incidence of arrhythmias among neonates with EA (about 5% to 10%) [17, 20, 21] seems to be lower than that of the older population of patients with EA (15% to 20%) [7, 13, 14, 26]. None of our patients had evidence of Wolff-Parkinson-White syndrome or accessory pathways. Although this may be fortuitous, it raises the interesting issue of whether the arrhythmias so prevalent in older patients with EA are part of the morphologic substrate of EA, or whether they are in part acquired over time secondary to chronic right heart failure and atrial distension. If this were so, it would mitigate strongly for earlier repair.

Recent data from two large institutions, experienced in the care of neonates with complex congenital heart disease, has identified risk factors for early death in neonates with EA, which represent perhaps the most comprehensive indications for neonatal surgical intervention currently available: (1) Celermajer and colleagues [2, 20] from Great Ormond Street in London have created an echocardiographic grading score for neonates with EA that appears to identify patients at highest risk for death; this is based on a four-chamber echocardiographic view of the heart, and represents the ratio of combined area of the right atrium and atrialized portion of the right ventricle to the functional right ventricle, left atrium, and left ventricle; if this ratio equals or is greater than 1.5 (grade 4), the observed mortality was 100% versus 15% for the rest. This has been confirmed by other investigators [17]. A ratio of 1.1 to 1.4 (grade 3) was associated with an observed early mortality of 10%, but a late mortality of about 45% usually in early childhood, whereas a ratio of 1.0 or less (grade 1 or 2) was associated with 92% survival. (2) Presence of cyanosis was associated with 50% mortality during the neonatal period [17]; this became 100% predictive of mortality when associated with a GOSE score of >1.0:1 (grade 3 or 4). (3) Associated cardiac defects such as anatomic or functional pulmonary atresia, large ASD, or severe tricuspid regurgitation was almost uniformly fatal. (4) Finally, cardiothoracic ratio more than 85% was associated with death in 100% of neonates [2, 17, 20].

On the basis of these findings and our own experience, we recommend that neonates undergo repair within the first 2 weeks of life. The proposed indications for neonatal repair of EA are as follows: in asymptomatic neonates (GOSE score grade 4; cardiothoracic ratio 0.80; and severe tricuspid regurgitation) and in symptomatic neonates (severe cyanosis; mild cyanosis and GOSE score grade 3 or 4; cardiothoracic ratio > 0.80; severe tricuspid regurgitation; and associated cardiac defects).

Preoperative aggressive supportive care is critically important in the very ill neonates. We suggest immediate intubation, continuous muscle paralysis, and high-dose fentanyl (4 to 8 µg · kg^-1 · h^-2) as a continuous infusion, standard pulmonary hypertensive precautions, adequate inotropic support (eg, dopamine 5 to 10 µg · kg^-1 · min^-2), and prostaglandin infusion to maintain ductal patency if significant cyanosis exists. As a second inotrope, isoproterenol has been shown to be beneficial in some neonates with EA [25]. Regular echocardiograms may identify signs of decreasing pulmonary vascular resistance, such as progressive forward flow through the pulmonary valve.

The techniques that we have used are directed at creating a largely competent tricuspid valve, obliterating the aneurismal dyskinetic atrialized portion of the right ventricle, reducing the volume and inefficiency of the gigantic right atrium, thus creating more room for the compressed lungs, maintaining left ventricular output in the presence of a compromised right heart by ensuring that a small ASD is present, and ensuring adequate prograde pulmonary blood flow without overloading the functional right ventricle. Although the technique evolved from studying and observing the repair that Danielson has perfected over many years [7, 12, 13], the technique of vertical plication and rotation of the anterior leaflet of the tricuspid valve shares many of the same principles of tricuspid repair advocated by Quaegebeur and colleagues in 1991 [14].

On the basis of the GOSE score (grade 3 or 4), cardiothoracic ratio (> 0.85 in all patients), presence of significant cyanosis in 2 patients, and the presence of associated cardiac defects in all 3 patients, our patients would not have survived the neonatal period without operation. Although we were very encouraged with the early results and have successfully applied the same techniques to other similar conditions (for example, valvular pulmonary atresia, associated with severe tricuspid regurgitation and giant cardiomegaly), we elected to delay publication of the data until adequate follow-up period had elapsed and the repair could be shown to be durable. Currently all of our patients are about 5 years old, and all lead fully active lives without medications. All 3 patients are in sinus rhythm without evidence of preexcitation, and all have trivial or mild residual tricuspid valve regurgitation. We acknowledge that all our patients had large anterior leaflets making the tricuspid valve repair easier, but the techniques are adaptable even to situations where the leaflet is tethered to the free wall of the right ventricle. However, in situations where the anterior leaflet is deficient or where the posterior leaflet is the dominant leaflet, an alternative operative technique, such as the Starnes operation, should be considered. Furthermore, if the pulmonary arteries are truly small despite adequate ductal blood flow, this repair may not be appropriate and a simple shunt should be considered

In summary, biventricular repair of EA present in the severely symptomatic neonate is feasible and the repair appears to be durable. Timing of surgical intervention is critical and the operative technique and perioperative management needs to be carefully tailored to the individual needs of the patient.

	Acknowledgments

 
We thank Karen Dale for assisting in the preparation of this manuscript and Krishnaswamy Chandrasekaran, MD, cardiologist and echocardiographer, for independently calculating the GOSE scores on our patients.

	References

Top Abstract Introduction Patients and methods Comment References

 

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Christopher J. Knott-Craig Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Knott-Craig, C. J. Articles by Razook, J. D. Search for Related Content PubMed PubMed Citation Articles by Knott-Craig, C. J. Articles by Razook, J. D.