Title: Non-cardiac surgery in neonate with PDA stent. Moderators:

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1 Title: Non-cardiac surgery in neonate with PDA stent Moderators: 1. Barbara A. Castro, MD Associate Professor Anesthesiology and Pediatrics University of Virginia Medical School 2. Terrance A. Yemen, MD Director Pediatric Anesthesia Associate Professor of Anesthesiology and Pediatric University of Virginia Medical School Goals: 1. Understand indications for PDA stents versus surgical shunts in management of complex congenital heart disease. 2. Discuss surgical timing of non-cardiac procedures in neonates with palliated congenital heart disease 3. Discuss ventilator strategies in neonates with shunt dependent pulmonary blood flow and how surgical positioning and approach may affect ventilator management. 4. Discuss anesthetic concerns including preoperative evaluation, hemodynamic monitoring, fluid management, and pain management Case History A two month old neonate with CHARGE association whose anomalies include Tetrology of Fallot with pulmonary atresia, tracheoesophageal fistula with long gap esophageal atresia, single right kidney, bilateral colobomas, and dysmorphic low set ears presents for repair of her long gap esophageal atresia. Her tracheoesophageal fistula was surgically ligated on DOL 3 however due to a long gap the esophageal atresia was not repaired and a gastrostomy tube was placed for nutrition and decompression. At 3 weeks o f age she was taken to the cath lab for placement of a PDA stent. Her hospital course has been complicated by chylothorax requiring multiple thoracenteses, multiple episodes of SVT which were unresponsive to amiodarone and flecainide now on a trial of Sotalol, non-occlusive thrombus formation in her IVC, right internal jugular and subclavian veins and a left hemisphere cerebral infarct. She is scheduled for a delayed repair of her long gap esophageal atresia via a left thoracotomy. She currently weighs 4.3 kg. She is on nasal CPAP with sats in the 70s on 40 % oxygen. She has a right sided chest tube to suction which has had 80 ml out over the past 24 hours. She has a single lumen tunneled central line in her right groin. She is on heparin at 10 units/kg/hour. 1. What are the advantages and disadvantages of PDA stents over traditional shunts for improving pulmonary blood flow? 2. Who are the best candidates for PDA stents?

2 3. Do patients with PDA stents require anticoagulation? 4. What factors affect pulmonary blood flow in shunt dependent patients? 5. What is the longevity of a PDA stent and should all patients with PDA stents have a cardiac cath to assess pulmonary blood flow prior to non-cardiac surgery? 6. Should elective surgical procedures be performed in patients with PDA stents? The primary cardiologist and surgeon are confident that she is stable and ready for anastomosis of her long gap esophageal atresia. 1. Do you agree? 2. What other information would you be interested in before agreeing to proceed? A recent echocardiogram confirmed the presence of TOF with a severely hypoplastic pulmonary valve annulus. The report stated that the stented PDA flow was not seen however continuous flow in confluent, moderately hypoplastic branch PAs was demonstrated. There were 2-3 atrial communications with bidirectional shunting and mildly reduced biventricular function. Her chest xray from yesterday shows a small right pleural effusion with a chest tube overlying the right hemidiaphragm, stable cardiomegaly, and a ductal stent. A review of the cardiac catheterization report from the time of stent placement reveals that she has a 3.5 mm X 12 mm bare metal coronary artery stent across her ductus arteriosus. Her most recent capillary blood gas was ph 7.35, pco2 50 mm Hg, po2 41 mm HG, base excess 1.1. Her Hgb is 14.7 g/dl and platelet count was 354,000. You agree to proceed. 1. How would you induce this neonate? 2. What monitors would you use during this procedure? 3. Will positioning affect pulmonary blood flow? 4. Is there any way to monitor pulmonary blood flow during the surgical procedure? 5. What is your plan for pain control? You do a mask induction with sevoflurane, paralyze with rocuronium and intubate without difficulty. A peripheral arterial line is placed and a baseline gas obtained, ph 7.39, pco2 47 mm Hg, po2 43 mm Hg and base excess -2. The infant is placed on conventional pressure controlled ventilation and anesthesia is maintained with sevoflurane, fentanyl is administered for pain control, and intermittent boluses of phenylephrine and 5% albumin are required to maintain blood pressure. Two hours into the procedure a repeat blood gas was obtained, ph 7.12, pco2 58 mm Hg, po2 54 mm Hg and base excess -11. A fluid bolus was administered as well as bicarbonate however the surgeons were having difficulty locating the esophageal edges to anastomose and 4 hours into the case the end tidal CO2 began to rise dramatically. A gas revealed ph 6.88, pco2 115 mm Hg, po2 47 mm Hg and base excess How would you respond? 2. Could this be a tet spell? 3. Could this be a problem with the PDA stent? 4. Would nitric oxide be of any help? 5. What other modes of ventilation would you consider?

3 You inform the surgeons of the difficulty you are having with ventilation so they can remove their retractor. You suction the endotracheal tube and manually ventilate to re-expand the lung. You administer another bolus of albumin and phenylephrine to increase blood pressure. You check to make sure the chest tube is on suction. You send a repeat ABG in 20 minutes with minimal improvement, ph 6.94, pco2 92 mm Hg, po2 52 mm Hg, base excess -14. The decision is made to abort the procedure so the surgeons tag the esophageal ends and close the chest. The infant is transferred to the ICU for further management and evaluation. Discussion A wide variety of congenital heart disease(s) results in severely insufficient pulmonary blood flow upon ductal closure. These conditions represent a high neonatal morbidity and mortality shortly after birth. For decades, the goal of those caring for such a child has been the preservation of pulmonary blood flow until the child can either spontaneously outgrow the problem, or until a more definitive, lower risk procedure can be surgically performed. In the short-term a prostaglandin E infusion can be used to maintain this flow, but in the longer term a surgical solution has been required. Drs. Blalock and Taussig devised the first of these surgical shunts in the 1940s with a direct endto-side anastomosis of the subclavian artery to the ipsilateral pulmonary artery. The additional use of a tube graft resulted in the so-called modified Blalock-Taussig shunt. Other systemic-pulmonary shunts were soon developed including the Potts and Waterston procedures. These later shunts were particularly plagued by pulmonary hypertension, cardiac failure and distortion of the pulmonary arteries and soon fell out of favor, leaving the modified Balock-Taussig shunt as one of the few options available as palliation to these infants. However even the modified Blalock-Taussig shunt is associated with a variety of surgical complications that include; pleural effusions, chylothorax, diaphragmatic paralysis, cardiac failure as a result of too much pulmonary blood flow, and distortion of the branch pulmonary arteries. Also, the procedure is difficult to perform in critically ill, small for gestational age, infants. Stenting of the ductus arteriosus is a viable alternative to surgical palliation, even in very small and/or high-risk infants. The use of a ductal shunt was first described in Using lambs, formaldehyde was surgically instilled into the ducts. This was followed by a 1975 study in newborns using a buffered formaldehyde solution. Subsequently there were balloon dilatations and radiofrequency thermal angioplasties reported in the literature. None of these techniques was clinically successful and all were gradually abandoned. In 1992 Gibbs first reported the use of implanted ductus arteriosus stents in two infants. Unfortunately those children died shortly after placement. Subsequent reports were plagued by the lack of appropriate technology and equipment, resulting in a high rate of vessel damage, thrombosis,

4 perforation, bleeding, and ductal rupture. As time progressed, improvements in stent technology and delivery systems resulted in better clinical results. Most recent studies over the past 10 years show little morbidity and no mortality from ductus arteriosus stent placement, although the results are from isolated and limited centers, hindering these results. The advantages of the ductal stent are several. Ductal stents can be placed in critically ill neonates, even those very small for gestational age. No surgical procedure is required, thereby reducing hospital stay, resources and costs. Blood flow from these shunts is more uniform and results in a near balanced growth of both lungs and their vessels. Overperfusion of the lungs is rare and oxygen saturations are equivalent over time with surgical shunts. In addition to the relatively easy sizing of these shunts, they may be dilated at a later time as the infant grows to accommodate the need for greater pulmonary blood flow. Recent studies have shown that although these stents are generally well incorporated into the vessel tissue and difficult to remove, the pulmonary artery architecture is generally well preserved and the shunts easily obliterated once a more definitive surgical procedure is required. Unfortunately, like all procedures, there are also problems with ductal shunts. Normal ductus arteriosus vessels are relatively easy to stent; they are short and straight. Unfortunately in many types of congenital heart disease they are not. This is particularly true with infants afflicted with Tetralogy of Fallot. The artery in those infants is often long and tortuous. Placement failures are common in this circumstance due either to the inability to safely navigate the stent into position, or a failure to measure the correct length of the duct and not stent the entire vessel. Stenosis of the pulmonary artery at the opening of the ductus can also occur. Histopathologic studies have demonstrated an active inflammatory response to the stents. Vascular smooth muscle cells proliferate at this site and are believe responsible for this complication. Additionally these vascular smooth muscle cells are believed to result in the neo-endothelial proliferation of the stent itself resulting in the narrowing and eventual obstruction of the ductal stent. This proliferation of cells occurs invariable within the first month of the stent placement, with most stents severely affected by 6 months. It is this proliferation of cells that distinguishes the occlusion of these stents from those used in coronary stenting. Platelet aggregation and adhesion is less of a factor with ductal stents as compared to coronary stents. As result, the use of aspirin and antiplatelet drugs are much less effective in preventing occlusion of the ductal stent. The prolonged need for a ductal stent commonly requires that the stent be dilated as time goes on. An interesting feature is the lack of literature and the limited use these stents in the USA. The vast majority of literature on this topic comes from abroad. This appears to be the result of several factors. The first is that restrictions by the FDA have prevented the use of stents more commonly available in Europe. Additionally, the abundance of skilled surgical congenital heart teams in the USA tends towards a greater use of surgical shunts. Many other countries prefer to use ductal stents as a palliation to reduce medical costs and/or because surgery is not an available option due to limited

5 physician and nursing resources. However, an ongoing multicentered study of the benefits and complications of this technique has recently started in the USA. The results of this study should be very interesting and a useful guide to the appropriate use of this relatively new procedure in these critically ill children. References: 1. Alwi M. Stenting the ductus arteriosus: Case selection, technique and possible complications. Ann Pediatr Cardiol. 2008; 1(1): Santoro G, Gaio G, Palladino MT, Esposito R et al. Arterial duct stenting: do we still need surgical shunt in congenital heart malformations with duct-dependent pulmonary circulation? J Cardiovasc Med, 2010; 11: Egan MJ, Trask AJ, Baker PB, Lawrence J et al. Histopathologic Evaluation of Patent Ductus Arteriosus Stents After Hybrid Stage I Palliation. Pediatr Cardiol 2011; 32: Nadorlik HA, Egan MJ, Hill SL, Cheatham JP et al. Predictors of Ductus Arteriosus In-Stent Stenosis in the Hybrid Approach to Hypoplastic Left Heart Syndrome. Pediatr Cardiol, Published online: 13 October Vida VL, Speggiorin S, Maschietto N, Padalino M et al. Cardiac Operations After Patent Ductus Arteriosus Stenting in Duct-Dependent Pulmonary Circulation. Ann Thorac Surg 2010; 90: Amoozgar H, Cheriki S, Borzoee M, Ajami G, Soltani M, Ahmadipour M, et al. Short-term Result of Ductus Arteriosus Stent implantation Compared With Surgically Created Shunts. Pediatr Cardiol. 2012; 33: Matter M, Almarsafawey H, Hafez M, Attia G, Abuelkheir M. Patent Ductus Arteriosus Stenting in Complex Congenital Heart Disease: Early and Midterm Results for a Single-Center Experience at Children Hospital, Mansoura, Egypt. Pediatr Cardiol. Published online: 13 December 2012.