Anesthesia for Patients With Patent Ductus Arteriosus
Introduction
The ductus arteriosus plays a crucial role in fetal circulation.[1] Functional closure typically occurs within 18 to 24 hours after birth due to smooth muscle constriction.[2] Anatomical closure of the ductal lumen is usually complete by 2 to 3 weeks of age.
A patent ductus arteriosus (PDA) results from delayed or interrupted closure of the ductus arteriosus. Although primarily diagnosed in neonates, PDA is occasionally identified as a cardiac defect in adults. A PDA functions as a persistent fetal shunt, allowing blood flow between the aorta and the pulmonary artery.
Several factors contribute to the development of PDA, including hypoxemia, low Apgar scores, prenatal rubella exposure, mechanical ventilation, and prematurity. Approximately 80% of neonates born at 25 to 28 weeks of gestation develop PDA.[3] Among congenital cardiac lesions, PDA accounts for 6% to 11% of cases and is a frequent concern for pediatric anesthesiologists. The incidence of PDA varies with gestational age. Preterm infants are 20% to 60% likely to develop PDA, compared to 0.2% to 0.4% in term births. PDA is also twice as common in female infants as in male infants.[4]
In preterm infants, PDA results in systemic hypoperfusion and excessive pulmonary blood flow. This condition is associated with necrotizing enterocolitis, prolonged mechanical ventilation, bronchopulmonary dysplasia, intraventricular hemorrhage, and neurodevelopmental delays. Treatment options range from conservative approaches, including nonsteroidal anti-inflammatory drugs, fluid restriction, and supportive care, to more invasive interventions, such as surgical ligation or catheter-based device closure.[5]
Infants with a ductus arteriosus-dependent congenital heart defect require the ductus to remain open for survival until surgical correction of the cardiac anomaly. Prostaglandin E1 (PGE1) infusion maintains ductal patency in these cases. These medically fragile infants often require anesthesia for procedures such as central line placement, exploratory laparotomy, congenital heart defect repair, PDA closure, and other neonatal emergencies. Anesthesiologists must understand the pathophysiology of this extracardiac left-to-right shunt and adjust ventilation, pharmacologic agents, and perfusion strategies to balance systemic and pulmonary circulations.[6][7]
Function
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Function
In utero, the ductus arteriosus remains open due to prostaglandins produced by the placenta and the hypoxic fetal environment. In fetal circulation, oxygenated blood from the placenta enters the right atrium, with most of this blood bypassing the lungs and flowing into the left atrium through the foramen ovale. The left heart then pumps oxygenated blood to the brain and peripheral tissues. The small portion of oxygenated blood that reaches the pulmonary artery is diverted to the aorta through the ductus arteriosus because of high pulmonary vascular resistance.[8]
After birth, the 1st breath expands the lungs with oxygen-rich air, leading to a significant decrease in pulmonary vascular resistance. Umbilical cord clamping increases systemic vascular resistance. As pulmonary vascular resistance declines, blood flow in the ductus arteriosus shifts from an in-utero right-to-left shunt to bidirectional flow. With increased pulmonary blood flow, the ductus arteriosus transitions into a left-to-right shunt, and rising left atrial pressure leads to foramen ovale closure.
Within hours of birth, a reduction in prostaglandin E levels and an increase in arterial oxygen tension trigger smooth muscle constriction in the ductus arteriosus. Blood flow through the ductus arteriosus beyond the first 3 days of life is considered pathological. Even after initial functional closure, factors such as stress, infection, inflammation, and prostaglandins can reopen the ductus, particularly in preterm neonates.
PGE1 is life-saving for neonates with ductus arteriosus-dependent cardiac lesions. PGE1 is a naturally occurring prostaglandin that maintains ductus arteriosus patency when administered postnatally as a continuous infusion. The initial dose ranges from 0.025 to 0.1 mcg/kg/minute. Anesthesia providers must ensure uninterrupted infusion while caring for these patients.
Approximately 60% to 80% of PGE1 undergoes 1st-pass metabolism in the pulmonary system, requiring continuous administration. If the infusion is discontinued, the neonate will experience hemodynamic deterioration. Restarting PGE1 typically reopens the ductus within 30 to 120 minutes, but the immediate clinical response depends entirely on ductal blood flow for survival.
The ductus arteriosus is deliberately kept open in cardiac lesions that restrict blood flow to the lungs or systemic circulation. Maintaining patency is also necessary when pulmonary and systemic vessels are transposed, as seen in the transposition of the great arteries. Ductus arteriosus-dependent cardiac lesions that may be encountered before corrective surgery are outlined in Table 1 (see Table 1. Ductus Arteriosus-Dependent Cardiac Lesions).
Table 1. Ductus Arteriosus-Dependent Cardiac Lesions
Restrictive Pulmonary Blood Flow | Restrictive Systemic Blood Flow | Cardiac Anomalies |
Pulmonary atresia | Aortic stenosis | Transposition of the great arteries |
Tetralogy of Fallot | Coarctation of the aorta | |
Tricuspid atresia | Interrupted aortic arch | |
Hypoplastic left heart syndrome [9] |
Issues of Concern
When providing anesthetic care for critically ill preterm neonates, surgery may not always take place in the operating room. In some cases, these infants are too unstable for transport, necessitating procedures in the neonatal intensive care unit (NICU). Common bedside surgeries requiring anesthesia include exploratory laparotomy and PDA ligation. These patients often require unconventional ventilation or more precise ventilatory support than an anesthesia machine can provide.
Although the NICU lacks the same infection control measures and air exchange standards as the operating room, performing surgery at the bedside may be the safest option to avoid transporting critically ill neonates. Transport increases the risk of hypothermia, disruption of infusions, loss of vascular access, accidental extubation, and ventilatory compromise, all of which can lead to clinical deterioration.[10]
Preoperatively, intubation may or may not be required, depending on the neonate’s size and the magnitude of the shunt. A significant left-to-right shunt through a PDA can result in pulmonary overcirculation, leading to systemic hypoperfusion (ductal steal), pulmonary edema, oliguria, and gut hypoperfusion, which increases the risk of necrotizing enterocolitis. Physical examination findings include wide pulse pressures, a coarse, continuous machine-like murmur that intensifies during systole at the left sternal border and radiates to the back, and a hyperdynamic precordium.
Before administering anesthesia, an echocardiogram should be obtained and reviewed, along with ventilator settings, fraction of inspired oxygen concentration (FiO2), ongoing infusions, and vascular access. The goal extends beyond survival. Optimal perioperative care should minimize long-term complications.
An appropriate anesthetic plan must be developed once the surgical location has been determined. Most patients will have preoperative intravenous access, and some will already be intubated.
High-dose fentanyl has been the anesthetic of choice for critically ill neonates since 1981 due to its ability to provide hemodynamic stability and adequate analgesia. Even today, fentanyl combined with a paralytic agent remains the preferred anesthetic approach for ductal ligation and other neonatal surgeries. A fentanyl dose of 25 mcg/kg can blunt the stress response, though doses as high as 100 mcg/kg have been used in neonatal surgery.[11]
For older, stable patients, a slow inhalational induction with sevoflurane may be an option, followed by vascular access establishment, paralytic agent administration, and intubation. However, careful monitoring of hemodynamic changes is essential when using sevoflurane for induction and maintenance. A decrease in systemic vascular resistance can reduce pulmonary blood flow and cause desaturation in patients with ductus arteriosus-dependent lesions. Additionally, increasing the inspired oxygen concentration can dilate the pulmonary vasculature, leading to systemic hypoperfusion.
Maintaining an appropriate balance between pulmonary and systemic blood flow is particularly critical in neonates with a large, nonrestrictive PDA. The lowest tolerated FiO2 should be used in these patients. The principles of managing PDAs closely resemble those used for managing ventricular septal defects.[12]
Table 2. Ventilatory and Oxygenation Strategies for Balancing Pulmonary and Systemic Blood Flow in Neonates with Patent Ductus Arteriosus
Increase Pulmonary Blood Flow/Decrease Systemic Blood Flow | Decrease Pulmonary Blood Flow/Increase Systemic Blood Flow |
Increase FIO2 | Decrease FIO2 |
Decrease PCO2 | Increase PCO2 |
PDA closure is feasible for infants weighing up to 1.5 kg, but determining its safety profile has been challenging due to various adverse events, including anesthesia-related complications. In healthy term infants, the ductus arteriosus closes naturally within 72 hours of birth. However, in 70% of extremely preterm infants, the ductus remains open, leading to potentially severe outcomes.
Treatment strategies have varied, with pharmacological therapy often used as the first approach. Nevertheless, pharmacological treatment fails in 30% to 50% of extremely preterm infants. Traditional surgical closure has been associated with multiple complications, prompting increased interest in alternative therapies.
Percutaneous closure is the preferred approach for adults and infants weighing over 6 kg, and emerging evidence supports its safety and feasibility for smaller and premature infants. The feasibility of percutaneous PDA closure, defined as successful device placement, is approximately 96%. Postprocedural adverse event risk appears to be linked to postnatal age, but existing studies vary significantly in defining and timing adverse events.
Current evidence suggests that percutaneous closure is associated with fewer cardiorespiratory complications than surgical ligation. However, studies have inconsistent data on the timing of procedures and the severity of illness among patients.[13]
A comparison of treatment options for PDA closure, including surgical ligation and transcatheter closure, was conducted using data from the Pediatric Health Information System database from 2016 to 2020. The study examined 678 patients younger than 1 year who underwent either transcatheter closure (n=503) or surgical ligation (n=175).
Surgical patients were generally younger and more premature than those who underwent transcatheter closure and had a higher mortality rate. After adjusting for multiple factors, transcatheter closure was associated with reduced intensive care unit admission rates, mechanical ventilation requirements, and hospital stays. Hospital charges and readmission rates were similar for both procedures. Among premature neonates and infants, surgical ligation was linked to longer hospital and postoperative stays.
Transcatheter closure was associated with lower mortality and reduced length of stay compared to surgical ligation. The proportion of PDA closures performed via transcatheter closure relative to surgical ligation has been increasing. When feasible, transcatheter closure should be considered over surgical ligation for PDA closure. However, both procedures carry procedural and anesthetic risks, and the optimal treatment for PDA remains a subject of ongoing debate.[14]
Clinical Significance
Advances in neonatal care have improved survival rates for extremely premature neonates. However, these infants face a higher risk of disrupted ductus arteriosus closure after birth, causing the ductus to remain patent. Not all premature infants receive care at dedicated pediatric hospitals. Many remain in NICUs at community hospitals. All anesthesiologists, not just those with pediatric fellowship training, must understand the physiology of a PDA and the anesthetic considerations necessary to optimize outcomes.
Other Issues
A PDA is rarely seen in older children or adults. On examination, these patients may present with a systolic murmur, cardiomegaly, and a hyperdynamic precordium. Chronic pulmonary overcirculation can lead to congestive heart failure, calcifications, pulmonary hypertension, and infective endocarditis, with these complications typically emerging by the 3rd decade of life. Endocarditis is the leading cause of death in adults with a PDA. Even small, hemodynamically insignificant PDAs are closed during childhood to prevent this risk.
Enhancing Healthcare Team Outcomes
Caring for these fragile patients requires coordination and communication among multiple subspecialists. Many neonates must be transported hundreds of miles to a pediatric hospital for PDA closure. A collaborative effort among neonatologists, cardiologists, nurses, cardiothoracic surgeons, and anesthesiologists is essential to ensure optimal care. An anesthesiologist must thoroughly understand the patient's cardiac anatomy and actively communicate preoperative, intraoperative, and postoperative treatment goals with the entire care team. Clear communication with the surgeon is critical, particularly regarding potential complications of PDA ligation, such as inadvertent ligation of the aorta or pulmonary artery. Awareness and coordination during test clamping can help prevent devastating outcomes.
Intervention may be necessary if a PDA significantly affects cardiac function. One option is transcatheter PDA closure (TCPC), a minimally invasive procedure that has been shown to be a safe and effective alternative for managing PDA in extremely low birth weight (ELBW) infants. A comprehensive outpatient follow-up strategy is an essential component of this intervention.
A team-based approach is essential, involving specialists from neonatology, cardiology, anesthesiology, pulmonology, cardiac surgery, and other healthcare fields. These experts collaborate to care for ELBW infants, a high-risk group due to their fragile physiology. This coordinated effort has enabled successful TCPC in hundreds of these infants, including those weighing less than 1 kg at the time of the procedure.
Key indicators of positive outcomes include reduced reliance on respiratory support, improved feeding tolerance, steady growth, and neurodevelopmental progress. Benefits of TCPC for ELBW infants include faster ventilator weaning, improved nutrition, and enhanced growth, ultimately leading to shorter hospital stays. Dedicated follow-up clinics play a crucial role in ensuring comprehensive long-term care, significantly improving overall outcomes.
This structured approach, integrating procedural management with interprofessional follow-up, has demonstrated effectiveness. By addressing both immediate medical needs and long-term developmental outcomes, this comprehensive strategy enhances the overall health and prognosis of ELBW infants with PDA.[15]
Skills
Managing PDA in the perioperative setting requires specialized knowledge of neonatal and pediatric cardiovascular physiology, anesthetic considerations, and surgical techniques. Each team member must be proficient in their role while understanding the broader implications of perioperative care, including hemodynamic stability, respiratory support, and potential complications.
Strategy
Effective perioperative management relies on continuous closed-loop communication among all members of the care team. Discussions should cover the procedure's necessity, the chosen technique, and potential management challenges. This approach ensures that all professionals involved, including anesthesiologists, neonatologists, cardiologists, cardiac surgeons, nurses, and respiratory therapists, remain aligned in their objectives and prepared to address intraoperative and postoperative concerns promptly.
Ethics
Thorough informed consent must be obtained before anesthesia induction. In cases where the patient lacks decision-making capacity, the designated and authorized decision-maker must be engaged in the consent process. Ethical practice also requires that all team members feel empowered to voice any concerns to the team, the patient, or the decision-maker. This open dialogue promotes transparency, ensures stakeholder buy-in, and provides additional oversight, which can help identify and address potential issues early in the process.
Responsibilities
Each team member must clearly communicate their role, responsibilities, and any concerns with the rest of the team. This ongoing exchange should occur in real-time as situations evolve, ensuring that all aspects of perioperative care are coordinated. Anesthesiologists must monitor hemodynamic changes and communicate with the surgeon regarding intraoperative adjustments, while nursing staff must ensure appropriate medication administration and patient monitoring.
Interprofessional Communication
Open and respectful communication is essential for the successful treatment of these patients. Team members should freely share critical information and concerns without fear of hostility or professional conflict. Constructive dialogue fosters collaboration and enhances patient safety by considering all perspectives.
Care Coordination
All interprofessional team members must work cohesively, avoiding disruptions to the workflow of others. Each professional should ensure that their actions do not inadvertently create additional challenges or burdens for their colleagues. Coordinated care is vital for optimizing patient outcomes, minimizing procedural risks, and ensuring efficient perioperative management.
References
Rios DR, Bhattacharya S, Levy PT, McNamara PJ. Circulatory Insufficiency and Hypotension Related to the Ductus Arteriosus in Neonates. Frontiers in pediatrics. 2018:6():62. doi: 10.3389/fped.2018.00062. Epub 2018 Mar 15 [PubMed PMID: 29600242]
Gournay V. The ductus arteriosus: physiology, regulation, and functional and congenital anomalies. Archives of cardiovascular diseases. 2011 Nov:104(11):578-85. doi: 10.1016/j.acvd.2010.06.006. Epub 2010 Sep 21 [PubMed PMID: 22117910]
Conrad C, Newberry D. Understanding the Pathophysiology, Implications, and Treatment Options of Patent Ductus Arteriosus in the Neonatal Population. Advances in neonatal care : official journal of the National Association of Neonatal Nurses. 2019 Jun:19(3):179-187. doi: 10.1097/ANC.0000000000000590. Epub [PubMed PMID: 30720481]
Level 3 (low-level) evidenceShinde SR, Basantwani S, Tendolkar B. Anesthetic management of patent ductus arteriosus in adults. Annals of cardiac anaesthesia. 2016 Oct-Dec:19(4):750-751. doi: 10.4103/0971-9784.191547. Epub [PubMed PMID: 27716713]
de Klerk JCA, Engbers AGJ, van Beek F, Flint RB, Reiss IKM, Völler S, Simons SHP. Spontaneous Closure of the Ductus Arteriosus in Preterm Infants: A Systematic Review. Frontiers in pediatrics. 2020:8():541. doi: 10.3389/fped.2020.00541. Epub 2020 Sep 11 [PubMed PMID: 33014935]
Level 1 (high-level) evidenceAw TC, Chan B, Singh Y. Transport and Anaesthesia Consideration for Transcatheter Patent Ductus Arteriosus Closure in Premature Infants. Journal of cardiovascular development and disease. 2023 Sep 1:10(9):. doi: 10.3390/jcdd10090377. Epub 2023 Sep 1 [PubMed PMID: 37754806]
Joffe DC, Shi MR, Welker CC. Understanding cardiac shunts. Paediatric anaesthesia. 2018 Apr:28(4):316-325. doi: 10.1111/pan.13347. Epub 2018 Mar 6 [PubMed PMID: 29508477]
Level 3 (low-level) evidenceRemien K, Majmundar SH. Physiology, Fetal Circulation. StatPearls. 2025 Jan:(): [PubMed PMID: 30969532]
Akkinapally S, Hundalani SG, Kulkarni M, Fernandes CJ, Cabrera AG, Shivanna B, Pammi M. Prostaglandin E1 for maintaining ductal patency in neonates with ductal-dependent cardiac lesions. The Cochrane database of systematic reviews. 2018 Feb 27:2(2):CD011417. doi: 10.1002/14651858.CD011417.pub2. Epub 2018 Feb 27 [PubMed PMID: 29486048]
Level 1 (high-level) evidenceWillis A, Pereiras L, Head T, Dupuis G, Sessums J, Corder G, Graves K, Tipton J, Sathanandam S. Transport of extremely low birth weight neonates for persistent ductus arteriosus closure in the catheterization lab. Congenital heart disease. 2019 Jan:14(1):69-73. doi: 10.1111/chd.12706. Epub [PubMed PMID: 30811788]
Wolf AR. Ductal ligation in the very low-birth weight infant: simple anesthesia or extreme art? Paediatric anaesthesia. 2012 Jun:22(6):558-63. doi: 10.1111/j.1460-9592.2012.03846.x. Epub 2012 Apr 10 [PubMed PMID: 22489639]
Shah SMA, Khan SA, Sadiq F, Gul R, Sadiq F, Khan MU, Khan MK, Uzma F, Khan A, Khan S. Comparison of the Effectiveness of Paracetamol and Ibuprofen in the Management of Patent Ductus Arteriosus in Preterm Neonates: A Randomized Controlled Trial. Molecular and cellular pediatrics. 2025 Jan 25:12(1):2. doi: 10.1186/s40348-025-00189-x. Epub 2025 Jan 25 [PubMed PMID: 39862321]
Level 1 (high-level) evidenceBarcroft M, McKee C, Berman DP, Taylor RA, Rivera BK, Smith CV, Slaughter JL, El-Khuffash A, Backes CH. Percutaneous Closure of Patent Ductus Arteriosus. Clinics in perinatology. 2022 Mar:49(1):149-166. doi: 10.1016/j.clp.2021.11.009. Epub 2022 Jan 21 [PubMed PMID: 35209997]
Kuntz MT, Staffa SJ, Graham D, Faraoni D, Levy P, DiNardo J, Maschietto N, Nasr VG. Trend and Outcomes for Surgical Versus Transcatheter Patent Ductus Arteriosus Closure in Neonates and Infants at US Children's Hospitals. Journal of the American Heart Association. 2022 Jan 4:11(1):e022776. doi: 10.1161/JAHA.121.022776. Epub 2021 Dec 31 [PubMed PMID: 34970919]
Apalodimas L, Waller Iii BR, Philip R, Crawford J, Cunningham J, Sathanandam S. A comprehensive program for preterm infants with patent ductus arteriosus. Congenital heart disease. 2019 Jan:14(1):90-94. doi: 10.1111/chd.12705. Epub [PubMed PMID: 30811791]