Pulmonary artery hypertension occurs in 2–5 of every 1,000 live births [13]. Acute pulmonary hypertension, which leads to hypoxemic respiratory failure during the transitional period, is characterized by a failure of the normal postnatal decline in pulmonary vascular resistance. The hypoxemia is related to impaired pulmonary blood flow and/or right ventricular dysfunction secondary to elevated pulmonary artery pressure and increased right ventricular afterload [14]. Consequently, severe PPHN in newborns often leads to profound hypoxemia, ultimately resulting in life-threatening circulatory and respiratory failure, with a mortality rate of approximately 50%[15, 16]. If respiratory failure persists despite standard treatment, ECMO therapy becomes necessary [17].

Cardiac dysfunction is more pronounced in neonates due to an underdeveloped contractile system with decreased compliance, reduced adaptability to changes in afterload, and an increased risk of diastolic dysfunction [18]. In the context of severe acute pulmonary hypertension, where there is significant right ventricular dysfunction and/or extremely low cardiac output, a continuous right-to-left shunt through the PDA can play a supportive role by reducing right ventricular pressure. The PDA should remain open during this time [19]. As treatment progresses and pulmonary vascular resistance and pulmonary artery pressure decrease, the PDA may develop a left-to-right shunt. Numerous studies have shown that when the PDA exhibits hemodynamically significant left-to-right shunting, closure of the PDA is necessary, as it can lead to complications such as pulmonary hemorrhage, renal failure, necrotizing enterocolitis, and even neonatal mortality [20, 21]. Hemodynamically significant PDA (HsPDA) is typically defined as a PDA with significant left-to-right shunting through the ductus arteriosus, confirmed by echocardiography and clinical evidence of systemic hypoperfusion and pulmonary overcirculation [22, 23]. For newborns with large PDAs, during ECMO treatment, when pulmonary artery pressure decreases, a large PDA can result in significant left-to-right shunting, leading to pulmonary congestion, hemorrhage, and reduced systemic circulation, among other adverse effects. Therefore, surgical closure of the PDA should be considered in newborns with severe PPHN and concomitant large PDAs during ECMO support. However, performing PDA ligation during ECMO carries a high risk. This study summarizes our clinical experience with performing PDA ligation during ECMO therapy in newborns.

Since PPHN in newborns is often self-limiting, pulmonary artery pressure decreases as the infant ages. Therefore, when ECMO-assisted therapy reduces pulmonary artery pressure to the point where left-to-right shunting occurs through the PDA, surgical closure of the PDA should be considered. If the PDA is large at this point, it can result in significant left-to-right shunting, leading to pulmonary congestion, pulmonary hemorrhage, and adverse effects on the already compromised lung function and the management of pneumonia, which can hinder successful ECMO removal [24, 25]. A significant reduction in systemic circulation can also lead to inadequate systemic perfusion, tissue ischemia, hypoxia, and complications such as elevated lactate levels and necrotizing enterocolitis [26]. Therefore, for newborns with severe respiratory failure and large PDAs undergoing ECMO-assisted therapy, closure of the PDA should be considered when pulmonary artery pressure decreases to the point where left-to-right shunting begins [24]. If significant pulmonary congestion, pulmonary hemorrhage, or elevated lactate levels occur, PDA ligation should be performed promptly. In the cases discussed in this study, all five patients had PDAs measuring 6 mm to 10 mm, which were close to or even exceeded the diameter of the aorta. Before PDA ligation, all five patients exhibited continuously rising lactate levels, and three experienced pulmonary hemorrhages. After PDA ligation, lactate levels significantly decreased, and pulmonary hemorrhages gradually resolved.

Due to the invasive nature of PDA ligation surgery and the need for heparin anticoagulation during ECMO therapy, the risk of intraoperative bleeding is relatively high [27]. To prevent bleeding, careful surgical techniques, avoidance of vascular and unnecessary tissue injury, and meticulous hemostasis are essential. We followed the approach recommended by Wang G, et al., [28] which involves maintaining the ACT within the range of 180–220 s, ensuring platelet counts above 60 × 10⁹/L, and using sodium nitroprusside to control the systolic blood pressure at 40–50 mmHg during PDA ligation. None of the five patients in our study experienced severe bleeding complications, with intraoperative bleeding volumes not exceeding 10 ml.

To improve the success rate of the surgery and minimize complications, we summarized the following key points from our experience: optimal exposure and a clear surgical field were crucial for the procedure’s success. Since ECMO support was available for cardiopulmonary function, we temporarily suspended mechanical ventilation during chest entry, retaining PEEP, and resumed ventilation only after completing the PDA ligation. This approach prevented respiratory movements from obstructing the surgical field, significantly improving visibility without causing circulatory changes. It is important to note that this brief pause in ventilation did not lead to lung perfusion issues, as the surgery duration was short. Newborns often had significant tissue edema due to their young age, heart failure, and ECMO support, making the aorta and PDA tissue very thin and susceptible to damage. Therefore, it was essential to perform the surgery meticulously and gently. The incision into the mediastinal pleura was extended as close as possible to the subclavian artery at the upper end and down to the pulmonary hilum, ensuring full exposure, with prompt application of electrocautery for hemostasis to minimize bleeding. To minimize the risk of damaging the PDA during ligation, we employed a technique where, after separating the upper and lower margins of the PDA with angled forceps, the PDA plane was freed from the outer posterior aspect of the descending aorta. We then inserted two 1 − 0 sutures, one above and one below the PDA margins, by passing them through the posterior aspect of the descending aorta. This approach simplified the procedure and minimized the risk of tissue damage during PDA ligation.

Our study had several limitations. It was a single-center retrospective study with a small sample size. This report reflects the early experience of our center and serves as an exploratory study. More objective and accurate conclusions will require studies with larger sample sizes in the future.