**1. Introduction**

Patent ductus arteriosus (PDA) was described a long time ago as a pathological entity in preterm babies [1]. From the physiological point of view, and outside the context of ductal-dependent lesions, PDA cannot be physiologically helpful when it comes to neonatal morbidity [2, 3].

In animal studies, there is significant engorgement and increased lymphatic conspicuity, secondary to dilated lymphatic architecture, in lambs with PDAs [4]. In primates, there is data suggesting that closing the PDA early makes a great difference in terms of the ventilation scores [4].

In humans, it takes only 3–7-day exposure to a moderate-large PDA shunt which significantly increases the incidence of bronchopulmonary dysplasia (BPD) [5] and BPD baseline incidence increases in preterm infants exposed to PDA [6].

PDA plays a critical role in the pathophysiology of many neonatal morbidities. This includes pulmonary hemorrhage [7, 8], myocardial changes in shape and size due to volume overload [9, 10], impaired bowel tissue oxygenation and other GI morbidities including necrotizing enterocolitis (NEC) [11–14], increased incidence of renal injury [15], mortality and intraventricular hemorrhage (IVH) [14].

Different approaches exist and vary between centers. In this chapter, we will concentrate on the pharmacological approach.

Role of targeted neonatal echocardiography in detecting hemodynamically significant PDA:

There has not been a standardized consensus to define hemodynamically significant PDA [16, 17].

Clinical assessment on its own was found not sensitive or specific in predicting PDA shunt volume especially in the first few days of life [18]. In addition, ductal size (diameter) only does not define the significance of the ductal shunt. There are large size PDAs that have no hemodynamic significance, and the opposite is true as well.

It appears that a detailed echocardiographic assessment is the key using targeted neonatal echocardiography (TnEcho). This comprehensive assessment includes multiple domains (**Figure 1**). PDA characteristics are crucial to look at, which includes the diameter, PDA flow Doppler pattern as well as PDA shape. It is interesting to think about the morphology of the duct and how is it different in preterm as opposed to less preterm babies. Initially, 5 types of ducts were described from A to E, however, with the increasing number of preterm babies being referred for catheter closure, a 6th type was recognized. The F type (fetal type) ductus is exclusively found in children born prematurely and is long, wide, tortuous and unlikely to close with pharmacological treatments [19].

Assessment of pulmonary circulation is important to establish using multiple parameters (**Figure 1**). Due to poor compliance, assessment of myocardial adaptation to the high shunt load is crucial. In addition, the atrial shunt needs to be assessed and established. Finally, any evidence of systemic compromise should be elaborated as well.

Recently, few biochemical markers were suggested as a part of ductal assessment especially in resource-limited areas. This includes cardiac troponin T (TnT), atrial natriuretic peptide (ANP), brain-type natriuretic peptide (BNP), N-terminal pro-BNP (NTpBNP) and urinary neutrophil gelatinase-associated lipocalin and urinary heart-type fatty acid-binding protein [20–23]. It appears that TnEcho is the proper tool to establish and define hemodynamically significant duct; only then treatment of PDA is shown to have an impact on neonatal outcomes [14, 17, 24, 25].






#### **Figure 1.**

*Targeted neonatal parameters needed to establish the hemodynamic significance of PDA.*
