VIDEO-THORACOSCOPIC DUCTAL CLOSURE IN THE PREMATURE AND NEWBORN

MICHAEL H. HINES, MD

Introduction

Depending on whether one chooses to categorize a patent ductus arteriosus (PDA) as a congenital heart defect (CHD) or a “residual” fetal defect without being a true congenital abnormality, the argument can be made that it is the most common heart defect, with an incidence of between 1 per 500 to 1 per 2000 live births.^1,2 And while proportionally a very small minority of patients will ever require intervention for a PDA, it remains a relatively common operation in tertiary or quaternary medical centers. However, prior to discussing surgical techniques, it is important to review the anatomy, physiology, diagnosis, and medical management of the neonatal PDA.

The Newborn PDA

In the first minutes to hours of life when the lungs expand and the pulmonary vascular resistance (PVR) falls, lung perfusion increases significantly and the flow across the ductus arteriosus reverses direction. This initiates several physiologic changes that stimulate contractile elements within the ductal wall, leading to effective physiologic closure of the ductus arteriosus within the first 24 to 48 hours of life, and anatomic closure in the subsequent weeks, leaving a fibrous band connecting the aorta (Ao) and the pulmonary artery (PA), the ligamentum arteriosum. During this transition, the ductus may still be responsive to an infusion of prostaglandins with relaxation of its walls, and reopening of the channel allowing flow across it once again. This is particularly important in certain newborns with congenital cyanotic heart lesions and valve disorders. In many premature infants and a small number of term infants, the normal sequence of events does not occur, leading to persistent patency of the ductus arteriosus. There are several theories as to the cause of this failure, each with supporting clinical evidence.³ Failure of the appropriate physiologic stimulus for spontaneous closure in the premature infant is supported by the commonly observed successful response to the exogenous stimulus with indomethacin. The possibility of abnormal receptors, a lack of responsiveness of receptors, or a lack of normal contractile elements in the ductal wall are all supported by the many premature infants with a PDA that does not respond to indomethacin, even when given in a timely manner, in addition to the many term neonates and infants in whom a PDA is discovered. In some cases, premature infants have had echocardiographic documentation of closure of the ductus, with later spontaneous reopening during an episode of sepsis. This may be related to endogenous production of prostaglandin, a common product of arachidonic acid metabolism initiated by sepsis. This may have a significant physiologic benefit in this population of patients as it allows the PDA to provide a pop-off for the commonly seen pulmonary hypertension in these septic premature neonates. And while our curiosity is piqued by these observations, the answer is actually irrelevant to the current discussion. Suffice it to say that it is not uncommon to have a premature infant, and the occasional term infant, with a PDA.

Indications for Closure

One of the most controversial areas in current neonatology practice surrounds management of the PDA in premature infants, with a range of opinions from never closing them to surgically closing all detected PDAs, although most centers lie somewhere in the middle.^4–7 While there are many publications supporting specific positions, it can be argued that the complexity of the physiology and the variety of conditions effecting the premature newborn make it extremely difficult to do any randomized trial of sufficient size to adequately answer the question. Instead, we will propose some simple logic to help guide individualized treatment.

There are 2 generally accepted indications for PDA closure: the treatment of overcirculation from a significant left-to-right shunt creating heart failure, failure to thrive, and the potential for the development of pulmonary hypertension; and the prevention of endocarditis, occasionally secondary to infection of the PDA itself, but more commonly from infection along the “callus” that forms on the intimal surface of the PA wall in response to the high-velocity flow through a restrictive ductus (which is rarely hemodynamically significant). Since the later indication involves primarily the non-neonate, we will limit our discussion to the decision process in determining the hemodynamic significance of the PDA.

In most cases, a PDA is discovered during the investigation of an audible murmur in the neonatal intensive care unit (NICU), although occasionally one is discovered during an echocardiogram obtained for hemodynamic instability in the absence of a murmur. This is often because of the lack of significant shunt through the PDA, particularly in premature infants with pulmonary hypertension. In any case, once discovered, it needs to be assessed for its significance. The direction and degree of shunting across a PDA is determined directly by the difference in the systemic vascular resistance (SVR) and PVR, as well as the actual size of the ductus. A pressure gradient may be estimated using the detected velocity of flow by Doppler, but must be interpreted with caution, as the gradient is not only based on the size of the ductal lumen, but also by the resistances. A large ductus in a patient with significantly elevated PVR may not have any detectable gradient, and also not have much flow and, in fact, may have bidirectional shunting. If the PVR is low, the same-sized PDA may have torrential flow. But if it is partially closed, say after a course of indomethacin, the flow may be somewhat restricted, leading to a significant gradient. The presence of left-to-right flow with a significant gradient does confirm that the PVR is likely low; however, it does not directly define the amount of shunting. This requires more indirect signs of volume loading or direct measurement with cardiac catheterization.

Echocardiographic evidence of volume loading from a PDA is primarily based on volume loading of the left atrium (LA) and left ventricle (LV), with several commonly applied measurements such as the LA to aortic ratios⁸ and recently the perfusion index.⁹ Experienced pediatric cardiologists may recognize this cardiac chamber enlargement in connection with a clinical picture of overcirculation and recommend closure with medical or surgical treatment. With small PDAs, many neonatologists and pediatric cardiologists prefer conservative management with diuretics and observation rather than surgery. As long as these patients are appropriately followed and not lost to follow-up, such management is perfectly appropriate. However, we have seen more than one occasion of the discharge of a patient with a “benign” PDA that was lost to follow-up, only to reappear with significant pulmonary hypertension.¹⁰ At times what is believed to be a “benign” PDAs in a premature infant based on low flow, can progress and demonstrate increased flow as the premature lungs develop and the PVR falls, only to rise again over time because of the PDA. Because of this, no PDA in a premature or term infant should ever be considered “benign” at the time of discharge, and the parents should be thoroughly educated as to the potential (although unlikely) risks, and the importance of close follow-up.

Unlike term newborns and infants with normal lungs, some infants with significant premature lung disease may benefit from PDA closure even though there is minimal or no observed LA or LV enlargement on echocardiography. In the face of significant lung disease, even a mild or moderate amount of left-to-right shunting may contribute to poor lung compliance and increased work of breathing in patients with lung function that is already compromised. They may remain in the NICU off the ventilator, show no signs of congestive heart failure, and yet still be unable to completely wean from oxygen therapy, or have persistent feeding issues secondary to their mild or moderate increased work of breathing. We have seen many such infants benefit from PDA closure with definite, and on occasion dramatic, improvement in their feeding and ability to wean from their respiratory support. In addition, there is a small population of premature infants with significant lung disease, often still ventilator dependent, who have a moderate or large PDA, but only mild-to-moderate shunting and increased PVR. These are perhaps the most difficult patients to manage and determine the most appropriate timing for intervention. Failure to address the left-to-right shunt can potentially prevent continued recovery of the elevated PVR, or even contribute to its progression. However, closure of a PDA that still has bidirectional shunting can lead to a serious pulmonary hypertensive crisis and right ventricular (RV) failure, even acute distention and fibrillation. There have been several publications describing a syndrome of RV dysfunction after PDA ligation presenting it as a possible unexpected complication of surgery.¹¹ However, we believe that this is due to closure of a PDA that has bidirectional shunting and intermittent right-to-left shunting that was not adequately recognized preoperatively. To add to the confusion in diagnosis, infants with premature lung disease may often have periods of desaturation due to their lung disease, and this may hinder recognition of any contribution of desaturation from right-to-left shunting across the PDA, particularly if it is not occurring during the time the echo is obtained (or especially if sedation is used to obtain better echocardiogram images). With close evaluation and careful attention to perioperative management, a logical plan can still be established in these most complex patients. With this type of approach we rarely see the RV dysfunction and hemodynamic instability previously reported.

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