Case November 2025 - PDA and Ligation at 35 weeks

Post-ligation cardiac syndrome (PLCS) is a well-recognized complication following surgical closure of a patent ductus arteriosus (PDA), typically occurring within the first 6 to 24 hours after ligation. It is characterized by acute hemodynamic instability, including hypo- or hypertension, low cardiac output, and impaired oxygenation. A subset of infants, particularly those with a robust pre-ligation systemic vascular tone due to endogenous systemic vasoconstriction and activation of the Renin-Angiotensin-Aldosterone System in the context of steal may instead present with systemic hypertension following ligation. This form of post-ligation hypertension reflects maladaptive cardiovascular adaptation to the abrupt elimination of the ductal shunt.

The pathophysiology of post-ligation hypertension involves a combination of increased systemic vascular resistance and altered ventricular loading conditions. Before ligation, the ductus arteriosus acts as a low-resistance pathway that allows left-to-right shunting of blood from the aorta to the pulmonary circulation. The sudden closure of this pathway increases effective systemic afterload, as the left ventricle must now eject into a higher resistance circuit without the offloading effect of the ductus. In the immediate postoperative period, the abrupt rise in systemic vascular resistance can lead to transient left ventricular dysfunction and diastolic impairment. Neurohumoral activation—particularly of the sympathetic nervous system and renin-angiotensin-aldosterone axis—further amplifies vasoconstriction and contributes to sustained hypertension in some infants. This is combined with a dramatic drop in left ventricular preload by decreased pulmonary blood flow to the left atrium from the cessation of the shunt. 

The management strategy focuses on carefully modulating systemic vascular resistance while supporting myocardial recovery. Continuous milrinone infusion is often initiated prior to ligation or continued/initiated postoperatively to provide afterload reduction and lusitropic support, promoting myocardial relaxation and preventing excessive blood pressure elevation. In cases of established hypertension, oral angiotensin-converting enzyme inhibitors such as captopril may be introduced once renal perfusion is stable, aiming to blunt neurohumoral activation and facilitate gradual normalization of vascular tone.

Close monitoring of systemic blood pressure, urine output, and echocardiographic parameters is essential to titrate therapy effectively. The goal is to balance afterload reduction with maintenance of adequate systemic perfusion and oxygen delivery. As the cardiovascular system adapts to the new post-ligation physiology and the myocardium recovers from transient stress, blood pressure typically stabilizes over several days. Understanding the interplay between vascular resistance, ventricular function, and neurohumoral responses remains key to optimizing postoperative management and minimizing the long-term sequelae of PDA ligation.