patent ductus arteriosus | The Journal of Critical Care Medicine

Congenital Heart Disease Requiring Maintenance of Ductus Arteriosus in Critically Ill Newborns Admitted at a Tertiary Neonatal Intensive Care Unit

Manuela Cucerea^1*, Marta Simon¹, Elena Moldovan², Marcela Ungureanu³, Raluca Marian¹, Laura Suciu¹

1 University of Medicine and Pharmacy Tirgu Mureș, Romania
2 Institute of Cardiovascular Disease and Transplant Tirgu Mureș, Romania
3 Department of Neonatal Intensive Care,County Clinical Emergency Hospital Tirgu Mureş, Romania

DOI: 10.1515/jccm-2016-0031

Introduction: Congenital heart diseases (CHD) have been reported to be responsible for 30 to 50% of infant mortality caused by congenital disabilities. In critical cases, survival of newborns with CHD depends on the patency of the ductus arteriosus (PDA), for maintaining the systemic or pulmonary circulation. The aim of the study was to assess the efficacy and side effects of PGE (prostaglandin E) administration in newborns with critical congenital heart disease requiring maintenance of the ductus arteriosus.
Material and method: All clinical and paraclinical data of 66 infants admitted to one referral tertiary level academic center and treated with Alprostadil were analyzed. Patients were divided into three groups: Group 1: PDA dependent pulmonary circulation (n=11) Group 2: PDA dependent systemic circulation (n=31) Group 3: PDA depending mixed circulation (n=24)
Results: The mean age of starting PGE1 treatment was 2.06 days, 1.91 (+/-1.44) days for PDA depending pulmonary flow, 2.39 (+/-1.62) days for PDA depending systemic flow and 1.71 (+/1.12) for PDA depending mixing circulation. PEG1 initiation was commenced 48 hours after admission for 72%, between 48-72 hours for 6%, and after 72 to 120 hours for 21% of newborns detected with PDA dependent circulation. Before PEG1 initiation the mean initial SpO2 was 77.89 (+/- 9.2)% and mean initial oxygen pressure (PaO2) was 26.96(+/-6.45) mmHg. At the point when stable wide open PDA was achieved their mean SpO2increased to 89.73 (+/-8.4)%, and PaO2 rose to 49 (+/-7.2) mmHg. During PGE1 treatment, eleven infants (16.7%) had apnea attacks, five children (7.5%) had convulsions, 33 (50%) had fever, 47 (71.2%) had leukocytosis, 52 (78.8%) had edema, 25.8% had gastrointestinal intolerance, 45.5% had hypokalemia, and 63.6% had irritability.
Conclusions: For those infants with severe cyanosis or shock caused by PDA dependent heart lesions, the initiation and maintenance of PGE1 infusion is imperative. The side effects of this beneficial therapy were transient and treatable.

Drug Closure of a Patent Ductus Arteriosus in an Extremely Low Birth Weight Premature Newborn. A Case Report

Elena Moldovan¹, Manuela Cucerea^1,2

¹ University of Medicine and Pharmacy Tîrgu-Mureş, Romania, 38 Gheorghe Marinescu street, Tirgu Mures, 540139, Romania

² Regional Center of Neonatal Intensive Care Unit UGON, 50 Gheorghe Marinescu street, Tirgu Mures, 540139, Romania

DOI: 10.1515/jccm-2015-0006

Introduction: Patent ductus arteriosus involves maintaining the permeability of the vascular ductus located between the pulmonary artery and the descending aorta, due to the failure of transition from foetal to adult type circulation. This malformation is characteristic to premature newborns with extremely low birth weight. The main pathophysiological factors identified in this pathology are immaturity of the smooth muscles, presence of vasodilator mediators and persistent hypoxaemia. Ductal-dependent cardiac malformations require drug therapy for keeping the permeability of the ductus arteriosus until the time of corrective surgery.
Case presentation: We present the case of an extremely low birth weight premature new-born, derived from twin pregnancy with suspected specific pathology, respectively feto-fetal transfusion syndrome, admitted to the Regional Centre of Neonatal Intensive Care Unit Tîrgu-Mureş.
Premature newborn with gestational age 31-32 weeks, extremely low birth weight, derived from twin pregnancy, with adequate prenatal follow up, was born by caesarean section for severe intrauterine growth restriction secondary to feto-fetal transfusion syndrome suspicion. The newborn developed respiratory distress syndrome by surfactant deficiency, intraventricular-haemorrhage grade I/II, and severe retinopathy. The detection of a systolic murmur in the second week of life, the diastolic theft revealed by trans-fontanellar ultrasound as well as lowered diastolic blood pressure values raised the suspicion of a patent ductus arteriosus and therefore specific treatment with ibuprofen, a cyclooxygenase inhibitor, was initiated. Progressive alteration of the newborn`s condition and the evidence of a coarctation of the aorta imposed the initiation of Prostaglandin E1 therapy and subsequent surgical correction.
Conclusions: Although beneficial, prophylactic or therapeutic closure of persistent ductus arteriosus may worsen the evolution of a newborn with a “silent” cardiac malformation and associated pathology.