Consequences of delayed surgical closure of patent ductus arteriosus in very premature infants.

BACKGROUND: Surgical closure of ductus arteriosus is commonly indicated in premature newborns. The aim of this study was to assess short-term and mid-term effects of delayed surgical closure of the ductus arteriosus on respiratory and digestive outcome in extremely preterm infants. METHODS: We retrospectively studied 58 infants less than 28 weeks gestational age who underwent surgical closure of ductus arteriosus between January 1997 and December 2002. Nine infants with intrauterine growth restriction and major congenital malformation were excluded from the study. Criteria for surgical closure of ductus arteriosus were: (1) medical treatment failure (ie, indomethacin or ibuprofen) and (2) hemodynamically patent ductus arteriosus: systemic arterial pressure less than gestational age in mm Hg, heart failure, left atrial-aortic root ratio greater than 1.6, mean velocity in the left pulmonary artery greater than 0.6 m/s, and ductus arteriosus diameter greater than 3 mm. Infants were divided into two groups: (1) the early group who had surgery before 21 days of life (n = 31), and (2) the late group who had surgery after 21 days of life (n = 27). Preoperative and postoperative criteria were compared between the two groups (ie, gestational age, birth weight, hemodynamic, ventilatory, and echographic [left atrial-aortic root ratio, mean velocity in the left pulmonary artery] parameters). RESULTS: Preoperative gestational age and birth weight did not differ between the two groups. In the early group, gestational age was 26 weeks (range, 23 to 28 weeks and birth weight was 800 g (range, 630 to 1,240 g). In the late group, gestational age was 26 weeks (range, 24 to 28 weeks) and birth weight was 840 g (530 to 1,130 g). Hemodynamic, ventilatory, and echographic parameters were similar in both groups. Rate of bronchopulmonary dysplasia was similar in both groups. However, at 24 hours post surgery, median FiO2 was higher in the late group (28% [range, 21% to 65%]) than in early group (21% [range, 21% to 60%]) (p < 0.05). Furthermore, full oral feeding was acquired later in the late group (57 days of life [range, 30 to 136 days]) than in the early group (37 days of life [range, 27 to 84 days]) (p < 0.01), and body weight at 36 weeks of post-conceptional age was higher in the early group at 1,800 g (range, 1,250 to 2,750 g) than in the late group at 1,607 g (1,274 to 2,200 g) (p < 0.05). CONCLUSIONS: Our findings show that early surgical closure of the ductus arteriosus (< 3 weeks of life) is associated with shortened delay for full oral feeding and improved body growth when compared with late surgical closure (> 3 weeks of life).

Preoperative ECMO in transposition of the great arteries with persistent pulmonary hypertension.

Persistent fetal circulation in transposition of the great arteries results in severe persistent pulmonary hypertension, which increases the risk of early mortality. We report the case of a newborn with transposition of the great arteries and intact ventricular septum associated with pulmonary hypertension. After the failure of immediate balloon atrial septostomy and supportive therapy including inhaled nitric oxide, preoperative extracorporeal membrane oxygenation reversed pulmonary hypertension and ventricular insufficiency and preceded a safe, delayed, cardiac surgical procedure. Unlike the authors of the other few case reports on this subject, we recommend a preoperative stabilization period after discontinuation of extracorporeal membrane oxygenation to avoid left ventricular "deconditioning" and postoperative deterioration related to recurrent persistent pulmonary hypertension.

Can generic paediatric mortality scores calculated 4 hours after admission be used as inclusion criteria for clinical trials?

INTRODUCTION: Two generic paediatric mortality scoring systems have been validated in the paediatric intensive care unit (PICU). Paediatric RISk of Mortality (PRISM) requires an observation period of 24 hours, and PRISM III measures severity at two time points (at 12 hours and 24 hours) after admission, which represents a limitation for clinical trials that require earlier inclusion. The Paediatric Index of Mortality (PIM) is calculated 1 hour after admission but does not take into account the stabilization period following admission. To avoid these limitations, we chose to conduct assessments 4 hours after PICU admission. The aim of the present study was to validate PRISM, PRISM III and PIM at the time points for which they were developed, and to compare their accuracy in predicting mortality at those times with their accuracy at 4 hours. METHODS: All children admitted from June 1998 to May 2000 in one tertiary PICU were prospectively included. Data were collected to generate scores and predictions using PRISM, PRISM III and PIM. RESULTS: There were 802 consecutive admissions with 80 deaths. For the time points for which the scores were developed, observed and predicted mortality rates were significantly different for the three scores (P < 0.01) whereas all exhibited good discrimination (area under the receiver operating characteristic curve >or=0.83). At 4 hours after admission only the PIM had good calibration (P = 0.44), but all three scores exhibited good discrimination (area under the receiver operating characteristic curve >or=0.82). CONCLUSIONS: Among the three scores calculated at 4 hours after admission, all had good discriminatory capacity but only the PIM score was well calibrated. Further studies are required before the PIM score at 4 hours can be used as an inclusion criterion in clinical trials.

Maternal Bartter's syndrome in pregnancy treated by amiloride.

BACKGROUND: Bartter's syndrome is a rare condition during pregnancy. The prenatal management is difficult to maintain normal potassium serum levels. CASE: We describe a 26-year-old woman with Bartter's syndrome. During pregnancy, she required increasing potassium and magnesium supplementations. Amiloride, a sparing potassium diuretic, was continued. She delivered an unaffected girl at term. CONCLUSION: When Bartter's syndrome is associated with pregnancy, the management must be careful. Amiloride can be used to support potassium supplementation.

Electro-stimulation in preterm neonates with congenital auriculo-ventricular block. Report of three cases.

UNLABELLED: Congenital auriculo-ventricular blocks (CAVB) are usually linked to maternal auto-immune diseases and their management remains controversial. We report three cases of CAVB in preterm newborns managed using electro-stimulation with an external, followed by an internal pacemaker. Results and long-term follow-up were satisfactory in all three children. CONCLUSION: the transitory placement of an external pacemaker seems necessary in low birth weight infants in order to allow weight gain and therefore the insertion of a permanent pacemaker. The prognosis seems good but a regular echocardiographic surveillance is of great importance in order to detect the onset of cardiac failure secondary to dilated cardiomyopathy.

Effects of antenatal glucocorticoids on pulmonary vascular reactivity in the ovine fetus.

OBJECTIVES: Although mechanisms of glucocorticoids-induced parenchymal lung maturation have been largely studied, little is known about the pulmonary vascular effects of antenatal glucocorticoids (GCs). We therefore hypothesized that antenatal GCs may alter the hemodynamic response to vasodilatory agents in the fetal lung. STUDY DESIGN: We tested the hemodynamic response to acetylcholine, increased PaO(2), and norepinephrine infusion before and after maternal GC administration in chronically prepared, late-gestation fetal lambs (135-137 days of gestational age, term = 147 days). RESULTS: We found that antenatal GCs (1). do not change the basal pulmonary vascular tone and (2). do not alter the vasodilatory response to acetylcholine and increased PaO (2) but enhanced the norepinephrine-mediated pulmonary vasodilation. CONCLUSION: Our results indicate that antenatal GCs alter the pulmonary vascular reactivity to catecholamines. We speculate that the benefits of antenatal GCs on the cardiovascular adaptation at birth may be related to potentiation of catecholamines vascular effects.

Role of the alpha2-adrenoceptors on the pulmonary circulation in the ovine fetus.

Recent in vitro studies reported that nitric oxide release and pulmonary vasorelaxation can be mediated by endothelial alpha2-adrenoceptor activation. As norepinephrine (alpha1-,alpha2-, and beta1-adrenoceptor agonist) was found to induce pulmonary vasodilation in the ovine fetus, we hypothesized that alpha2-adrenoceptors may modulate basal pulmonary vascular tone and mediate the vascular effect of norepinephrine during fetal life. To determine the role of alpha2-adrenoceptors and the mechanisms of norepinephrine-mediated vasodilation in the fetal pulmonary circulation, we tested, in chronically prepared late-gestation fetal lambs, the hemodynamic response to 1). yohimbine (alpha2 antagonist); 2). UK 14304 (alpha2 agonist) with and without l-nitro-arginine (nitric oxide synthase inhibitor); and 3). norepinephrine infusion with and without yohimbine. We found that yohimbine increased mean pulmonary artery pressure by 15% (p < 0.05), decreased pulmonary flow by 22% (p < 0.01), and increased pulmonary vascular resistance by 51% (p < 0.01). UK 14304 increased pulmonary flow by 145% (p < 0.01) and decreased pulmonary vascular resistance by 58% (p < 0.01). l-Nitro-arginine abolished the UK 14304-mediated pulmonary vasodilation. Norepinephrine (0.5 microg x kg(-1)x min(-1) increased both pulmonary flow by 61% (p < 0.01) and pulmonary arterial pressure by 13% (p < 0.01) and decreased pulmonary vascular resistance by 33% (p < 0.01). Yohimbine abolished the norepinephrine-induced pulmonary vasodilation. This study suggests that 1). a basal alpha2-adrenoceptor activation-induced pulmonary vasodilation exists during fetal life; 2). the pulmonary vascular effects of alpha2-adrenoceptor activation are related at least in part to nitric oxide production; and 3). the norepinephrine-mediated pulmonary vasodilation involves alpha2-adrenoceptor activation. As a surge of norepinephrine exists at birth, we speculate that norepinephrine and endothelial alpha2-adrenoceptor activation may play a significant role in pulmonary vasodilation at birth.