Aim:  Intrauterine conditions may interfere with foetal brain development. We compared the neurodevelopmental outcome between infants <32 weeks gestational age after maternal preeclampsia or chorioamnionitis and controls. Methods:  Case‐control study on infants with maternal preeclampsia, chorioamnionitis and controls (each n = 33) matched for gestational age. Neurodevelopment at 2 years was assessed with the Bayley Scales of Infant Development II. Results:  A total of 99 infants were included with a median gestational age of 29 weeks (range 25–32). Median mental developmental index (MDI) was 96 in the control, 90 in the chorioamnionitis and 86 in the preeclampsia group. Preeclampsia infants had a lower MDI compared with the control group (univariate p = 0.021, multivariate p = 0.183) and with the chorioamnionitis group (univariate p = 0.242; multivariate p = 0.027). Median psychomotor index was 80.5 in the control, 80 in the preeclampsia and 85 in the chorioamnionitis group and was not different between these three groups (p > 0.05). Chorioamnionitis or preeclampsia exposure was not associated with major neurodevelopmental impairments (cerebral palsy, MDI<70, PDI<70). Conclusion:  The results of this preliminary study suggest that preeclampsia and chorioamnionitis play a relatively minor role among risk factors for adverse neurodevelopment outcome. Postnatal factors such as ventilation and bronchopulmonary dysplasia may have a greater impact on neurodevelopmental outcome.

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Our retrospective study presents and evaluates clinical ethics consultations (CECs) in pediatrics as a structure for implementing hospital-wide ethics. We performed a descriptive and statistical analysis of clinical ethics decision making and its implementation in pediatric CECs at Zurich University Children's Hospital. Ninety-five CECs were held over 5 years for 80 patients. The care team reached a consensus treatment recommendation after one session in 75 consultations (89 %) and on 82 of 84 ethical issues (98 %) after two or more sessions (11 repeats). Fifty-seven CECs recommended limited treatment and 23 maximal treatment. Team recommendations were agreed outright by parents and/or patient in 59 of 73 consultations (81 %). Initial dissensus yielded to explanatory discussion or repeat CEC in seven consultations (10 %). In a further seven families (10 %), no solution was found within the CEC framework: five (7 %) required involvement of the child protection service, and in two families, the parents took their child elsewhere. Eventual team-parent/patient consensus was reached in 66 of 73 families (90 %) with documented parental/patient decisions (missing data, n = 11). Patient preference was assessable in ten CECs. Patient autonomy was part of the ethical dilemma in only three CECs. The Zurich clinical ethics structure produced a 98 % intra-team consensus rate in 95 CECs and reduced initial team-parent dissensus from 21 to 10 %. Success depends closely on a standardized CEC protocol and an underlying institutional clinical ethics framework embodying a comprehensive set of transparently articulated values and opinions, with regular evaluation of decisions and their consequences for care teams and families.

The incidence of RD in infants admitted to neonatal units doubled over the last 30 years in a geographically defined neonatal population. This rise can predominantly be ascribed to infants with birth weight >2500 g and may reflect the corresponding increase in the rate of caesarean section.

Skin development is a continuous process, but some discrete patterns are strongly related to fetal age, are easy to recognize, and are insensitive to artifacts. In our institution, they have become indispensable in evaluating fetal and neonatal pathology.

Aims: To compare the effect of fasting period duration on complication rates in neonates managed conservatively for necrotizing enterocolitis (NEC) Bell stage II. Methods: We conducted a multicenter study to analyze retrospectively multiple data collected by standardized questionnaire on all admissions for NEC between January 2000 and December 2006. NEC was staged using modified Bell criteria. We divided the conservatively managed neonates with NEC Bell stage II into two groups (those fasted for -5 days and those fasted for )5 days) and compared the complication rates. Results: Of the 47 conservatively managed neonates Bell stage II, 30 (64%) fasted for -5 days (range 1-4 days) and 17 (36%) for )5 days (range 6-16 days). There were no significant differences for any of the patient characteristics analyzed. One (3%) and four (24%) neonates, respectively, developed post-NEC bowel stricture. One (3%) and two neonates (12%) suffered NEC relapse. None and five (29%) neonates developed catheter-related sepsis. Conclusion: Shorter fasting after NEC appears to lower morbidity after the acute phase of the disease. In particular, shorter-fasted neonates have significantly less catheter-related sepsis. We found no benefit in longer fasting.

A 4-year old boy with D-transposition of the great arteries, pulmonary atresia with intact ventricular septum, and a hypoplastic left ventricle with mitral atresia underwent a Fontan operation. He had previously been treated with neonatal balloon atrial septostomy followed by a left modified Blalock-Taussig shunt and, at the age of 2 years, a Hemi-Fontan operation was performed. The Fontan operation was completed with an extracardiac conduit (Goretex) from the inferior vena cava to the superior vena cava. High central venous pressures and bilateral chylothoraces complicated the postoperative course. Despite 6 weeks of conservative treatment with fat-free nutrition and subsequent total parenteral nutrition, pleural fluid loss remained excessive, and a pleurodesis was performed bilaterally. A few days postoperatively, acute respiratory failure occurred due to bronchial casts. Cast analysis showed high triglyceride and protein concentrations (cast triglyceride, 0.96 mmol/L; cast protein, 66 g/L; serum triglyceride, 0.36 mmol/L; and serum protein, 47 g/L). Bronchoscopic attempts to remove the bronchial casts failed, and the child died of cardiorespiratory failure.At autopsy, the bronchial system was completely plugged by casts resembling bronchial tree anatomy (Figure 1). Thromboses obliterated the left innominate vein partially and reduced the lumen of the extracardiac conduit by 50%. These thromboses occurred despite full anticoagulation and were not detected by previous transthoracic echocardiography. Histopathology demonstrated massively dilated pulmonary lymph vessels within the whole lung (Figure 2). Ruptures of lymphatic vessels and the influx of chyle into the alveoli could clearly be demonstrated (Figure 3). The material in the alveoli was proven to be chyle by lipid staining (Figure 4). The mechanism of lymphatic leakage leading to the formation of bronchial casts has been discussed, 1 but it had not been demonstrated histologically before. This condition must be distinguished from mucus hypersecretion as an unusual response of the pulmonary epithelium to elevated venous pressure (classified as type II or as acellular mucin casts by Seear et al), 2 where no alveolar flooding with chyle is present. Respir Crit Care Med. 1997;155:364 -370.

A 20-month-old male child died during an episode of acute bronchitis. The autopsy revealed massive hypertrophy and acute dilatation of the right heart which was caused by pulmonary hypertension exhibiting plexogenic arteriopathy and necrotizing arteriitis of small lung vessels. Further examination revealed complete old fibrotic occlusion of the extrahepatic portal vein and a large porto-systemic shunt. Esophageal varices indicating portal hypertension were not present. Histology showed enlarged hepatic arteries within the portal tracts while branches of the portal vein were lacking. The placenta had been examined at the time of birth and multiple chorangiomas reported. Furthermore, multiple old and florid occlusions of fetal vessels had been detected together with focal lymphoplasmocytic inflammation, which may indicate that intrauterine infection and vascular compromise were the cause of the complete closure of the portal vein around birth. The association of pulmonary hypertension with liver disease is well known, and portal hypertension has been considered a key factor in the pathogenesis of pulmonary hypertension. However, this case illustrates that portal hypertension is not a requisite for the development of pulmonary hypertension. It rather suggests that plexogenic arteriopathy of the lungs can be caused by porto-caval shunting independent of liver damage and portal hypertension. Toxic metabolites of nutrients or residual activity of pancreatic enzymes reaching the pulmonary vascular bed may be involved in the pathogenesis.