Respiratory distress syndrome results from inadequate functional pulmonary surfactant and is a significant cause of mortality in preterm infants. Surfactant is essential for regulating alveolar interfacial surface tension, and its synthesis by Type II alveolar epithelial cells is stimulated by leptin produced by pulmonary lipofibroblasts upon activation by peroxisome proliferator-activated receptor γ (PPARγ). As it is unknown whether PPARγ stimulation or direct leptin administration can stimulate surfactant synthesis before birth, we examined the effect of continuous fetal administration of either the PPARγ agonist, rosiglitazone (RGZ; Study 1) or leptin (Study 2) on surfactant protein maturation in the late gestation fetal sheep lung. We measured mRNA expression of genes involved in surfactant maturation and showed that RGZ treatment reduced mRNA expression of LPCAT1 (surfactant phospholipid synthesis) and LAMP3 (marker for lamellar bodies), but did not alter mRNA expression of PPARγ, surfactant proteins (SFTP-A, -B, -C, and -D), PCYT1A (surfactant phospholipid synthesis), ABCA3 (phospholipid transportation), or the PPARγ target genes SPHK-1 and PAI-1. Leptin infusion significantly increased the expression of PPARγ and IGF2 and decreased the expression of SFTP-B. However, mRNA expression of the majority of genes involved in surfactant synthesis was not affected. These results suggest a potential decreased capacity for surfactant phospholipid and protein production in the fetal lung after RGZ and leptin administration, respectively. Therefore, targeting PPARγ may not be a feasible mechanistic approach to promote lung maturation.

Respiratory infections among infants constitute a major burden to health care systems in developed nations, yet the course and risk factors leading to these conditions are poorly understood. We examine the longitudinal patterns of respiratory infection hospitalisation (RIH) and how these patterns are influenced by neonatal pulmonary morbidities. We included all live births (n = 429 058) occurring in the Australian state of Queensland between January 2009 and December 2015. Data were structured so that each participant had a record (present/absent) of RIH for each month from birth to 12 months. Initially, latent class growth analysis was used to identify the trajectories of RIH adjusted for spatial–temporal factors; using the identified trajectories of RIH as outcomes, we built a multinomial logistic regression model to identify neonatal predictors of RIH trajectories. Our results indicated that a four-class solution was the best fit to the data, comprising a ‘no-risk’ trajectory, a ‘low-risk’ trajectory, an ‘early-risk’ trajectory and a ‘chronic-risk’ trajectory. Compared with the no-risk trajectory, membership in the other trajectories was predicted by a range of neonatal pulmonary morbidities, with transient tachypnoea of newborn showing a specific relationship with the early-risk group and sleep apnoea showing a specific and strong risk with the chronic-risk group. Our findings suggest the possibility of identifying neonates at risk of recurrent RIH and implementing effective intervention strategies prior to neonatal discharge.

Fetal lung maturity assessment in twin pregnancy has been discussed, but is still controversial. The purpose of this study is to predict the occurrence of respiratory distress syndrome (RDS) using lamellar body count (LBC) and analyze the validity of LBC for fetal lung maturity assessment in twin pregnancy. Three-hundred two amniotic fluid samples were obtained at cesarean section from 29 to 38 weeks of gestation. Samples were analyzed immediately with no centrifugation and the number of lamellar bodies was counted using a platelet channel on the Sysmex SF-3000. There were 18 neonates (6.0%) suffering from RDS. An LBC cut-off value of 2.95 × 104/μL resulted in 91.5% sensitivity and 83.3% specificity for predicting RDS. This cut-off value for predicting RDS was the same as that in singleton pregnancy. Moreover, the median LBC value in RDS cases was significantly lower than in non-RDS cases (1.50 ± 1.1 × 104/μL vs. 10.6 ± 7.5 × 104/μL; p < .001). This is the first report on the validity of LBC in twin pregnancy and also the largest study on fetal lung maturity assessment in twin pregnancy. An LBC value of >2.95 × 104/μL means reassuring findings for RDS even in twin pregnancy. We believe the data in this study provide valuable, new information for the management of twin pregnancies.

Fetal growth restriction in singletons has been shown to enhance fetal lung maturation and reduce the risk of respiratory distress syndrome due to increased endogenous steroid production. However, data on lung maturation in growth-discordant monochorionic (thus, identical) twins are lacking. Our objective was to compare the risk of severe neonatal morbidity between the larger and the smaller twin in monochorionic twins with birth weight discordance (BWD). We included in the study all consecutive monochorionic diamniotic pregnancies with severe BWD (≥25%) and two live-born twins delivered at our center (n = 47 twin pairs). We compared the incidence of neonatal morbidity, particularly respiratory distress syndrome (RDS), and cerebral lesions between the larger and the smaller co-twin. The incidence of severe neonatal morbidity in the larger and smaller twin was 38% (18/47) and 19% (9/47), respectively (odds ratio (OR) 2.66, 95% confidence interval (CI) 0.94–7.44) and was due primarily to the higher incidence of RDS, 32% (15/47) and 6% (3/47), respectively (OR 6.88, 95% CI 1.66–32.83). In conclusion, this study shows that the larger twin in monochorionic twin pairs with BWD is at increased risk of severe neonatal morbidity, particularly RDS, compared to the smaller twin.

Glial heterotopia is a rare disorder. However, it must be considered in the differential diagnosis of airway obstruction in the newborn. Differentiation of this lesion from nasal glioma and encephalocele is important.

In this paper we report a midline glial heterotopia, which presented with upper airway obstruction in a newborn. The origin of a glial heterotopia from the midline of the nasopharynx has not been reported before.

We present a review of the literature and discuss the clinical, radiological and pathological features of nasopharyngeal brain heterotopia in an infant.

Summary

Background and objective: We evaluated the effect of duration of mechanical ventilation with different tidal volumes (VT) on ventilator-induced lung injury in healthy rats. Methods: Anaesthetized rats were ventilated with VT between 9 and 45 mL kg−1 for 1 or 7 h with a positive end-expiratory pressure of 2.5 cmH2O. Results: After 1 h, rats ventilated even with the highest applied VT (36 and 45 mL kg−1, resulting in average peak airway pressures of 30 ± 3 and 37 ± 4 cmH2O), had no detectable alterations in dynamic or static lung mechanics, gas exchange or pulmonary permeability, but a moderate degree of lung inflammation (neutrophil accumulation in broncho-alveolar lavage) observed in all groups. In contrast, after 3 h of ventilation, rats ventilated with the highest VT (36 and 45 mL kg−1) died from progressive circulatory failure and high-permeability pulmonary oedema, manifested by hypoxaemia, an increased alveolar–arterial protein concentration ratio and a reduced static lung compliance (mortality rate at 7 h, 62.5% and 100%). Animals with lower VT all survived and presented no changes in the measured variables. Conclusion: These results in normal rats demonstrate the preponderant effect of the duration (>3 h) of ‘aggressive’ ventilation and the cut-off value of the level of VT applied (>27 mL kg−1).

We report the case of a young man who presented with a clinical picture of acute pyelonephritis. Within 3 h of admission, the patient developed acute respiratory distress associated with tachycardia and shock, and he was transferred to the intensive care unit. Mechanical ventilation of the lungs and symptomatic treatment were started immediately. Abdominal ultrasound revealed the presence of an adrenal tumour with central necrosis indicating a probable phaeochromocytoma. There was no sign of pyelonephritis. Ventricular fibrillation followed by asystole occurred soon after admission. The suddenness of the patient’s death did not allow time for further investigation and therapy. The severity of the clinical signs was probably related to a massive release of catecholamines because of necrosis of the tumour, which may have been worsened by the diagnostic procedures performed to investigate the clinical symptoms and signs of acute pyelonephritis.

Background and objective Pressure-controlled inverse ratio ventilation was compared with controlled mechanical ventilation in patients after cardiac surgery.

Methods Ten patients were ventilated after sternal closure using a Siemens Servo 900C ventilator to a target end–tidal PCO2 of 4.0 kPa. They were randomized to receive controlled mechanical ventilation or pressure–controlled inverse ratio ventilation. CO2-based data were recorded on a laptop personal computer, which together with arterial PCO2 permitted measurement of the respiratory dead space. Once measurements were complete the ventilator was switched to the other mode and new measurements taken. Results PaCO2 and VCO2 were virtually the same in both modes. Peak airway pressure (17.2±2.7 vs. 20.8±2.5 cmH2O, P < 0.01) and minute ventilation (4.9±1.1 vs. 5.3±1.1 cmH2O, P < 0.01) were less during pressure–controlled inverse ratio ventilation. Physiological dead space fraction (0.39±0.06 vs. 0.51±0.05, P <0.001), airway dead space (56±15 vs. 81±15 mL, P <0.001) and alveolar dead space fraction (0.25±0.07 vs. 0.31±0.09, P<0.01) were all less during pressure–controlled inverse ratio ventilation. There were no differences in heart rate or mean arterial pressure.

Conclusions The prolonged inspiratory period and pressure–controlled flowpattern of pressure–controlled inverse ratio ventilation reduce the alveolar and airway dead spaces, and give lower peak airway pressures, compared with conventional ventilation, in cardiac surgical patients.

Amniotic fluid elastolytic activity was assessed in a group of 120 women who delivered preterm infants and in 35 women who delivered at term. Amniotic fluid elastolytic activity decreases as pregnancy progresses. The lecithin-to-sphingomyelin (L/S) ratio in women's amniotic fluid was determined by the method developed by Gluck and associates [6] and elastolytic activity by that developed by Mehdi and associates. A significant negative correlation was found between the amniotic fluid L/S ratio and amniotic fluid elastolytic activity (r = −0.932; p<0.001).

The border value of elastolytic activity that indicates lung maturity (L/S ratio equal to or greater than 2) is 2.01 ± 0.05 mmol/min ml. In the amniotic elastolytic activity test, it is the value that differentiates mature from immature lungs. The amniotic fluid elastolytic activity test is characterized by high sensitivity (91.43%) and specificity (91.67%), high positive prognostic value (76.19%) and low negative prognostic value (2.65%). The test parameters do not therefore differ greatly from those of the Gluck test. Moreover, the amniotic fluid elastolytic activity test is cheaper and takes less time to perform.

During a screening protocol of early echocardiographic diagnosis (ATL MK 600) and treatment of “silent” PDA in RDS preterms with BW ≤ 1.750 kg, clinical data on premature twins were collected, including diagnosis of both PDA and BPD, to investigate whether twin birth influences PDA incidence and BPD development. Out of the 290 RDS preterms evaluated, 96 (33%) showed evidence of PDA, and a total of 79 (27%) developed BPD, 47 (16%) with associated PDA and 32 (11%) without PDA. Out of 238 singletons, 74 (31%) presented “silent” PDA and a total of 75 (31%) developed BPD, 44 (18%) with associated PDA, and 31 (13%) without PDA. In 52 other twins (18% of the total number of babies studied), 22 (42% of this subgroup) presented evidence of “silent” PDA, and 4 (8% of the subgroup), developed BPD, 3 with associated PDA (6% of the subgroup), and 1 without PDA (2% of the subgroup). From these data, it is inferred that that low-birthweight twins are at high risk for PDA hemodynamic complications during RDS, and may benefit from early induced ductal closure. Instead, in RDS twins, BPD was statistically less frequent (at the 99% C.L.) probably because twinning enhances fetal lung maturity, influencing enzymatic and nonenzymatic protective systems of lung defence.

The incidence and evolution of patent ductus arteriosus (PDA) was evaluated in twins and preterm singletons with birth weight ≤ 1750 g admitted to our Department in 1987 for respiratory distress syndrome (RDS). Screening by echocardiography and Doppler-flow studies (AT MK 600) was performed on the third day of life. Out of 91 neonates who needed intubation and ventilation during this 12-month period (23.8% of admissions), 40 weighed less than 1750 g and of these 40, 14 were twins (35%). Hemodynamically significant PDA was documented in 13 patients; of these, only 5 were preterm singletons and 8 were twins. Two twins weighing < 1000 g received no therapy for ductus closure; one ductus closed spontaneously, the other had an early demise. Three twins and 2 preterm singletons received indomethacin; one of the twins needed a second cycle for definitive ductus closure. Three twins and three preterm singletons underwent surgery, while one twin died on the 10th postoperative day. Screening and early therapy of PDA during RDS could be of great clinical importance. Twinning seems to play a role in the incidence and evolution of PDA and this needs to be evaluated in further studies.

Four hundred and thirty four twins occurring in 220 women were studied during a period of 11 years (1969–1979) at Notre-Dame Hospital.

Perinatal mortality (< 28 days) was compared before and after 1974, and the impact of ultrasound technique upon perinatal outcome was assessed during the second period (1974–1979). The main factor associated with perinatal mortality was low birth weight caused by either prematurity or intrauterine growth retardation.

While fetal mortality remained unchanged within the two study periods, neonatal mortality decreased from 68.2/1,000 to 28.9/1,000 mainly due to increased survival rate of twins below 1,500 g at birth.

With identical perinatal care during the same period, perinatal mortality and incidence of intrauterine growth-retarded twins remained unchanged despite early diagnosis by ultrasound.