Neonatology最新文献

Background: Although a major cause of infant mortality for centuries, little research was done on the causes of infants' diarrhea. Artificial feeding, teething, and summer heat were believed to cause the severe disease that spared breastfed infants.

Summary: Since antiquity, infants' digestive disorders were termed dyspepsia, flux of the belly, diarrhea, gastroenteritis, watery gripes, the runs, dysentery, or cholera, without definitions. Alois Bednar discerned 3 grades (dyspepsia, diarrhea, and cholera) of the same disease. Infants' neurologic symptoms were interpreted as alimentary toxicosis. Chronic diarrhea caused emaciation and dehydration. In 1950, Laurence Finberg found diarrhea with hypernatremia causing cerebral damage. Seasonal influence was known since Hippocrates. Baudelocque recommended obtaining infant milk fresh from the cow because it decomposes in the summer heat. In the cities, summer diarrhea caused a third of total infant mortality. Physicians debated whether heat acted directly on the infant or spoiled the food. The discovery of microorganisms in the 1860s revolutionized medical understanding. However, influential researchers such as Adalbert Czerny classified nutritional disturbances by assumed pathogenesis ("ex alimentation, ex infection, ex constitution"), but denied the possibility of bacterial infection via milk. Heating baby food, practiced for centuries, was introduced in Denmark, Sweden, and France, whereas in Britain and Germany, professional and public debate on pasteurization persisted.

Key messages: It took half a century to implement effective hygienic measures once the bacterial origin became known. Foodborne infection was rejected, and the prejudice that raw milk possesses essential "living" properties, adopted by influential scientists, contributed to delaying pasteurization.

Introduction: Perinatal asphyxia initiates cytokine release and complement activation with risk of brain damage. We assessed the effect of nicotine on innate immunity and hypothesized that nicotine infusion in a newborn piglet model of asphyxia would decrease the immune response and be neuroprotective.

Methods: Newborn piglets (n = 41) were randomized to one of three groups after hypoxia: two groups receiving nicotine, (1) 18 µg/kg/h (n = 17), (2) 46 µg/kg/h (n = 15), and (3) control group receiving saline (n = 9). C3a, IL-6, TNF, and IL-10 were measured in plasma and IL-6 and IL-8 in microdialysis fluid from cerebral periventricular white matter, using immuno-assays.

Results: Plasma C3a and IL-6 increased significantly from start to end hypoxia (mean 4.4 ± 0.55 to 5.6 ± 0.71 ng/mL and 1.66 ± 1.04 to 2.68 ± 0.71 pg/mL, respectively), while IL-10 and TNF increased significantly after 4 h (mean 1.4 ± 1.08 to 2.9 ± 1.87 and 3.3 ± 0.67 to 4.0 ± 0.58 pg/mL, respectively) (p < 0.001 for all). IL-6 increased significantly (p < 0.001) in microdialysis samples from end hypoxia to end experiment (mean 0.65 ± 0.88 to 2.78 ± 1.84 ng/mL). No significant differences were observed between the nicotine groups and the control group neither in plasma nor in microdialysis samples.

Conclusion: Hypoxia leads to rapid release of cytokines in plasma and cerebral microdialysis fluid, and complement activation measured on C3a. However, low-dose nicotine administration did not affect the immune response.

Introduction: Compromised neonatal intensive care unit neonates are at risk of acquiring late-onset infections (late-onset sepsis [LOS]). Neonates born with congenital anomalies (CAs) could have an additional LOS risk.

Methods: Utilising the population-based Australian and New Zealand Neonatal Network data from 2007 to 2017, bacterial LOS rates were determined in very preterm (VPT, <32 week), moderately preterm (MPT, 32-36 weeks), and term (FT, 37-41 weeks) neonates with or without CA. Stratified by major surgery, the association between CA and bacterial LOS was evaluated.

Results: Of 102,808 neonates, 37.7%, 32.8%, and 29.6% were born VPT, MPT, and FT, respectively. Among these, 3.4% VPT, 7.5% MPT, and 16.2% FT neonates had CA. VPT neonates had the highest LOS rate (11.1%), compared to MPT (1.8%) and FT (1.8%) neonates. LOS rates were higher in CA neonates than those without (8.2% versus 5.1% adjusted relative risk [aRR] 1.67, 95% confidence interval [CI]: 1.45-1.92). Neonates with surgery had a higher LOS rate (14.2%) than neonates without surgery (4.4%, p < 0.001). Among the neonates without surgery, CA neonates had consistently higher LOS rates than those without CA (VPT 14.3% vs. 9.6% [aRR 1.32, 95% CI: 1.11-1.57]; MPT 4% vs. 0.9% [aRR 4.45, 95% CI: 3.23-6.14]; and FT 2% vs. 0.7% [aRR 2.87, 95% CI: 1.97-4.18]). For the neonates with surgery, CAs were not associated with additional LOS risks.

Conclusion: Overall, we reported higher rates of LOS in neonates with CA compared to those without CA. Regardless of gestation, CA was associated with an increased LOS risk among non-surgical neonates. Optimisation of infection prevention strategies for CA neonates should be explored. Future studies are needed to evaluate if the infection risk is caused by CA or associated complications.

Introduction: Neonatal linear immunoglobulin A (IgA) bullous dermatosis (NLABD) is a rare, life-threatening, mucocutaneous bullous disorder. The pathogenesis and optimal treatment remain poorly defined and raise critical clinical challenges.

Case presentation: We present a case of a full-term female infant with severe cutaneous and respiratory symptoms due to NLABD. Diagnosis was confirmed by immunofluorescence on the infant's skin biopsy, while IgAs directed against the basement membrane of the skin and mucosa were identified in the mother's milk. The infant fully recovered after nearly 8 weeks of intensive multidisciplinary care, including non-invasive ventilation, nutritional support, wound care, systemic corticoid treatment, and breastfeeding discontinuation.

Conclusion: This case underscores the importance of timely adequate diagnosis and management of this rare and serious condition. Moreover, it adds novel evidence documenting the presence of pathogenic IgAs in breastmilk.

Introduction: In Canada, newborn morbidity far surpasses mortality. The neonatal adverse outcome indicator (NAOI) summarizes neonatal morbidity, but Canadian trend data are lacking.

Methods: This Canada-wide retrospective cross-sectional study included hospital livebirths between 24 and 42 weeks' gestation, from 2013 to 2022. Data were obtained from the Canadian Institute of Health Information's Discharge Abstract Database, excluding Quebec. The NAOI included 15 newborn complications (e.g., birth trauma, intraventricular hemorrhage, or respiratory failure) and seven interventions (e.g., resuscitation by intubation and/or chest compressions), adapted from Australia's NAOI. Rates of NAOI were calculated by gestational age. Unadjusted rate ratios (RR) and 95% confidence interval (CI) were calculated for neonatal mortality, neonatal intensive care unit (NICU) admission, and extended hospital stay, each in relation to the number of NAOI components present (0, 1, 2, 3, 4, or ≥5).

Results: Among 2,821,671 newborns, the NAOI rate was 7.6%. NAOI increased from 7.3% in 2013 to 8.0% in 2022 (p < 0.01). NAOI prevalence was highest in the most preterm infants. Compared to no NAOI, RRs (95% CI) for mortality were 8.5 (7.6-9.5) with 1, 118.1 (108.4-128.4) with 3, and 395.3 (367.2-425.0) with ≥5 NAOI components. Respective RRs for NICU admission were 6.7 (6.6-6.7), 11.2 (10.9-11.3), and 11.9 (11.6-12.2), and RR for extended hospital stay were 6.6 (6.4-6.7), 12.2 (11.7-12.7), and 26.4 (25.2-27.5). International comparison suggested that Canada had a higher prevalence of NAOI.

Conclusion: The Canadian NAOI captures neonatal morbidity using hospitalization data and is associated with neonatal mortality, NICU admission, and extended hospital stay. Newborn morbidity may be on the rise in recent years.

Introduction: Intrauterine herpes simplex virus (HSV) infection is uncommon and challenging to diagnose, requiring detection of HSV in skin lesions within 48 h post-birth.

Case presentation: A preterm female infant presented with the typical triad of blisters, microcephaly, and chorioretinitis, but the initial diagnostic approach was elusive due to negative results for TORCH pathogens from vesicles/serum. Referred at 7 months for developmental delay and epilepsy, her brain imaging showed calcification and cortical dysplasia. Polymerase chain reaction (PCR) of her preserved dried umbilical cord detected HSV-2 DNA, diagnosing intrauterine HSV infection. HSV-2 was later found in relapsed blisters at 8 months but not in cerebrospinal fluid or brain tissue. A literature review identified 104 congenital/intrauterine HSV cases; 28.8% presented the typical triad, and 50% were diagnosed using specimens collected 48 h post-birth.

Conclusion: This case marks the first retrospective diagnosis of intrauterine HSV infection via PCR on preserved umbilical cord, underscoring its diagnostic value.

Introduction: Optimal oxygen saturation targets remain unknown for extremely preterm infants.

Methods: Cohort analysis of eligible preterm infants born <29 weeks' gestation admitted between 2011 and 2018 to centers submitting data to the Canadian Neonatal Network (CNN) database. Site questionnaires to determine saturation targets, alarm settings, and date of change, allowed assignation of centers to intermediate (88-93%) or high (90-95%) saturation targets. A 6-month washout period was applied to sites which switched targets during the study period. Our primary outcome was survival free of major morbidity. Secondary outcomes were death, necrotizing enterocolitis (NEC), bronchopulmonary dysplasia (BPD), treated retinopathy of prematurity, and evidence of brain injury during admission. Generalized estimating equations were applied to compensate for demographic differences and site practices.

Results: There were 2,739 infants in the high (mean gestational age [GA] 26 ± 1.6 weeks) and 6,813 infants in the intermediate (mean GA 26.2 ± 1.6 weeks) saturation target group. Survival without morbidity was higher in the intermediate target group (adjusted odds ratio [aOR] 1.59; 95% CI: 1.04, 2.45). There was no difference in mortality between groups (aOR 0.81; 95% CI: 0.59, 1.11), in NEC, treated retinopathy, or brain injury. On subgroup analysis, restricting data to sites which switched targets during the study, intermediate saturation targets were associated with lower rates of BPD (aOR 0.45; 95% CI: 0.28, 0.72).

Conclusion: For neonates <29 weeks' gestation, intermediate saturation target was associated with higher odds of survival without major morbidity compared to higher oxygen saturation target.

Introduction: Probiotics have shown potential in reducing the occurrence of atopic eczema in high-risk infants. We aimed here to assess whether the preventive effect of maternal probiotic administration stems from compositional changes in early gut microbiota.

Methods: This study included 46 mother-infant pairs from an original randomized controlled trial assessing the impact of maternal probiotic intervention with either the combinations of Lacticaseibacillus rhamnosus LPR and Bifidobacterium longum BL999, or Lacticaseibacillus paracasei ST11 and Bifidobacterium longum BL999, or placebo beginning 2 months before expected delivery and ending 2 months after birth. All children were vaginally delivered, full term and breastfed. During the 2-year follow-up period, the children were clinically evaluated by physicians for atopic eczema, and their gut microbiota was profiled at 1 and 6 months of age by 16S rRNA gene sequencing using an Illumina sequencing platform.

Results: Altogether, 19 of 46 children developed atopic eczema by the age of 2 years. At 1 and 6 months of age, gut microbial diversity was similar between children who developed atopic eczema and their healthy controls, but at the age of 6 months, children who developed atopic eczema manifested with significantly higher relative abundance of Clostridia. Probiotic intervention did not significantly influence microbial diversity, and the effects on microbial composition were not consistent with the changes associated with the development of atopic eczema.

Conclusion: The reduction of the risk of atopic eczema achieved by perinatal maternal probiotic intervention does not seem to require substantial gut microbiota modulation.