Respiratory syncytial virus (RSV) prophylaxis with the monoclonal antibody Nirsevimab has shown high efficacy in preventing severe lower respiratory tract infections in infants. However, the sequences of immunopathological phenomena leading to breakthrough infections and the role of RSV in causing extrapulmonary disease remain poorly understood. We report on a former preterm infant who developed an unusually severe form of necrotizing enterocolitis (NEC) requiring multiple emergency laparotomies and prolonged intensive care treatment in the context of severe RSV-bronchiolitis 22 days after passive immunization with Nirsevimab. RSV RNA was retrospectively detected using a validated RSV PCR assay in resected intestinal tissue obtained during the acute disease phase but was not detected in tissue collected during later surgical reconstruction. Our case highlights the need for clinicians to maintain a high index of suspicion for intestinal complications in infants with severe RSV infection. Although these findings raise the possibility of intestinal RSV involvement, a causal relationship between Nirsevimab prophylaxis, antibody-dependent enhancement (ADE), and NEC cannot be established from this single case. Confirmation in additional clinical and translational studies is required. Further clinical and translational studies are required to clarify the potential role of RSV in intestinal disease and the mechanisms underlying severe breakthrough infections.
Introduction: An Apgar score of 0 at 10 minutes is considered an indicator of poor prognosis and has historically influenced decisions regarding neonatal resuscitation. However, mortality estimates are largely based on small heterogeneous studies. We examined infant mortality among infants with Apgar score 0 at 10 minutes and compared mortality with that among infants with Apgar scores of 1, 2, or 3. Methods: This nationwide population-based cohort study included 2,638,291 singleton live births in Sweden from 1999 to 2024. Analyses included 1,608 infants born at ≥36 weeks’ gestation with an Apgar score of 0 to 3 at 10 minutes after birth. The primary outcome was all-cause infant mortality. Adjusted risk ratios (aRRs) with 95% confidence intervals (CIs) were estimated using modified Poisson regression. Results: Of 1,608 infants, 277 had an Apgar score of 0, 327 a score of 1, 398 a score of 2, and 606 a score of 3 at 10 minutes. Among infants with Apgar score 0, 143 infants (51.6%) died within the first year. The aRRs (95% CIs) for infant mortality were 1.16 (0.98-1.37) compared with Apgar score 1, 2.48 (1.99-3.09) compared with Apgar score 2, and 2.85 (2.32-3.51) compared with Apgar score 3. Conclusion: Infant mortality did not differ statistically significantly between infants with Apgar scores of 0 and 1 at 10 minutes, and was higher in both groups than among infants with Apgar scores of 2 or 3. These findings are consistent with resuscitation guidelines emphasizing individualized decision-making.
Background/Objectives Preterm survivors, with or without bronchopulmonary dysplasia (BPD) have decreased and progressive lung function decline. As neonatal care has improved survival, limited studies have compared lung function trajectories across birth epochs. Methods Retrospective study of subjects born <33 weeks who completed ≥1 pulmonary function test (PFT). BPD was classified per 2019 NICHD criteria. We analyzed spirometry values and Dysanapsis Ratio (DR). Birth epochs included Epoch A(<2000), B (2000-2009), and C(2010-2019). Results We analyzed 2,216 PFTs from 707 subjects; 319 (45.1%) had BPD. Pulmonary function decreased with increasing BPD severity. FEV1 decreased monotonically, from 92.0%(80.1-102.0) in preterm without BPD to 73.1%(57.7-84.9) in Grade 3, with consistent decreases in FVC (99.0%(87.0-110.0) to 85.2%(71.5-93.4). FEV₁/FVC remained largely constant, with a small decrease in Grade 3. Due to divergence in FEV1 and FVC trend with increasing age, FEV1/FVC yearly decline slope tripled in more recent epochs in subjects with BPD (Epoch A:-0.4%/yr(-0.8 to 0.05), B:-0.8%/yr(-1.1 to -0.5),, C:-1.4%/yr(-1.8 to -0.9). Similarly, DR decreased with age, with steeper decline in more recent epochs (Epoch A:-0.01/yr(-0.02 to -0.0004), B:-0.02/yr(-0.03 to -0.01), C:-0.04/yr(-0.05 to -0.03). Similar declines were noted for FEV1/FVC and DR in children without BPD. Conclusion In preterm survivors, lung function declined with increasing BPD severity and age. Lung function was reduced and declined in preterm children without BPD. Recent birth epochs exhibited faster decline in FEV1/FVC and worsening DR, indicating evolving airway-parenchymal growth mismatch despite advances in neonatal care, highlighting the need for longitudinal follow-up and targeted interventions to improve long-term outcomes.
Introduction Catheter-related bloodstream infection remains a major complication of neonatal central venous access. Although taurolidine lock therapy has been used in neonatal populations, experience with taurolidine locking in ultra-small (1–2 Fr) neonatal peripherally inserted central catheters (n-PICCs) remains extremely limited. This study describes the feasibility of repeated 2% taurolidine lock therapy in neonates requiring prolonged central vascular access. Methods We retrospectively reviewed three neonates who received repeated 2% taurolidine lock therapy during routine care in a tertiary neonatal intensive care unit. Locks were administered using a standardized local protocol for therapeutic or prophylactic indications. Collected data included catheter characteristics, lock administration and aspiration, flushing requirements, catheter patency, adverse events, and clinical outcomes. Results Taurolidine lock therapy was performed in 1–2 Fr n-PICCs, with all 30 planned procedures completed. Aspiration after the dwell period was unsuccessful in every procedure, requiring flushing of the residual solution. Catheter patency was maintained, with no occlusion, thrombosis, mechanical complications, or taurolidine-related adverse events. Bloodstream infection resolved with concomitant systemic antimicrobials in the therapeutic case, while no catheter-related bloodstream infection occurred during prophylactic locking. Conclusion This preliminary clinical experience demonstrates the technical feasibility of repeated 2% taurolidine lock therapy in ultra-small n-PICCs while maintaining catheter patency. The consistent inability to aspirate the lock solution represents an important practical observation for future investigation. These findings support further prospective evaluation of the feasibility and safety of taurolidine lock therapy as a catheter-preserving strategy in neonates. A multicentre randomized controlled trial is planned to further investigate this approach.
Introduction: Persistent pulmonary hypertension of the newborn (PPHN) is a life-threatening condition requiring intensive cardiopulmonary support. The optimal systemic blood pressure target in this population remains unknown. We evaluated the association between clinician-selected mean arterial pressure (MAP) targets and in-hospital outcomes in infants with PPHN. Methods: We conducted a retrospective cohort study of infants ≥35 weeks’ gestation with PPHN treated with inhaled nitric oxide (iNO) who had a clinician-documented MAP target within the first 48 hours of age. Infants were classified as having a MAP target <50 mmHg or ≥50 mmHg. The primary outcome was the composite of extracorporeal membrane oxygenation (ECMO) and/or death. Results: Among 109 infants, 82 (75%) were in the MAP target group < 50 mmHg and 27 (25%) were in the ≥ 50 mmHg MAP target group. Compared with a < 50 mmHg MAP target, a ≥ 50 mmHg MAP target was associated with higher rates of ECMO cannulation (33% vs 11%, p=0.01) and ECMO/death (48% vs 20%, p<0.01). Use of epinephrine and hydrocortisone, use of more than two vasoactive agents, and the vasoactive-inotropic score were also higher in the ≥ 50 mmHg MAP target group. After adjustment for HIE, pneumothorax, and initial oxygenation index, the ≥ 50 mmHg MAP target remained associated with ECMO cannulation (aOR 4.8; 95% CI 1.6, 15.0) and ECMO/death (aOR 5.9; 95% CI 2.0, 17.3). Conclusion: Among neonates treated with iNO for PPHN, clinician-selected MAP targets ≥ 50 mmHg were independently associated with ECMO cannulation and ECMO/death. Randomized trials are needed to define safe MAP targets in PPHN.
