BackgroundCongenital esophageal atresia (CEA) type III is a common neonatal digestive malformation, and recurrent tracheoesophageal fistula (rTEF) is a refractory long-term postoperative complication. Combined suspension laryngoscopy and flexible bronchoscopy minimally invasive fistula repair is a novel therapeutic strategy, yet standardized perioperative nursing experience targeting adolescents with multiple failed transthoracic surgeries remains scarce. Conventional nursing cannot simultaneously manage compound risks including severe malnutrition, tracheomalacia, adolescent anxiety and airway edema. This case report aimed to summarize multidisciplinary team (MDT) individualized full-cycle nursing protocols for this rare patient population.Case presentationA 17.5-year-old male patient with rTEF, 17.5 years after neonatal primary congenital esophageal atresia repair, with two failed transthoracic fistula closures, presented persistent feeding choking, recurrent pneumonia and severe malnutrition (BMI=15.5 kg/m2). MDT refined airway management, quantitative staged nutrition, whole-course psychological intervention and predictive complication prevention were implemented before and after endoscopic fistula repair. No severe complications occurred during hospitalization. Esophagography and bronchoscopy on postoperative day 10 confirmed complete fistula healing. The patient was discharged on postoperative day 14 with a 0.8 kg weight gain, and one-month follow-up showed sustained fistula repair and continuous weight improvement.ConclusionMDT-driven individualized perioperative nursing effectively reduces airway and nutritional complications and promotes fistula healing in adolescent rTEF patients receiving endoscopic minimally invasive surgery. This case provides replicable evidence-based nursing references for similar complex rare esophageal malformation cases.
BackgroundRetinopathy of prematurity (ROP) is a major cause of childhood visual impairment. Although neonatal hyperglycemia has drawn research interest, its independent effect on ROP remains controversial. This study explores the association between neonatal hyperglycemia and ROP among infants with gestational age <32 weeks.MethodsIn this multi-center retrospective cohort of 308 preterm infants, multivariable Cox proportional-hazards models adjusted for perinatal factors, maternal comorbidities and neonatal complications. Sensitivity analyses further accounted for invasive/non-invasive ventilation duration, total oxygen therapy time, peak inspired oxygen fraction and glucose infusion rate; Firth penalized regression corrected sparse-data bias. Additional sensitivity analyses examined the dose-response association with neonatal peak glucose levels.ResultsOur findings revealed that hyperglycemic infants had significantly lower birth weights and gestational ages compared to their non-hyperglycemic counterparts. After controlling for confounding variables, hyperglycemia was identified as an independent risk factor for ROP, with an adjusted hazard ratio (aHR) of 2.54 (95% CI: 1.45–4.44, P = 0.001). This association persisted after further adjustment for respiratory support variables and glucose infusion rate (aHR=2.46, 95% CI: 1.40–4.31) and in Firth penalized analysis (aHR=2.36, 95% CI: 1.36–4.11). Notably, a pronounced dose-response relationship was detected, with risks escalating markedly at peak glucose levels exceeding 8.33 mmol/L (150 mg/dL) (aHR=2.72) and intensifying further above 10 mmol/L (180 mg/dL) (aHR=3.64), indicating an approximately 50%–80% average risk increase per glucose tier across model specifications (all P-trend < 0.001), a gradient that was unchanged after further adjustment for neonatal complications, respiratory support, and glucose infusion rate. In exploratory analysis, severe ROP (stage ≥3, n = 13) was not significantly associated with hyperglycemia after penalized adjustment (OR = 1.45, 95% CI: 0.36–7.31).ConclusionThis study establishes neonatal hyperglycemia as a significant, dose-dependent predictor of ROP and associated multi-organ injury in preterm infants, independent of traditional risk factors. Clinically, this underscores the imperative for stringent glycemic monitoring, with a candidate vigilance threshold of 8.33 mmol/L (150 mg/dL), the clinical benefit of which requires prospective validation. Future prospective studies integrating continuous glucose monitoring and mechanistic investigations are essential to refine glycemic thresholds and optimize metabolic management strategies aimed at enhancing visual outcomes in this susceptible population.
BackgroundT-box transcription factor 4 (TBX4) is a critical regulator of lung and pulmonary vascular development. Pathogenic TBX4 variants are associated with developmental lung disease, pulmonary hypertension, and neonatal respiratory failure.Case presentationWe report two siblings with lethal neonatal respiratory failure. The first, a term female infant, died at 11 h of life, and her late-preterm male sibling died at 9 h despite maximal intensive care. Both developed severe hypoxemia and pulmonary hypertension. Autopsy demonstrated marked pulmonary hypoplasia. Whole-exome sequencing identified a novel heterozygous TBX4 variant, c.741G>C (p.Lys247Asn), inherited from their unaffected father. Preimplantation genetic testing detected the variant in seven of 10 embryos.ConclusionThese cases expand the spectrum of TBX4-associated developmental lung disease and support consideration of TBX4 testing in neonates with unexplained respiratory failure and pulmonary hypertension.
IntroductionProtein S deficiency is a predominant form of hereditary thrombophilia in Asian populations. Pediatric venous thromboembolism (VTE) is exceedingly rare, with an incidence of only 0.2%–0.6%, and acute massive pulmonary embolism (PE) requiring extracorporeal membrane oxygenation (ECMO) support in children with thrombophilia presents exceptional clinical challenges. The core therapeutic dilemma lies in reconciling the hypercoagulable state inherent to protein S deficiency with the high bleeding risk following thrombolytic therapy, compounded by the obligatory anticoagulation requirement during ECMO. This case report describes the nursing management of a pediatric patient with protein S deficiency and acute PE who successfully underwent ECMO-supported interventional treatment under high bleeding risk.OutcomeThe patient was successfully weaned from ECMO after 98 h of support, extubated on day 6, and discharged in stable condition after 30 days of hospitalization. At 6-month follow-up, no thrombus recurrence was observed, and the patient had fully resumed normal life and academic activities.ConclusionThis case demonstrates that an individualized low-dose heparin anticoagulation strategy, guided by the PEACE consensus and supported by meticulous monitoring, can effectively balance the competing risks of thrombosis and hemorrhage in pediatric ECMO patients with underlying thrombophilia and recent thrombolysis. Notably, as a single case report, this finding cannot be broadly generalized to all pediatric ECMO patients with thrombophilia. Instead, this case provides a potential framework for individualized anticoagulation and nursing management that requires further validation in larger pediatric cohorts. The nursing experience provides a practical reference for managing similar complex cases in pediatric critical care.
