Introduction: Newborns treated in a neonatal intensive care unit (NICU) are susceptible to several complications one of them being vein thrombosis. Aim: The study aims to evaluate risk factors of catheter-related venous thrombosis, clinical manifestations, treatment, and the outcomes of thrombotic events (TE) during the neonatal period. Methods: This work is a case-control retrospective study performed on patients in the tertiary NICU between January 2013 and June 2016. The analysis includes data from infants with CVC diagnosed with thrombosis and infants with CVC, not being diagnosed with thrombosis (control group). Statistica 10 software was used for statistical analysis. Results: Vein thrombosis was diagnosed in 19 NICU infants including 16 cases of catheter-related vein thrombosis (84% of complicated cases). Other statistically significant risk factors were asphyxia, infection, and the duration of CVC use. The incidence of thrombosis in our population increased during the study which may result from a statistically significant increase in the number of inserted CVC (294 vs 435), and more frequent diagnosis of incidental thrombosis (1 vs 9). Conclusion: Vein catheterization, asphyxia, infection, and prolonged CVC use are critical risk factors for thrombosis in the neonatal period. Given the hereinbefore mentioned increased number of central line catheterizations in the NICU, it would be useful to conduct a prospective study with a scheduled routine ultrasound protocol applied not only as a tool to diagnose thrombosis but also to prevent it by determining a proper catheter for a particular vein.
Persistent pulmonary hypertension of the newborn (PPHN) results from disrupted fetal–neonatal circulatory transition, characterized by elevated pulmonary vascular resistance (PVR), right-to-left shunting, and refractory hypoxemia. Despite improved perinatal care, PPHN remains a major source of neonatal morbidity and mortality. This review details PPHN phenotypes, pathophysiology, etiology, diagnostics including echocardiography and biomarkers like B-type Natriuretic Peptide (BNP) or N-terminal pro-B-type Natriuretic Peptide (NT-proBNP), and current therapeutic modalities, from lung recruitment and surfactant to targeted vasodilator therapy (iNO, sildenafil, milrinone, bosentan) and extracorporeal membrane oxygenation (ECMO). We emphasize the role of endothelial and molecular mechanisms in precision therapy and outline guidelines for clinical decision-making in diverse care settings.
Objective: This study aims to evaluate the performance of the fabian-Predictive-Intelligent-Control-of-Oxygenation (PRICO) system for automated control of the fraction of inspired oxygen (FiO2).Design: Multicentre randomised cross-over study.Setting: Five neonatal intensive care units experienced with automated control of FiO2and the fabian ventilator.Patients: 39 infants: median gestational age of 27 weeks (IQR: 26–30), postnatal age 7 days (IQR: 2–17), weight 1120 g (IQR: 915–1588), FiO20.32 (IQR: 0.22–0.43) receiving both non-invasive (27) and invasive (12) respiratory support.Intervention: Randomised sequential 24-hour periods of automated and manual FiO2control.Main outcome measures: Proportion (%) of time in normoxaemia (90%–95% with FiO2>0.21 and 90%–100% when FiO2=0.21) was the primary endpoint. Secondary endpoints were severe hypoxaemia (98% with FiO2>0.21) and prevalence of episodes ≥60 s at these two SpO2extremes.Results: During automated control, subjects spent more time in normoxaemia (74%±22% vs 51%±22%, p<0.001) with less time above and below (<90% (9%±8% vs 12%±11%, p95% with FiO2>0.21 (16%±19% vs 35%±24%) p<0.001). They spent less time in severe hyperoxaemia (1% (0%–3.5%) vs 5% (1%–10%), p<0.001) but exposure to severe hypoxaemia was low in both arms and not different. The differences in prolonged episodes of SpO2were consistent with the times at extremes.Conclusions: This study demonstrates the ability of the PRICO automated oxygen control algorithm to improve the maintenance of SpO2in normoxaemia and to avoid hyperoxaemia without increasing hypoxaemia.
Chronic renal disease (CRD) is a well-known risk factor for bleeding complications in acute coronary syndrome patients. To determine the impact of CRD with ST segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI) on periprocedural complications. 103 patients with STEMI treated with pPCI were prospectively observed for in-hospital complications and analysed according to kidney function status. Endpoints included clinical and periprocedural outcomes. Major and minor bleedings were reported according to TIMI, REPLACE2 and EASY classifications. Patients with CRD were at greater risk of major bleeding defined by RAPLACE-2 (20.0% vs. 2.7%; p = 0.007) and TIMI(13.3% vs. 1.3%, p = 0.018) classifications and had more grade 2 EASY scale haematomas (20.0% vs. 2.7%; p = 0.007). Vascular access crossover during PCI occurred eight-fold more often among CRD patients (33.3% vs. 4.0%, p < 0.001). Grade 3 TIMI flow was achieved less frequently in CRD patients (60% vs. 89.3%, p = 0.004). CRD predisposed to contrast-induced nephropathy (35.7% vs. 5.7%; p < 0.001) and ischaemic stroke (14.3% vs. 0.0%; p = 0.004). CRD in STEMI patients undergoing pPCI is a risk factor for major and minor bleeding complications including major bleeding, moderate haematomas, contrast-induced nephropathy and ischaemic stroke. Treatment and diagnostic measures should be taken in CRD patients to reduce the severity of periprocedural complications.