Management of oxygen saturation monitoring in preterm newborns in the NICU: the Italian picture.

BACKGROUND: Although many studies emphasize the importance of using oxygen saturation (SpO2) targets in the NICUs, there is a wide variability in used saturation ranges among centers. Primary aim was to draw a representative picture on how the management of oxygen monitoring is performed in the Italian NICUs. Second aim was to identify healthcare-professionals related factors associated with oxygen targeting in the preterm population. METHODS: Cross-sectional study with data collection via an electronic survey form. A questionnaire containing pre-piloted and open questions on monitoring and management of the SpO2 was administered to neonatologists across the network of the Italian Society of Neonatology. The questions focused on: the infrastructure, specific training, healthcare professionals and patients-related factors. The results of the survey were anonymously collected, summarized and analyzed. RESULTS: Out of 378 questionnaires, 93 were correctly filled. Thirty-six different SpO2 ranges were observed. Centers using written standard operating procedures on oxygen management and SpO2 monitoring maintained a correct average range of SpO2 90-95%, avoided hyperoxia and reconsidered saturation targets in relation to comorbidities. 39.8% of responders disabled alarms during neonatal care. One center used biomarkers for complete monitoring of neonatal oxygenation status. CONCLUSIONS: There is considerable variation in SpO2 targets for preterm infants in the Italian NICUs. Standard operating procedures and specific training for health care personnel are the main factors playing a role for the correct maintenance of the recommended oxygen targets in preterms.

Brain susceptibility to oxidative stress in the perinatal period.

Oxidative stress (OS) occurs at birth in all newborns as a consequence of the hyperoxic challenge due to the transition from the hypoxic intrauterine environment to extrauterine life. Free radical (FRs) sources such as inflammation, hyperoxia, hypoxia, ischaemia-reperfusion, neutrophil and macrophage activation, glutamate and free iron release, all increases the OS during the perinatal period. Newborns, and particularly preterm infants, have reduced antioxidant defences and are not able to counteract the harmful effects of FRs. Energy metabolism is central to life because cells cannot exist without an adequate supply of ATP. Due to its growth, the mammalian brain can be considered as a steady-state system in which ATP production matches ATP utilisation. The developing brain is particularly sensitive to any disturbances in energy generation, and even a short-term interruption can lead to long-lasting and irreversible damage. Whenever energy failure develops, brain damage can occur. Accumulating evidence indicates that OS is implicated in the pathogenesis of many neurological diseases, such as intraventricular haemorrhage, hypoxic-ischaemic encephalopathy and epilepsy.

Oxidative injury in neonatal erythrocytes.

Erythrocytes are continuously exposed to free radicals (FR) injury due to their high cellular oxygen concentration and heme iron. The autoxidation of oxyhaemoglobin to methaemoglobin, generating superoxide anion radical, represents the main source of FR in erythrocytes. The erythrocyte membrane is particularly sensitive to oxidative damage due to its high polyunsaturated fatty acid content, and hence, it represents an important system to evaluate the effect of oxidative stress (OS). Information on how red cells OS is triggered and mechanisms of erythrocytes oxidative pressure from plasma may provide a partial answer to questions about the causes of the anaemia of prematurity and about red cell involvement in hypoxia. The recent insights about the mechanism of oxidative injury of red cells and the evidence of relationships between erythrocyte, OS and hypoxia suggest that increased haemolysis is induced by severe hypoxia and acidosis in the perinatal period.

Biomarkers of oxidative stress in fetal and neonatal diseases.

Oxidative stress (OS) is strongly involved in the pathogenesis of many fetal and newborn diseases. A low efficient antioxidant systems in preterm babies are not able to counteract the harmful effects of free radicals (FRs), leading to "FRs-related disease" of newborns promoting cellular, tissue and organ damages. The dangerous effects of FRs are linked to their property of being very unstable molecules and their ability to react with lipids, proteins, polysaccharides, nucleic acids, causing functional alterations within the cell, until cell death. OS is difficult to be measured in vivo, because FRs have a very short half-life. Actually, measurements of lipid peroxidation reach high specificity and sensitivity with the discovery of stable compounds, isoprostanes. Recent studies evaluating the damaging effects of FRs in the perinatal period, have observed a direct relation between the degree of OS and the severity of oxidative damage in the course of pregnancy and in perinatal period, with an interesting predictive role of OS biomarkers for diseases resulting from oxidative injury. The validation of a biomarker profile for early identification of newborns at high risk of OS, will pave the way to new clinical preventative or therapeutic approaches to reduce the prevalence of neonatal disability.

New pharmacologic and therapeutic approaches for hypoxic-ischemic encephalopathy in the newborn.

Hypoxic-ischemic encephalopathy is still an important cause of neonatal mortality and long-term disabilities. The understanding of the differential responses to hypoxia-ischemia as an initial insult leading to cellular degeneration in brain has opened the way to develop new pharmacologic and therapeutic approaches. Due to the complex pathophysiology, therapies can target early pathways such as oxidative stress, inflammation and apoptosis or delayed pathways such as the privation of growth factors and cell death. Pharmacological interventions should start at different points of time according to their mechanisms of action. The association of moderate hypothermia with neuroprotective drugs may decrease cell injury and optimize endogenous repair. More basic science research focusing on the mechanisms of injury are required. Moreover, clinical trials are needed to detect safely and effectiveness drugs and to establish the optimal time of action for each one.