Factors associated with umbilical artery acidemia in term infants with low Apgar scores at 5min

Locatelli, Anna; Incerti, Maddalena; Ghidini, Alessandro; Greco, Massimiliano; Villa, Elisabetta; Paterlini, Giuseppe

doi:10.1016/j.ejogrb.2008.01.003

Cited by 60 publications

(48 citation statements)

References 18 publications

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“…Similar observations were seen in Kacho MA et al, 7 Anyaegbunam A et al, 10 Locatelli A et al 11 and Modarressnejad V et al 5 studies, whereas Manganaro R et al 12 studied in both term and preterm infants.…”

Section: Gestational Agesupporting

confidence: 74%

Correlation Between Umbilical Arterial Blood Gas Parameters and Apgar Score in High-Risk Pregnancy

Kumaran¹,

Sucindar²,

Ashok³

2017

jemds

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Section: Gestational Agesupporting

confidence: 74%

Correlation Between Umbilical Arterial Blood Gas Parameters and Apgar Score in High-Risk Pregnancy

Kumaran¹,

Sucindar²,

Ashok³

2017

jemds

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“…Vascular disease [23] and increased uterine activity associated with the use of oxytocin [24] appeared to be the most important risk factors for acidemia in the neonate. Indeed, during uterine contractions, reduced uteroplacental circulation causes fetal hypoxemia and a vascular redistribution towards vital organs from peripheral organs and viscera, which accumulate anaerobic metabolites [25] .…”

Section: Discussionmentioning

confidence: 99%

Arterial Cord Blood Lactate at Birth Correlates with Duration of Pushing Efforts

Dessolle

Lebrec²,

Daraı̈³

2009

Fetal Diagn Ther

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Objective: To evaluate the impact of the duration of pushing efforts on arterial cord blood lactate values. Methods: This was a prospective observational study of 124 consecutive normal vaginal deliveries in a tertiary teaching hospital. Arterial cord blood lactate was determined immediately at birth with a test strip method. Univariate and multivariate analyses were performed to check for clinical determinants of lactate levels. The main measure was lactate according to the duration of pushing efforts. Results: Arterial cord lactates increased significantly and were strongly correlated with the duration of pushing efforts, independent of gestational age and birthweight. Women pushing for more than 20 min had higher arterial cord blood lactates (4.9 ± 1.4 vs. 3.3 ± 1.16 mM, respectively) and a higher rate of lactates >6 mM (18 vs. 3%) than those pushing for less than 20 min. Conclusion: At normal delivery, arterial cord blood lactates increase significantly with the duration of pushing efforts. Pushing for more than 20 min is associated with an increased risk of metabolic acidosis in the neonate. Further studies are required to evaluate the clinical significance of these observations.

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“…Despite limitations in the quantity and quality of evidence, current reports indicate that placental abnormality is often associated with neonatal encephalopathy, perinatal stroke, 28 low Apgar scores, [29][30][31] and term stillbirth. 32,33 However, the nature of the placental abnormality differs in several ways, supporting the aetiological diversity of these clinical syndromes.…”

Section: The Placentamentioning

confidence: 99%

Does aetiology of neonatal encephalopathy and hypoxic–ischaemic encephalopathy influence the outcome of treatment?

McIntyre

Badawi

Blair

et al. 2015

Develop Med Child Neuro

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HIE Hypoxic-ischaemic encephalopathyNeonatal encephalopathy, a clinical syndrome affecting term-born and late preterm newborn infants, increases the risk of perinatal death and long-term neurological morbidity, especially cerebral palsy. With the advent of therapeutic hypothermia, a treatment designed for hypoxic or ischaemic injury, associated mortality and morbidity rates have decreased. Unfortunately, only about one in eight neonates (95% confidence interval) who meet eligibility criteria for therapeutic cooling apparently benefit from the treatment. Studies of infants in representative populations indicate that neonatal encephalopathy is a potential result of a variety of antecedents and that asphyxial complications at birth account for only a small percentage of neonatal encephalopathy. In contrast, clinical case series suggest that a large proportion of neonatal encephalopathy is hypoxic or ischaemic, and trials of therapeutic hypothermia are specifically designed to include only infants exposed to hypoxia or ischaemia. This review addresses the differences, definitional and methodological, between infants studied and investigations undertaken, in population studies compared with cooling trials. It raises the question if there may be subgroups of infants with a clinical diagnosis of hypoxic-ischaemic encephalopathy (HIE) in whom the pathobiology of neonatal neurological depression is not fundamentally hypoxic or ischaemic and, therefore, for whom cooling may not be beneficial. In addition, it suggests approaches to future trials of cooling plus adjuvant therapy that may contribute to further improvement of care for these vulnerable neonates.Neonatal encephalopathy is a clinical syndrome of disordered neurological function occurring in the first days of life in term-born and late preterm neonates and is characterized by difficulty initiating and maintaining respiration, an abnormal level of consciousness, depression of tone and reflex responses, and often seizures. This symptom complex affects about 3 in every 1000 births, and is an important predictor of perinatal death and a major contributor to long-term adverse neurological outcomes, particularly cerebral palsy (CP). 1,2 Evidence from clinical and experimental studies agrees that some instances of neonatal encephalopathy are related to hypoxic-ischaemic injury, but the proportions of neonatal encephalopathy attributed to recent asphyxial events vary with the definitions used and the methodology of the investigations. Studies of infants in representative populations indicate that asphyxial complications at birth account for only a minority of neonatal encephalopathy. These population-based studies also identify other factors that contribute to increased risk of neonatal encephalopathy, such as intrauterine exposure to inflammation or fetal growth restriction, and note that some non-asphyxial factors can produce a clinical picture that closely mimics hypoxia-ischaemia. [3][4][5] In contrast, studies of neonatal cooling have approached this topic from the ...

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Factors associated with umbilical artery acidemia in term infants with low Apgar scores at 5min

Cited by 60 publications

References 18 publications

Correlation Between Umbilical Arterial Blood Gas Parameters and Apgar Score in High-Risk Pregnancy

Correlation Between Umbilical Arterial Blood Gas Parameters and Apgar Score in High-Risk Pregnancy

Arterial Cord Blood Lactate at Birth Correlates with Duration of Pushing Efforts

Does aetiology of neonatal encephalopathy and hypoxic–ischaemic encephalopathy influence the outcome of treatment?

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