Preventing The Human Factor: Organisational Aspects Linked to Foetal Asphyxia.

Background: the aim of this study was to identify prepartum, intrapartum and organisational risk factors for foetal asphyxia. We focused on modifiable factors such as organisational factors, maternal Body Mass Index, Assisted Reproductive Technology pregnancies, smoking and number of clinical checks.Methods: This is a retrospective analytical observational study.It was carried out in a teaching hospital in Northern Italy. The data for this study was obtained from maternal and neonatal medical records,obstetric and neonatal hospital discharge summaries and birth assistance certificates.162 cases of mothers whose children experienced foetal asphyxia were compared to 162 controls where this condition did not occur. The different variables were analysed using the Fisher test, the Mann Whitney U test and logistic regression. The association probability was estimated by the odds ratio with a confidence interval of 95%. The alpha level of 0,05 was considered significant.Results: giving birth at night (p<0.001), lack of one to one assistance during labour (p <0.001), birth on a day of high volume activity(p<0.001), Assisted Reproductive Technology obtained pregnancies (p<0.001), number of clinical checks during pregnancy (p <0.001 ), smoking during pregnancy (p<0.001), high maternal body mass index (p<0.001 ), as well as other traditionally associated risk factors like shoulder distocia (p<0.001) or age>35 (p <0.001) all increased the risk in a statistically significant way.Conclusions: giving birth on a high activity day, at night or without one-to one care are organisational factors that statistically increase the risk of foetal asphxia.Our paper proposes strategies to try and modify these risk factors and therefore limit the incidence of foetal asphyxia and of its life changing consequences like cerebral palsy.

No Take Home Baby After Caesarian Birth for Foetal Distress in Women with Risk

Sometimes interventions are done for the baby in women with risks but it turns out to be unnecessary caesarian section (CS). However it may be delayed decision and / or delayed execution of intervention, CS too, with no take home baby. While lack of adverse outcome reflected that the decision was not for a compromised foetus, still birth or asphyxiated baby at birth meant delayed decision and / or execution. Recent studies revealed an estimated 9.04 million perinatal deaths related to birth asphyxia. Of them 1.02 million were intrapartum deaths leading to still births, many after CB for foetal concern. Birth asphyxia is a significant global health problem, responsible for around 1.2 million neonatal deaths each year worldwide [1-3]. Those who survive often suffer from a range of disorders. Chauhan et al. conducted, a meta analysis comprising of 169 articles and 37 reports and concluded that the overall risk of prompt CB for fetal concern was 3.1 % (43,340 of 13,98,9740 cases) [4,5]. From time to time several hospital based studies have proved the role of various antepartum or intrapartum maternal & foetal risk factors which lead to foetal asphyxia. It is known that some disorders which could cause foetal asphyxia are obvious during pregnancy, some are labour related, be it mother or baby. Kaye reported association of primiparity, anaemia, hypertensive disorders of pregnancy, foetal growth restriction, malpresentation, antepartum haemorrhage, premature rupture of membranes, prematurity, fever, oxytocin augmentation of labour, umbilical cord prolapse, as risk factors ,with complex interplay between factors which predispose foetuses to poor outcome, due to decreased oxygenation, ACOG reported that foetal hypoxemia which if not compensated or corrected in time progressed to birth asphyxia and even death, either in utero or immediately after birth [6,7]. Gaffineet and James have reported, intrapartum hypoxia complicating around 1% of labours, resulting in foetal / neonatal deaths in 0.5/1000 pregnancies and cerebral palsy in 1 in 1000 cases diagnosed after swift delivery for clinically diagnosed “fetal distress’’ [8]. Earlier Murphy et al had suggested that reduced uterine perfusion uteroplacental vascular disease, low fetal reserve foetal asphyxia, foetal sepsis and cord compression with other gestational and antepartum factors could affect the fetal response which needed to be known. However diagnosis of FD also has to be correct and timely [9]. Cardiotocography (CTG) has been criticized for unnecessary high rate of operative delivery [10-12]. In the study by Roy, non-reassuring fetal heart rate (FHR) detected by CTG did not correlate well with neonatal outcome [13]. In the era of defensive practices, ‘play safe’ attitude results in high CS rate for non-reassuring FHR. The concept of detecting fetal acidosis, using fetal scalp blood appeared attractive, but practical difficulties in carrying it out restricted its use [14,15]. Roy et al suggested that since non-reassuring FHR detected by CTG did not correlate well with adverse neonatal outcome and resulted in unnecessary CS, fetal ECG needed to be introduced in addition to conventional CTG, wherever possible [13]. There are many such issues about timely appropriate authentic diagnosis and action.