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