Perinatal Mortality

MONITORING PERINATAL MORTALITY: A Pathophysiological Approach

Assess improvable care factors in late preterm mortality, defined as death of a child during labour or in the first 28 days thereafter between 32 + 0 and 36 + 6 weeks gestation, in the Netherlands.

Perinatal audit has been coordinated and supported at the national level, with selection of nationwide audit themes, and audit sessions are performed at the local level across the country as multidisciplinary meetings with primary and secondary level health care professionals, organised in local perinatal cooperation units. In 2017–2019, late preterm mortality was such a theme. We compiled and systematically categorised all improvable care factors formulated during local audit meetings in a national perinatal audit database.

In total, 27 cases were discussed in local perinatal audits and analysed locally and at the national level. Altogether, 52 improvable care factors were identified. Most identified improvable care factors concerned inadequate foetal monitoring by cardiotocography during labour, factors related to care organisation, particularly unclarity around local assigning of responsibilities and work procedures, and poor communication between involved health care professionals especially in transfer of care.

Several critical improvable care factors were identified through nationwide perinatal audit of late preterm deaths in the Netherlands.

To analyse the factors associated with preventable of infant mortality, in Espirito Santo, Brazil.

Data were collected from records of notifiable of infant death of the Mortality Information System. A total of 5,089 infant deaths were classified as preventable and non-preventable according to the International Collaborative Effort on Infant Mortality (ICE) and the State System of Data Analysis Foundation (SEADE) methods. To investigate the factors associated with preventable of deaths, it was applied the logistic regression.

Approximately, 73% of the deaths were preventable according to the ICE, while 76% were preventable according to the SEADE method. Using to both methods, it was observed that preterm birth, postneonatal death and birth weight between 3000 and above 4,000 g represented higher chances for preventable infant deaths. Furthermore, the medical care was more likely to preventable infant death only for ICE method.

The factors related to the quality of care offered in the prenatal, prepartum and childbirth periods were more relevant for the occurrence of preventable infant death. Accordingly, it is recommended to strengthen mother-child care to detect risk pregnancies during prenatal care, as well as a hierarchical, regionalized and integrated perinatal network.

Stillbirth is a devastating adverse pregnancy outcome that may occur without any obvious reason or may occur in the context of fetal growth restriction, preeclampsia, or other obstetric complications. There is increasing evidence that women who experience stillbirths are at greater risk of long-term cardiovascular disease, but little is known about their risk of chronic kidney disease and end-stage renal disease. We conducted the largest study to date to investigate the subsequent risk of maternal chronic kidney disease and end-stage renal disease following stillbirth.

To identify whether pregnancy complicated by stillbirth is associated with subsequent risk of maternal chronic kidney disease and end-stage renal disease, independent of underlying medical or obstetric comorbidities.

We conducted a population-based cohort study using nationwide data from the Swedish Medical Birth Register, National Patient Register, and Swedish Renal Register. We included all women who had live births and stillbirths from 1973 to 2012, with follow-up to 2013. Women with preexisting renal disease were excluded. Cox proportional hazard regression models were used to estimate adjusted hazard ratios and 95% confidence intervals for associations between stillbirth and maternal chronic kidney disease and end-stage renal disease respectively. We controlled for maternal age, year of delivery, country of origin, parity, body mass index, smoking, gestational diabetes, preeclampsia, and small for gestational age deliveries. Women who had a history of medical comorbidities, which may predispose to renal disease (prepregnancy cardiovascular disease, hypertension, diabetes, lupus, systemic sclerosis, hemoglobinopathy, or coagulopathy), were excluded from the main analysis and examined separately.

There were 1,941,057 unique women who had 3,755,444 singleton pregnancies, followed up over 42,313,758 person-years. The median follow-up time was 20.7 years (interquartile range, 9.9–30.0 years). 13,032 women (0.7%) had at least 1 stillbirth. Women who had experienced at least 1 stillbirth had a greater risk of developing chronic kidney disease (adjusted hazard ratio, 1.26; 95% confidence interval, 1.09–1.45) and end-stage renal disease (adjusted hazard ratio, 2.25; 95% confidence interval, 1.55–3.25) compared with women who only had live births. These associations persisted after removing all stillbirths that occurred in the context of preeclampsia, and small for gestational age or congenital malformations (for chronic kidney disease, adjusted hazard ratio, 1.33; 95% confidence interval, 1.13–1.57; for end-stage renal disease, adjusted hazard ratio, 2.95; 95% confidence interval, CI 1.86–4.68). There was no significant association observed between stillbirth and either chronic kidney disease or end-stage renal disease in women who had preexisting medical comorbidities (chronic kidney disease, adjusted hazard ratio, 1.13; 95% confidence interval, 0.73–1.75 or end-stage renal disease, adjusted hazard ratio, 1.49; 95% confidence interval, 0.78–2.85).

Women who have a history of stillbirth may be at increased risk of chronic kidney disease and end-stage renal disease compared with women who have only had live births. This association persists independently of preeclampsia, and small for gestational age, maternal smoking, obesity, and medical comorbidities. Further research is required to determine whether affected women would benefit from closer surveillance and follow-up for future renal disease.

Most fetal deaths are unexplained. Long QT syndrome is a genetic disorder of cardiac ion channels. Affected individuals, including fetuses, are predisposed to sudden death. We sought to determine the risk of fetal death in familial long QT syndrome, in which the mother or father carries the long QT syndrome genotype. In addition, we assessed whether risk differed if the long QT syndrome genotype was inherited from the mother or father.

This was a retrospective review of pregnancies in families with the 3 most common heterozygous pathogenic long QT syndrome genotypes in KCNQ1 (LQT1), KCNH2 (LQT2), or SCN5A (LQT3), which occur in approximately 1 in 2000 individuals. The purpose of our study was to compare pregnancy and birth outcomes in familial long QT syndrome with the normal population and between maternal and paternal carriers of the long QT syndrome genotype. We hypothesized that fetal death before (miscarriage) and after (stillbirths) 20 weeks gestation would be increased in familial long QT syndrome compared with the normal population and that the parent of origin would not affect birth outcomes.

Our study was a multicenter observational case series of 148 pregnancies from 103 families (80 mothers, 23 fathers) with familial long QT syndrome (60 with LQT1, 29 with LQT2, 14 with LQT3) who were recruited from 11 international centers with expertise in hereditary heart rhythm diseases, pediatric and/or adult electrophysiology, and high-risk pregnancies. Clinical databases from these sites were reviewed for long QT syndrome that occurred in men or women of childbearing age (18–40 years). Pregnancy outcomes (livebirth, stillbirth, and miscarriage), birthweights, and gestational age at delivery were compared among long QT syndrome genotypes and between maternal vs paternal long QT syndrome–affected status with the use of logistic regression analysis.

Most offspring (80%; 118/148) were liveborn at term; 66% of offspring (73/110) had long QT syndrome. Newborn infants of mothers with long QT syndrome were delivered earlier and, when the data were controlled for gestational age, weighed less than newborn infants of long QT syndrome fathers. Fetal arrhythmias were observed rarely, but stillbirths (fetal death at >20 weeks gestation) were 8 times more frequent in long QT syndrome (4% vs approximately 0.5%); miscarriages (fetal death at ≤20 weeks gestation) were 2 times that of the general population (16% vs 8%). The likelihood of fetal death was significantly greater with maternal vs paternal long QT syndrome (24.4% vs 3.4%; P=.036). Only 10% of all fetal deaths underwent postmortem long QT syndrome testing; 2 of 3 cases were positive for the family long QT syndrome genotype.

This is the first report to demonstrate that mothers with long QT syndrome are at increased risk of fetal death and to uncover a previously unreported cause of stillbirth. Our results suggest that maternal effects of long QT syndrome channelopathy may cause placental or myometrial dysfunction that confers increased susceptibility to fetal death and growth restriction in newborn survivors, regardless of long QT syndrome status.