Dataset Information

Trends and predictors of in-hospital mortality among babies with hypoxic ischaemic encephalopathy at a tertiary hospital in Nigeria: A retrospective cohort study.

ABSTRACT:

Background

Globally, approximately 9 million neonates develop perinatal asphyxia annually of which about 1.2 million die. Majority of the morbidity and mortality occur in Low and middle-income countries. However, little is known about the current trend in incidence, and the factors affecting mortality from hypoxic ischaemic encephalopathy (HIE), in Nigeria.

Objective

We assessed the trends in incidence and fatality rates and evaluated the predictors of mortality among babies admitted with HIE over five years at the Lagos University Teaching Hospital.

Methods

A temporal trend analysis and retrospective cohort study of HIE affected babies admitted to the neonatal unit of a Nigerian Teaching Hospital was conducted. The socio-demographic and clinical characteristics of the babies and their mothers were extracted from the neonatal unit records. Kaplan-Meir plots and Multivariable Cox proportional hazard ratio was used to evaluate the survival experienced using Stata version 16 (StataCorp USA) statistical software.

Results

The median age of the newborns at admission was 26.5 (10-53.5) hours and the male to female ratio was 2.1:1. About one-fifth (20.8%) and nearly half (47.8%) were admitted within 6 hours and 24 hours of life respectively, while majority (84%) of the infants were out-born. The prevalence and fatality rate of HIE in our study was 7.1% and 25.3% respectively. The annual incidence of HIE among the hospital admissions declined by 1.4% per annum while the annual fatality rate increased by 10.3% per annum from 2015 to 2019. About 15.7% died within 24 hours of admission. The hazard of death was related to the severity of HIE (p = 0.001), antenatal booking status of the mother (p = 0.01) and place of delivery (p = 0.03).

Conclusion

The case fatality rate of HIE is high and increasing at our centre and mainly driven by the pattern of admission of HIE cases among outborn babies. Thus, community level interventions including skilled birth attendants at delivery, newborn resuscitation trainings for healthcare personnel and capacity building for specialized care should be intensified to reduce the burden of HIE.

SUBMITTER: Ezenwa BN

PROVIDER: S-EPMC8075215 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:ObjectivesTo determine whether parents cuddling infants during therapeutic hypothermia (TH) would affect cooling therapy, cardiorespiratory or neurophysiological measures. The secondary aim was to explore parent-infant bonding, maternal postnatal depression and breastfeeding.DesignProspective observational study.SettingTwo tertiary neonatal intensive care units (NICU).ParticipantsParents and their term-born infants (n=27) receiving TH and intensive care for neonatal hypoxic-ischaemic encephalopathy.InterventionsCuddling up to 2 hours during TH using a standard operating procedure developed in the study (CoolCuddle).Main outcome measuresMean difference in temperature, cardiorespiratory and neurophysiological variables before, during and after the cuddle. Secondary outcomes were parental bonding, maternal postnatal depression and breastfeeding.ResultsDuring 70 CoolCuddles (115 cumulative hours), there were measurable increases in rectal temperature (0.07°C (0.03 to 0.10)) and upper margin of amplitude-integrated electroencephalogram (1.80 µV (0.83 to 2.72)) and decreases in oxygen saturations (-0.57% (-1.08 to -0.05)) compared with the precuddle period. After the cuddle, there was an increase in end-tidal CO2 (0.25 kPa (95% CI 0.14 to 0.35)) and mean blood pressure (4.09 mm Hg (95% CI 0.96 to 7.21)) compared with the precuddle period. From discharge to 8 weeks postpartum, maternal postnatal depression declined (13 (56.5%) vs 5 (23.8%), p=0.007); breastfeeding rate differed (71% vs 50%, p=0.043), but was higher than national average at discharge (70% vs 54.6%) and mother-infant bonding (median (IQR): 3 (0-6) vs 3 (1-4)) remained stable.ConclusionIn this small study, CoolCuddle was associated with clinically non-significant, but measurable, changes in temperature, cardiorespiration and neurophysiology. No infant met the criteria to stop the cuddles or had any predefined adverse events. CoolCuddle may improve breastfeeding and requires investigation in different NICU settings.

Project description:BackgroundHypoxic ischaemic encephalopathy (HIE) in newborns can cause significant long-term neurological disability. The insult is a complex injury characterised by energy failure and disruption of cellular homeostasis, leading to mitochondrial damage. The importance of individual metabolic pathways, and their interaction in the disease process is not fully understood. The aim of this study was to describe and quantify the metabolomic profile of umbilical cord blood samples in a carefully defined population of full-term infants with HIE.Methods and findingsThe injury severity was defined using both the modified Sarnat score and continuous multichannel electroencephalogram. Using these classification systems, our population was divided into those with confirmed HIE (n = 31), asphyxiated infants without encephalopathy (n = 40) and matched controls (n = 71). All had umbilical cord blood drawn and biobanked at -80 °C within 3 hours of delivery. A combined direct injection and LC-MS/MS assay (AbsolutIDQ p180 kit, Biocrates Life Sciences AG, Innsbruck, Austria) was used for the metabolomic analyses of the samples. Targeted metabolomic analysis showed a significant alteration between study groups in 29 metabolites from 3 distinct classes (Amino Acids, Acylcarnitines, and Glycerophospholipids). 9 of these metabolites were only significantly altered between neonates with Hypoxic ischaemic encephalopathy and matched controls, while 14 were significantly altered in both study groups. Multivariate Discriminant Analysis models developed showed clear multifactorial metabolite associations with both asphyxia and HIE. A logistic regression model using 5 metabolites clearly delineates severity of asphyxia and classifies HIE infants with AUC = 0.92. These data describe wide-spread disruption to not only energy pathways, but also nitrogen and lipid metabolism in both asphyxia and HIE.ConclusionThis study shows that a multi-platform targeted approach to metabolomic analyses using accurately phenotyped and meticulously biobanked samples provides insight into the pathogenesis of perinatal asphyxia. It highlights the potential for metabolomic technology to develop a diagnostic test for HIE.

Project description:Hypoxic-ischaemic encephalopathy remains a global health burden. Despite medical advances and treatment with therapeutic hypothermia, over 50% of cooled infants are not protected and still develop lifelong neurodisabilities, including cerebral palsy. Furthermore, hypothermia is not used in preterm cases or low resource settings. Alternatives or adjunct therapies are urgently needed. Exendin-4 is a drug used to treat type 2 diabetes mellitus that has also demonstrated neuroprotective properties, and is currently being tested in clinical trials for Alzheimer's and Parkinson's diseases. Therefore, we hypothesized a neuroprotective effect for exendin-4 in neonatal neurodisorders, particularly in the treatment of neonatal hypoxic-ischaemic encephalopathy. Initially, we confirmed that the glucagon like peptide 1 receptor (GLP1R) was expressed in the human neonatal brain and in murine neurons at postnatal Day 7 (human equivalent late preterm) and postnatal Day 10 (term). Using a well characterized mouse model of neonatal hypoxic-ischaemic brain injury, we investigated the potential neuroprotective effect of exendin-4 in both postnatal Day 7 and 10 mice. An optimal exendin-4 treatment dosing regimen was identified, where four high doses (0.5 µg/g) starting at 0 h, then at 12 h, 24 h and 36 h after postnatal Day 7 hypoxic-ischaemic insult resulted in significant brain neuroprotection. Furthermore, neuroprotection was sustained even when treatment using exendin-4 was delayed by 2 h post hypoxic-ischaemic brain injury. This protective effect was observed in various histopathological markers: tissue infarction, cell death, astrogliosis, microglial and endothelial activation. Blood glucose levels were not altered by high dose exendin-4 administration when compared to controls. Exendin-4 administration did not result in adverse organ histopathology (haematoxylin and eosin) or inflammation (CD68). Despite initial reduced weight gain, animals restored weight gain following end of treatment. Overall high dose exendin-4 administration was well tolerated. To mimic the clinical scenario, postnatal Day 10 mice underwent exendin-4 and therapeutic hypothermia treatment, either alone or in combination, and brain tissue loss was assessed after 1 week. Exendin-4 treatment resulted in significant neuroprotection alone, and enhanced the cerebroprotective effect of therapeutic hypothermia. In summary, the safety and tolerance of high dose exendin-4 administrations, combined with its neuroprotective effect alone or in conjunction with clinically relevant hypothermia make the repurposing of exendin-4 for the treatment of neonatal hypoxic-ischaemic encephalopathy particularly promising.