Risk Factors For Hypoxic-ischemic Encephalopathy Research Articles

Risk factors for hypoxic-ischemic encephalopathy in cases of severe acidosis: A case-control study.

The aim of the study was to identify the obstetric risk factors for hypoxic-ischemic encephalopathy (HIE) in infants with asphyxia at birth. This multicenter case-control study covered the 5-year period from 2014 through 2018 and included newborns ≥36weeks of gestation with an umbilical pH at birth ≤7.0. Cases were newborns who developed moderate or severe HIE; they were matched with controls with pH ≤7.0 at birth over the same period without moderate or severe HIE. The factors studied were maternal, gestational, intrapartum, delivery-related, and neonatal characteristics. A multivariable analysis was performed to study the maternal, obstetric, and neonatal factors independently associated with moderate or severe HIE. Our review of the records identified 41 cases and 98 controls. Compared with controls, children with moderate or severe HIE had a lower 5-min Apgar score, lower umbilical artery pH, and higher cord lactate levels at birth and at 1h of life. Obstetric factors associated with moderate or severe HIE were the occurrence of an acute event (adjusted odds ratio [aOR] 6.4; 95% confidence interval [CI] 1.8-22.5), maternal fever (aOR 3.5; 95% CI 1.0-11.9), and thick meconium during labor (aOR 2.9; 95% CI 1.0-8.6). HIE is associated with a lower 5-min Apgar score and with the severity of acidosis at birth and at 1h of life. In newborns with a pH <7.0 at birth, the occurrence of an acute obstetric event, maternal fever, and thick meconium are independent factors associated with moderate or severe HIE.

THE OUTCOMES OF PERINATAL HYPOXIC-ISCHEMIC ENCEPHALOPATHY IN PREMATURE NEWBORNS

Hypoxic-ischemic damage of the fetal and newborn brain are an actual medical and social problem of modern medicine, as these patients increase the number of children with disabilities. Premature infants have a high risk of developing neurodevelopmental defects, with cognitive impairment ranging from 20% in late preterm infants and up to 64% in extremely low birth weight infants.The aim of the study was to assess the importance of timely diagnosis of hypoxia of the premature fetus during pregnancy and childbirth and the proposed preventive measures to reduce adverse neurological disorders in newborns and children.Material and methods. We monitored 120 pregnant women who gave birth prematurely at 26-34 weeks of pregnancy. The main group consisted of 60 pregnant women in whom preterm birth was programmed for various indications, such as progression of preeclampsia, fetal growth retardation and antenatal distress. The comparison group consisted of 60 pregnant women who gave birth prematurely. Neuroprotection with magnesium sulfate was performed only in pregnant women of the main group, whose gestation period was up to 32 weeks. In addition, pregnant women of the main group received drugs docosahexaenoic acid.Results and discussion. Among children born to pregnant women of the main group, at the age of 18-24 months, only 18.8% of children had minor neurological disorders, such as delayed physical and mental development. Only 1 child (2.1%) had cerebral palsy (birth weight 1200.0, the mother had severe preeclampsia, fetal growth retardation, antenatal distress). Children born to pregnant women in the comparison group were 3 times more likely to have delayed physical and mental development, in 2 cases cerebral palsy developed (these newborns had extremely low body weight, were born to pregnant women with abruption of placenta and low Apgar score).Conclusions. Thus, perinatal risk factors for hypoxic-ischemic encephalopathy in premature infants were gestational age (up to 32 weeks of pregnancy), placenta previa with bleeding and placental abruption in this period. To prevent severe outcomes of HIE for children, it is important timely diagnosis of antenatal and intranatal fetal distress, to conduct neuroprotection with magnesium sulfate and prophylaxis of fetal respiratory distress syndrome

ФАКТОРИ РИЗИКУ ГІПОКСИЧНО-ІШЕМІЧНОЇ ЕНЦЕФАЛОПАТІЇ НЕДОНОШЕНИХ НОВОНАРОДЖЕНИХ

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Association of perinatal risk factors with neurological outcome in neonates with hypoxic ischemic encephalopathy

Objective Neonates exposed to perinatal insults typically present with hypoxic ischemic encephalopathy (HIE). The aim of our study was to analyze the association between known risk factors for HIE and the severity of encephalopathy after birth and neurological outcome in neonates during the first 4 d of life. Methods Retrospective cohort study including 174 neonates registered between 2011 and 2013 in the National Asphyxia and Cooling Register of Switzerland. Results None of the studied perinatal risk factors is associated with the severity of encephalopathy after birth. Fetal distress during labor (OR, 2.06; 95% CI, 1.02–4.25, p = .049) and neonatal head circumference (HC) above 10th percentile (p10) at birth (OR, 1.33; 95% CI, 1.05–1.69, p = .02) were associated with neurological benefit in the univariate analysis. Fetal distress on maternal admission for delivery was the only risk factor for neurological harm in the univariate (OR, 0.26; 95% CI, 0.12–0.57, p < .01) and the multivariate analysis (OR, 0.15; 95% CI, 0.04–0.67, p = .013). We identified two different patient scenarios: the probability for neurological benefit during the first 4 d of life was only 20% in neonates with the combination of all the following risk factors (gestational age >41 weeks, chorioamnionitis, fetal distress on maternal admission for delivery, fetal distress during labor, sentinel events during labor, HC below 10th percentile), whereas in the absence of these risk factors the probability for neurological benefit increased to 80%. Conclusions We identified a constellation of risk factors that influence neurological outcome in neonates with HIE during the first 4 d of life. These findings may help clinicians to counsel parents during the early neonatal period. (ClinicalTrials.gov NCT02800018).

PERINATAL RISK FACTORS FOR HYPOXIC-ISCHEMIC ENCEPHALOPATHY IN PRETERM INFANTS

The article presents the results of an assessment of risk factors for the development of hypoxic-ischemic encephalopathy in premature newborns. We examined 75 pregnant women who gave 92 premature newborns, patients with hypoxic-ischemic encephalopathy (main group). The comparison group included 75 pregnant women, who gave birth to 82 preterm infants, did not have GIE symptoms. In pregnant women of the main group who gave birth to children with GIE, more accurate were such extragenital pathology as hypertension (9.3%), chronic pyelonephritis (18.6%), thyroid disease (12 0%), tuberculosis and HIV infection, trichomoniasis, chlamydia. Among the complications of pregnancy in both groups was a high percentage of the threat of termination of pregnancy in all trimesters. Placental dysfunction and fetal growth retardation were in every fifth pregnant woman in both groups. Complications of labor, such as preterm premature rupture of amniotic membranes (PPROM) was in 32% of women, placenta previa with bleeding (8%) and abruption of placenta (14 6%) were significantly more frequent in the main group. The urgent cesarean section was performed in 41.4% of cases in the main group, 2.5 times greater than in the comparison group. Pregnant of the main group significantly more often gave birth to children with extremely low body weight (up to 30 weeks of pregnancy), 2 times more likely to give birth to children at 32 weeks of gestation. Among the 92 children of the main group, the Apgar scores of 3 points were -5-5.4%, 4-5 points - 18-19.5%, 6 points-28-30.4%, 7 and higher - 41-44, 5%. One of four children had severe fetal distress at birth. In the comparison group, the Apgar scores of 4-5 points were only 9.7%, 6 points - 14.6%, the other 75.7% had a satisfactory condition at birth. Artificial ventilation was performed in 58-63.1% of the newborns in the main group and only 10% in the comparison groupThus, perinatal risk factors for hypoxic-ischemic encephalopathy in premature newborns are the factories that lead to the development of placental dysfunction, fetal growth retardation, antenatal fetal distress and premature birth. The most important factor in the development of GIE is gestation (up to 32 weeks gestation), placenta previa with bleeding and premature placental abruption in the given time.

Ante- and intrapartum risk factors for neonatal hypoxic ischemic encephalopathy

Purpose: To identify obstetrical risk factors for the diagnosis of neonatal hypoxic ischemic encephalopathy (HIE). A secondary aim was to determine the incidence of HIE. Materials and methods: A retrospective cohort study including 36,086 women with singleton term pregnancies giving live births in Sweden between 2009 and 2013. Cases of HIE were identified from three different sources. Risk factors for HIE were evaluated using univariate and multivariate analyses. Cases of HIE were extracted from available Swedish Medical Health registers to determine incidence. Results: A diagnosis of HIE was associated with: acute obstetrical events, mode of delivery other than unassisted vaginal birth, abnormal CTG admission test, and nulliparity. The incidence of HIE was 1.7/1000 infants born. Conclusions: Acute obstetrical events will always occur, and some of the risk factors for these events are not responsive to interventions, but a careful risk assessment could lower the risk associated with acute obstetrical events. By alertness to early symptoms and timely measures taken by a trained staff at the delivery unit, damage could be reduced.

Monitoring of neurological parameters in newborns with hypoxic-ischemic encephalopathy

Asphyxia i a condition caused by lack of oxygen in tissues and organs. The basic pathogenic mechanisms of asphyxia are: 1)hypoxemia, 2) ischemia. The effects of perinatal asphyxia on the brain of a neonatal baby are critical in development of hypoxic-ischemic encephalopathy. The diagnosis of hypoxic-ischemic encephalopathy is based on clinical data including course of pregnancy and delivery (Apgar score) and especially on the neurological status of the newborn (consciousness, tonus, convulsions, reflexes, vegetative functions, etc.) and it can be confirmed by biochemical analysis and neurological examinations. The aim of this paper is to determine the importance of prenatal and perinatal risk factors for hypoxic-ischemic encephalopathy, as well as their effects on the development of neurological complications and further neurological problems. The research included 148 newborn infants born in the period from January 1, 1996 to January 1, 1999, with gestational age of 27 to 42 weeks, with hypoxic ischemic lesions of the central nervosus system. The control group included 58 children of the same age and the same gestation, with generalized hypotonia ("floppy infant") but without any signs of hypoxic ischemic lesions of the central nervous system. In the group of examined newborn infants with hypoxic ischemic lesions, from 149 children 1 (0.67%) died, 87 (53.89%) had normal findings, whereas the handicap was established in 61 (40.94%). Perinatal asphyxia affects the fetus and newborn infants not by individual factors, but with at least three or four associated factors. The disorders caused by asphyxia are in inverse proportion to the duration and intensity of hypoxic insults and the gestational age of the newborn.

Influence of Maternal, Obstetric and Fetal Risk Factors on the Prevalence of Birth Asphyxia at Term in a Swedish Urban Population

Birth asphyxia is a perinatal occurrence that, in serious cases, may lead to permanent adverse consequences or death. This retrospective case-control study of term neonates with birth asphyxia, defined as a 5-minute Apgarscore less than 7, had as its goal to explore risk factors for birth asphyxia itself, related hypoxic-ischemic encephalopathy (HIE), and asphyxia-related disability and death. Infants who died of nonasphyxial causes, such as infection or maternal sedation, were not included. Among more than 42,000 live births reviewed for the years 1985 through 1991 in an urban Swedish population were 225 cases of birth asphyxia that were matched with nonasphyxial control cases. The study group included 75 infants with both asphyxia and HIE. Surviving infants were followed for 18 months or longer, and those viewed as neurologically disabled were followed for 1.5 to 3 years longer. Twenty-two infants in the asphyxia group died or developed asphyxia-related neurological disability. Rates of birth asphyxia, pure birth asphyxia, and asphyxia-related HIE during the 7-year review period were, respectively, 6.9, 5.4, and 1.9 per 1000 live births. The asphyxia-related mortality rate was 0.26 per 1000 live births, and the rate of neurological impairment at the 18-month follow-up was 0.2 per 1000. Factors associated with birth asphyxia included single marital status (odds ratio [OR] = 7.1), intrauterine meconium release (OR = 4.1), operative delivery (OR = 8.7), breech delivery (OR = 20.3), and oxytocin augmentation (OR = 2.9). Other associated parameters were cord complications (OR = 15.8) and external compression to aid delivery (OR = 6.2). Significant cardiotocographic (CTG) correlates included repeated late decelerations (OR = 29.4), occasional late or variable decelerations (OR = 2.2), and a lack of accelerations (OR = 5.2). All groups of infants with asphyxia were delivered operatively or instrumentally more often than were the matched control infants. No association was evident between asphyxia and maternal age, smoking, illnesses, time of delivery (day vs. night or seasonal), or previous cesarean delivery. Independent risk factors for HIE included intrauterine meconium release, CTG score, and operative delivery. This is one of the few population-based studies of risk factors for asphyxia and perhaps the first to separately examine risk factors for pure asphyxia, HIE, and asphyxia-related death and disability. Asphyxia was strongly associated with CTG abnormalities, particularly the absence of baseline variability. CTG monitoring definitely is indicated for women given oxytocin augmentation, one of the factors associated with asphyxia in this study.