Risk Factors For Neonatal Encephalopathy Research Articles

INTERRELATIONSHIP BETWEEN INDICATORS OF LOCAL AND SYSTEMIC INFLAMMATORY REACTION IN NEWBORNS WITH NEONATAL ENCEPHALOPATHY

Introduction. Neonatal encephalopathy is one of the most common diseases in newborns. Several factors influence the development of neonatal encephalopathy including adverse obstetric history, fetal distress, meconium-containing amniotic fluid and cesarean section. In moderate and severe neonatal encephalopathy, damage to internal organs, local and systemic inflammation may occur. Cytokines, which are activated in the central nervous system and released in response to its damage, play an important role in brain inflammation caused by neonatal encephalopathy. C-reactive protein is also a possible biomarker of neonatal encephalopathy severity, being considered a protein of the innate immune system with anti-inflammatory properties. The state of the inflammatory response can be influenced by a local inflammatory reaction, as a result of which children with neonatal encephalopathy have been shown to have increased levels of fecal calprotectin in the first weeks of life. Also, one of the results of the transferred inflammatory reaction is a change in the composition of the neonatal intestinal microbiome. Objective. To study risk factors for neonatal encephalopathy in newborns, the features of the relationship between local and systemic inflammatory response parameters in asphyxia of varying degrees, and the features of severity and control of inflammatory response parameters. Materials and methods. The study was conducted in 119 full-term newborns, of which 87 children had neonatal encephalopathy and 32 healthy children. To determine the features of severity and control of inflammatory response parameters, group A was identified, which included 60 newborns, 46 of them with moderate neonatal encephalopathy, 14 with severe neonatal encephalopathy. The study was conducted using a culture method to determine the composition of the intestinal microbiome in feces. Using a semi-automated Thermo Scientific Multiskan FC enzyme immunoassay analyzer, the level of fecal calprotectin in feces and C-reactive protein and interleukins 1β and 10 in the blood serum were estimated by the enzyme immunoassay. The results were analyzed using SPSS version 28.0. The correlation between the parameters was analyzed using the Pearson correlation coefficient. The odds ratio was used to quantitatively describe the closeness of the relationship between the features in the statistical population. Binary logistic regression was used to determine the dependencies of the severity of the inflammatory reaction and create a model for calculating its severity. Results. Risk factors for neonatal encephalopathy included mother’s acute respiratory infections and fetal distress. Bifidobacterium levels were positively correlated throughout the study, and there was also a relationship with lactobacilli in the control and non-probiotic treated neonatal encephalopathy groups. E. coli values were positively associated with opportunistic pathogens in the control and probiotic treated groups. Fecal calprotectin was negatively correlated with birth weight and height, Apgar scores, and gestational age. Fecal calprotectin levels were positively correlated with E. coli and opportunistic pathogens in healthy neonates. In children with neonatal encephalopathy interleukin 1β and 10 values were positively associated with fecal calprotectin, interleukin 1β were positively correlated with interleukin 10 and C-reactive protein. Conclusions. The most significant risk factors for the development of neonatal encephalopathy are mother’s acute infectious diseases and fetal distress. The severity of hypoxia/asphyxia at birth correlated with the levels of interleukin 1β and 10 at 2 and 5 weeks of life, and Bifidobacterium at 2 weeks of life. The severity of the inflammatory response in the study population was characterized by a change in the level of interleukin 1β and Bifidobacterium at 2 weeks and a change in the level of interleukin 10 at 5 weeks

Risk factors for neonatal encephalopathy in late preterm and term singleton births in a large California birth cohort.

The objective was to investigate maternal and pregnancy characteristics associated with neonatal encephalopathy (NE). We queried an administrative birth cohort from California between 2011 and 2017 to determine the association between each factor and NE with and without hypothermia treatment. From 3 million infants born at 35 or more weeks of gestation, 6,857 cases of NE were identified (2.3 per 1000 births), 888 (13%) received therapeutic hypothermia. Risk factors for NE were stronger among cases receiving hypothermia therapy. Substance-related diagnosis, preexisting diabetes, preeclampsia, and any maternal infection were associated with a two-fold increase in risk. Maternal overweight/obesity, nulliparity, advanced maternal age, depression, gestational diabetes or hypertension, and short or long gestations also predicted NE. Young maternal age, Asian race and Hispanic ethnicity, and cannabis-related diagnosis lowered risk of NE. By disseminating these results, we encourage further interrogation of these perinatal factors.

Perinatal risk factors for neonatal encephalopathy: an unmatched case-control study

ObjectiveNeonatal encephalopathy (NE) is the third leading cause of child mortality. Preclinical studies suggest infection and inflammation can sensitise or precondition the newborn brain to injury. This study examined perinatal...

Intrapartum risk factors for neonatal encephalopathy leading to cerebral palsy in women without apparent sentinel events.

To determine intrapartum factors associated with neonatal encephalopathy leading to cerebral palsy (NE-CP). A total of 70 NE-CP patients who fulfilled study criteria (cephalic singleton pregnancy with attempted vaginal delivery [AVD] at gestational week [GW] ≥36; intrapartum occurrence of non-reassuring fetal status without apparent cause following reassuring fetal status on admission; and development of NE-CP) were compared with 210 AVD controls who had 1- and 5-min Apgar score ≥8 matched for GW, maternal parity, and use of uterotonics. Suboptimal care was defined as delayed reaction due to misinterpretation of fetal heart rate (FHR) tracing, or inappropriate trial of instrumental delivery (TOID). Successful and failed TOID were defined as vaginal and cesarean delivery after TOID, respectively. The 210 controls were assumed not to have had suboptimal care. The rates of successful (34% vs 12%) and failed TOID (11% vs 0.0%), cesarean section (34% vs 14%), suboptimal care (57% vs 0.0%), pregnancy-induced hypertension (11% vs 2.4%), birthweight ≥3800 g (8.6% vs 1.9%), subgaleal hemorrhage (16% vs 0.0%) were significantly higher in NE-CP patients than in controls. Selection with the stepwise method and logistic regression analysis identified four independent risk factors for NE-CP: suboptimal intrapartum care (OR, 2.21; 95%CI: 1.99-2.47), cesarean section (OR, 1.19; 95%CI: 1.08-1.31), successful TOID (OR, 1.14; 95%CI: 1.03-1.25), and hypertension (OR, 1.20; 95%CI: 1.01-1.42). Training programs for improved interpretation of FHR tracing and appropriate TOID are required to prevent NE-CP among healthy and mature fetuses in Japan.

Antepartum and Intrapartum Risk Factors for Neonatal Encephalopathy at Term

We investigated antepartum and intrapartum risk factors for neonatal encephalopathy (NE) in term infants. We performed a case-controlled study in which characteristics of singleton term infants who developed NE from 1993 to 2003 were compared with those of randomly selected controls. Antenatal risk factors (including obesity, diabetes, thyroid dysfunction, previous cesarean delivery, preeclampsia, fetal growth restriction, abnormal amniotic fluid volume, and abnormal fetal heart rate [FHR] tracing before labor) and intrapartum risk factors (acute intrapartum sentinel events and other risk factors like suspicious or ominous FHR tracing and clinical chorioamnionitis) were related to occurrence of NE. From the study cohort of 30,580 infants, 27 (0.09%) developed NE and were compared with 100 controls. Neonates with encephalopathy had more frequent antepartum (74% versus 18%, P < 0.001) and intrapartum (67% versus 19%, P < 0.001) risk factors, including acute intrapartum events (33% versus 2%, P < 0.001), than controls. On the whole, 26% of cases of NE had only antepartum risk factors, 22% had only intrapartum risk factors, and 44% had a combination of the two. In 2/27 (7%) cases, no risk factors were recognizable. In conclusion, 44% of cases of NE following term deliveries can be attributed to a combination of antepartum and intrapartum variables.

The Relationship Between Intrapartum Maternal Fever and Neonatal Acidosis as Risk Factors for Neonatal Encephalopathy

Impey, L.W.; Greenwood, C.E.; Black, R.S.; Yeh, P.S.; Sheil, O.; Doyle, P. Author Information

The relationship between intrapartum maternal fever and neonatal acidosis as risk factors for neonatal encephalopathy

This study was undertaken to investigate the relationship among maternal intrapartum fever, neonatal acidosis, and the risk of neonatal encephalopathy. Cohort study of pregnancies at term. Logistic regression was used to estimate the effect of maternal fever and acidosis on the risk of neonatal encephalopathy. The potential interaction between maternal fever and acidosis was included in the models. Of 8299 women, 25 neonates (0.3%) had encephalopathy develop. These were more often born acidotic (adjusted odds ratio 11.5; 95% CI, 5.0-26.5) or after a maternal intrapartum fever (adjusted odds ratio 8.1; 95% CI, 3.5-18.6). Where both risk factors coexisted, the risk was 12.5% (adjusted odds ratio 93.9; 95% CI, 28.7-307.2). Although this effect is multiplicative, there was no evidence of statistical interaction (P = .93); the effect of maternal fever on the risk of encephalopathy was similar in infants with (adjusted odds ratio 8.7; 95% CI, 2.4-31.7) and without acidosis (adjusted odds ratio 7.4; 95% CI, 2.4-21.9). The combination of a maternal fever with cord acidosis greatly increases the risk of neonatal encephalopathy, but there is evidence against interaction between them, suggesting that they represent 2 separate causal pathways.

Neonatal encephalopathy: etiology and outcome

The original study by Badawi et al. investigated risk factors for neonatal encephalopathy (NE) and/or neonatal seizures in term infants. They used a broad definition appropriate for examining etiology and capable of asking such questions as: what proportion of NE arises after birth asphyxia? The answer was: some, but not much. That study was, and still is, the only large population-based investigation of multiple potential risk factors for NE, and it identified novel risk factors such as maternal thyroid disease, family history of seizures, and placental abnormalities. Several of these factors have been found to be risk factors for NE, neonatal seizures, or cerebral palsy (CP) in other studies.

MRI for neonatal encephalopathy in full-term infants

Encephalopathy in an infant within the first few days of birth often reflects a major neurological disorder with a significant risk of long-term disability. 1 Ellenberg JH Nelson KB Cluster of perinatal events identifying infants at high risk for death or disability. J Pediatr. 1988; 113: 546-552 Summary Full Text PDF PubMed Scopus (113) Google Scholar Determining the cause and prognosis remains challenging. Signs of neonatal encephalopathy include seizures, lethargy or coma, poor tone and feeding, and difficulty maintaining respiration; and early descriptions focused on intrapartum asphyxia as the primary cause. In 1976 Sarnat and Sarnat 2 Sarnat HB Sarnat MS Neonatal encephalopathy following fetal distress. Arch Neurol. 1976; 33: 696-705 Crossref PubMed Scopus (1979) Google Scholar pointed out the importance of staging encephalopathy with behavioural and electroencephalographic criteria, and 10 years later Levene et al 3 Levene MI Grindulis H Sands C Moore JR Comparison of two methods of predicting outcome in perinatal asphyxia. Lancet. 1986; 1: 67-69 Summary PubMed Google Scholar reported that rating the clinical severity of encephalopathy is better than the Apgar score for predicting neurological outcome after asphyxia. Evidence, especially from the Western Australian case-control study by Badawi et al, 4 Badawi N Kurinczuk JJ Keogh JM et al. Antepartum risk factors for newborn encephalopathy: the Western Australian case-control study. BMJ. 1998; 317: 1549-1553 Crossref PubMed Scopus (750) Google Scholar suggests that a diverse group of disorders, many beginning antenatally, in addition to asphyxia are associated with encephalopathy in newborn babies. These disorders include maternal and fetal infections, maternal thyroid and nutritional deficiencies, placental disorders, and genetic diseases including Prader-Willi and Angelman's syndromes, Rett's syndrome, myotonic dystrophy, non-ketotic hyperglycinaemia, thrombophilic disorders, brain malformations, and family history of epilepsy. 4 Badawi N Kurinczuk JJ Keogh JM et al. Antepartum risk factors for newborn encephalopathy: the Western Australian case-control study. BMJ. 1998; 317: 1549-1553 Crossref PubMed Scopus (750) Google Scholar , 5 Ellis M Manandhar N Manandhar DS Costello AM Risk factors for neonatal encephalopathy in Kathmandu, Nepal, a developing country: unmatched case-control study. BMJ. 2000; 320: 1229-1236 Crossref PubMed Scopus (106) Google Scholar , 6 Grether JK Nelson KB Maternal infection and cerebral palsy in infants of normal birth weight. JAMA. 1997; 278: 207-211 Crossref PubMed Google Scholar , 7 Geerdink N Rotteveel JJ Lammens M et al. MECP2 mutation in a boy with severe neonatal encephalopathy: clinical, neuropathological and molecular findings. Neuropediatrics. 2002; 33: 33-36 Crossref PubMed Scopus (55) Google Scholar , 8 Richer LP Shevell MI Miller SP Diagnostic profile of neonatal hypotonia: an 11-year study. Pediatr Neurol. 2001; 25: 32-37 Summary Full Text Full Text PDF PubMed Scopus (77) Google Scholar , 9 Smith A Wiles C Haan E et al. Clinical features in 27 patients with Angelman syndrome resulting from DNA deletion. J Med Genet. 1996; 33: 107-112 Crossref PubMed Scopus (90) Google Scholar In the Western Australian study, 28% of infants with encephalopathy had birth defects compared with 4% of controls, and these defects were judged to have contributed to the encephalopathy in 37% of these cases. 10 Felix JF Badawi N Kurinczuk JJ Bower C Keogh JM Pemberton PJ Birth defects in children with newborn encephalopathy. Dev Med Child Neurol. 2000; 42: 803-808 Crossref PubMed Google Scholar Origin and timing of brain lesions in term infants with neonatal encephalopathyAlthough our results cannot exclude the possibility that antenatal or genetic factors might predispose some infants to perinatal brain injury, our data strongly suggest that events in the immediate perinatal period are most important in neonatal brain injury. Full-Text PDF

Risk factors for neonatal encephalopathy in Kathmandu, Nepal, a developing country: unmatched case-control study

Objective: To determine the risk factors for neonatal encephalopathy among term infants in a developing country.Design: Unmatched case-control study.Setting: Principal maternity hospital of Kathmandu, Nepal.Subjects: All 131 infants with neonatal...