Neonatal Hyperbilirubinemia is one of the important causes of neonatal morbidity and mortality in developing countries 14&15. It is also a primary reason of avoidable brain damage, physical and mental disabilities, and early losses among newborns in several communities16.As regard the results of this study, regarding the etiology of neonatal hyperbilirubinemia in the present study, the most common cause was exaggerated physiological jaundice (40.8%) followed by ABO incompatibility (25.4%), RH incompatibility (16.6%), sepsis (8.9%) and G6PD deficiency (%8.3).These results were similar to the results obtained by Abdel Moktader et al, (2019)17. Concerning the recognition of jaundice by the parents, we found that most of them 76.4% recognized jaundice of their babies during the second week or the awareness of it after the first week ,this may be due to lack of knowledge of the parents about neonatal jaundiced and its complications. Also, it was found that working mother had good knowledge towards neonatal jaundiced18.
Concerning different etiologies of jaundice ,the incidence of exaggerated physiological jaundice was the commonest ,this could be explained by that physiological jaundice is the result of increased bilirubin production from the breakdown of fetal red blood cells combined with transient limitations in the conjugation of bilirubin by the immature neonatal liver for most of these infants, jaundice is mild and resolves without treatment 19.The incompatibility of the ABO blood groups of the mother and fetus was 25.4% when the mother has the blood group O and the newborn has the A or B blood group, Murray and Roberts, (2007) 20 found that it was 15–20% of all pregnancies. Babies with O-blood group mothers should be closely checked for and discharged after72 h where routine cord blood screening is not recommended for newborns with O-group mothers21.Regarding different outcomes of the studied neonates, most of them 128 (75.8%) were recovered and discharged, 20 (11.8%) died and 21 (12.4%) survived with complications (Table 2).
Comparison between different outcomes as regard the etiology of neonatal hyperbilirubinemia, table (3) showed that neonates with exaggerated physiological jaundice were statistically significant recovered more than those with other causes while neonates with sepsis were more significantly died or developed complications (P value = 0.01).This could be explained by that in sepsis there increased oxidative stress with damage of the neonatal red blood cells22.
Concerning the predictors of the outcome of NJ, the current study found that newborns who recovered and discharged were significantly full term (55%) ,with proper weight and proper breast feeding while newborns who died were more presented as the first order (65%), had lower birth weight, more frequently presented under the third centile (95%), previous jaundiced baby ,significantly preterm (54%), had higher bilirubin level, lower HB level and higher CRP than who survived. There are many explanations for these findings where first birth order baby usually had higher frequency of NJ because of maternal breastfeeding complications, such as engorgement, cracked nipples, and fatigue, and neonatal factors, such as ineffective suck, which may result in ineffective breastfeeding if they are not properly educated during antenatal care visits. Moreover, preterm infants are more likely to experience difficulty in establishing successful breastfeeding than term infants where they may not fully empty the breast because of increased sleepiness, fatigue, and/or difficulty maintaining a latch because their oro-buccal coordination and swallowing mechanisms are not fully matured. As a result, additional support and close monitoring are warranted for this group of infants and their mothers. Family history of previous jaundiced baby or early infant death are suggestive of pathological jaundice in neonates23.Concerning lower weight association with neonatal hyperbilirubinemia ,This result is similar to the finding by Mojtahedi et al, (2018)24. This could be explained by that low calorie intake with lower weight is associated with increased hepatic circulation of bilirubin25. Figure (1) showed that bilirubin level at admission was a significant predictor for the good outcome (survival) of neonatal hyperbilirubinemia where (AUC = 0.79 ± 0.05 P = 0.001). This could be explained by that bilirubin which is a known antioxidant at low concentrations but a potent neurotoxin at high concentrations26..The transition from progressive hyperbilirubinemia to acute bilirubin encephalopathy is often rapid and unpredictable because of a very narrow margin of safety .Jaundice attributable to physiological immaturity which usually appears between 24–72 h of age and between 4th and − 5th days can be considered as its peak in term neonates and in preterm at 7th day, it disappears by 10–14days of life27. The bilirubin level does not usually rise above200 µmol/L and the baby remains well28.