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

INTRODUCTION: The aim of the study was to identify the obstetric risk factors for hypoxic-ischemic encephalopathy (HIE) in infants with asphyxia at birth. MATERIAL AND METHODS: This multicenter case-control study covered the 5-year period from 2014 through 2018 and included newborns ≥36 weeks 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. RESULTS: 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 1 h 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). CONCLUSIONS: HIE is associated with a lower 5-min Apgar score and with the severity of acidosis at birth and at 1 h 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.

Perinatal outcome and need of care for term asphyxiated newborns without moderate or severe hypoxic-ischemic encephalopathy.

AIM: Birth asphyxia can lead to organ dysfunction, varying from isolated biological acidosis to hypoxic-ischemic encephalopathy (HIE). Pathophysiology of moderate or severe HIE is now well known and guidelines exist regarding the care required in this situation. However, for newborns without moderate or severe HIE, no consensus is available. Our objective was to describe the immediate neonatal consequences and need for care of asphyxiated newborns without moderate or severe HIE. METHODS: Multicentre retrospective study from January 2015 to December 2017 in two academic centres, including neonates ≥37 gestational weeks with pathological foetal acidemia (umbilical arterial pH<7.00 and/or lactate≥10 mmol/L). RESULTS: Among 18 550 births, 161 (0.9%) had pathological foetal acidemia. 142 (88.0%) were not diagnosed with moderate or severe HIE. Among them, 82 (58.0%) were hospitalised. 13 (9.0%) had respiratory failure and required nutritional support. 100 (70.0%) underwent blood sampling, which showed at least one biological anomaly in 66 (66.0%) of cases. CONCLUSION: Newborns born with pathological foetal acidemia without the occurrence of moderate or severe HIE had metabolic disorders and could need organ support. A prospective study describing this vulnerable population would help to establish consensus guidelines for the management of this population.

Diagnostic contribution of metabolic workup for neonatal inherited metabolic disorders in the absence of expanded newborn screening.

Inherited metabolic disorders (IMDs) in neonates are a diagnostic and therapeutic challenge for the neonatologist, with the priority being to rapidly flag the treatable diseases. The objective of this study was to evaluate the contribution of targeted metabolic testing for diagnosing suspected IMDs on the basis of suggestive clinical setting or family history in neonates. We conducted an observational study over five years, from January 1st, 2010 to December 31, 2014 in the neonatal intensive care unit (NICU) at Robert Debré University Hospital, Paris, France. We assessed the number of neonates for whom a metabolic testing was performed, the indication for each metabolic test and the diagnostic yield of this selected metabolic workup for diagnosing an IMD. Metabolic testing comprised at least one of the following testings: plasma, urine or cerebrospinal fluid amino acids, urine organic acids, plasma acylcarnitine profile, and urine mucopolysaccharides and oligosaccharides. 11,301 neonates were admitted at the neonatal ICU during the study period. One hundred and ninety six neonates underwent metabolic testing. Eleven cases of IMDs were diagnosed. This diagnostic approach allowed the diagnosis, treatment and survival of 4 neonates (maple syrup urine disease, propionic acidemia, carnitine-acylcarnitine translocase deficiency and type 1 tyrosinemia). In total, metabolic testing was performed for 1.7% of the total number of neonates admitted in the NICU over the study period. These included 23% finally unaffected neonates with transient abnormalities, 5.6% neonates suffering from an identified IMD, 45.4% neonates suffering from a non-metabolic identified disease and 26% neonates with chronic abnormalities but for whom no final causal diagnosis could be made. In conclusion, as expected, such a metabolic targeted workup allowed the diagnosis of classical neonatal onset IMDs in symptomatic newborns. However, this workup remained normal or unspecific for 94.4% of the tested patients. It allowed excluding an IMD in 68.4% of the tested neonates. In spite of the high rate of normal results, such a strategy seems acceptable due to the severity of the symptoms and the need for immediate treatment when available in neonatal IMDs. However, its cost-effectiveness remains low especially in a clinically targeted population in a country where newborn screening is still unavailable for IMDs except for phenylketonuria in 2019.