Lactate and S100 protein as early biochemical indicators of birth neonatal asphyxia caused by intrauterine umbilical cord strangulation: a medicolegal view

Abstract

Background: From a forensic pathologist's perspective, there are several aspects of the perinatal postmortem that are particularly important if the baby was born alive or dead. In cases of litigation for perinatal morbidities occurring in hospitals, access to the obstetric and neonatal notes if the baby is born alive and dies a few hours or days later is essential to reach a correct interpretation and conclusion. Hypoxic ischemic encephalopathy (HIE) after prenatal asphyxia is an important cause of neonatal morbidity and long-term neurological disability. It has many causes including intrauterine strangulation by umbilical cord (nuchal cord). Failure of early diagnosis of neonatal asphyxia and its treatment is considered a medicolegal negligence against the doctors. Aim: The present study aimed to use cord blood lactate & S100 protein levels as early markers of neonatal hypoxia caused by nuchal cord to minimize the risk of medicolegal liabilities against the doctors and hospitals. Methods: This is a comparative cross-sectional study conducted on 30 hypoxic neonates due to intrauterine cord strangulation. Lactate & S100 protein levels in the cord blood were measured. These were compared to 30 apparently healthy neonates matched in age, sex and body weight as a control group. Results: Lactate & S100 protein levels in cord blood were a higher significant difference in HIE neonates than control group. In conclusion: lactate & S100 protein levels in cord blood could be used as an early marker for diagnosis of neonatal HIE.

The Usefulness of Serum Brain Damage Biomarkers in Detection and Evaluation of Hypoxic Ischemic Encephalopathy in Calves with Perinatal Asphyxia

“…In the present study, a statistically significant increase was found in the S100B concentration of calves with perinatal asphyxia compared to healthy calves at the time of admission, 24, 48, and 72 h. Higher S100B concentrations in calves with perinatal asphyxia compared to healthy calves have been associated with the development of hypoxic-ischemic encephalopathy [ 50 , 51 ]. In our study, the concomitant elevation of S100B, lactate [ 52 , 53 ], and UCHL1 concentrations in calves with perinatal asphyxia supports the development of hypoxic-ischemic encephalopathy.…”

“…In term and preterm infants with hypoxic-ischemic encephalopathy, S100B concentration was found to be elevated within the first 72 h [ 50 ]. In contrast, Nagdyman et al [ 51 ] reported that S100B is rapidly released in hypoxic brain injury and returns to normal ranges within 48 h. Previous studies showed that in the umbilical cord blood of infants born with neonatal asphyxia S100B and lactate concentrations were increased, and these markers could be helpful as an early predictive marker for diagnosis of neonatal hypoxic-ischemic encephalopathy [ 52 , 53 ]. In the present study, a statistically significant increase was found in the S100B concentration of calves with perinatal asphyxia compared to healthy calves at the time of admission, 24, 48, and 72 h. Higher S100B concentrations in calves with perinatal asphyxia compared to healthy calves have been associated with the development of hypoxic-ischemic encephalopathy [ 50 , 51 ].…”