Perinatal Asphyxia: A Review from a Metabolomics Perspective

Abstract

Perinatal asphyxia is defined as an oxygen deprivation that occurs around the time of birth, and may be caused by several perinatal events. This medical condition affects some four million neonates worldwide per year, causing the death of one million subjects. In most cases, infants successfully recover from hypoxia episodes; however, some patients may develop HIE, leading to permanent neurological conditions or impairment of different organs and systems. Given its multifactor dependency, the timing, severity and outcome of this disease, mainly assessed through Sarnat staging, are of difficult evaluation. Moreover, although the latest newborn resuscitation guideline suggests the use of a 21% oxygen concentration or room air, such an approach is still under debate. Therefore, the pathological mechanism is still not clear and a golden standard treatment has yet to be defined. In this context, metabolomics, a new discipline that has described important perinatal issues over the last years, proved to be a useful tool for the monitoring, the assessment, and the identification of potential biomarkers associated with asphyxia events. This review covers metabolomics research on perinatal asphyxia condition, examining in detail the studies reported both on animal and human models.

Urinary gas chromatography mass spectrometry metabolomics in asphyxiated newborns undergoing hypothermia: from the birth to the first month of life

“…In newborns with perinatal asphyxia, a small number of metabolomics studies have been published in the literature (22)(23)(24)(25)(26)(27); each of them has depicted the metabolic snapshot of the disease. As recapitulated in a recent review (28), human metabolomics studies have found that the most impaired molecular pathway during perinatal asphyxia and TH are the TCA cycle and the osmoregulation system.…”

Preliminary case control study to establish the correlation between novel peroxidation biomarkers in cord serum and the severity of hypoxic ischemic encephalopathy

“…In the experimental setting metabolomic studies performed in animal models of hypoxia reoxygenation have shown that oxidative stress associated metabolites strongly correlate with brain injury. The most specific and reliable biomarkers identified have been isoprostanes, neuroprostanes, non-protein bound iron, and 4-HNE proteins adducts [15][16][17]. F2-isoprostanes have been determined to be both biomarkers and mediators of oxidative stress in numerous diseases [18].…”

Neonatal Central Diabetes Insipidus Caused by Severe Perinatal Asphyxia

“…Perinatal asphyxia affects some four million neonates worldwide each year, causing the death of one million of them [8]. In most cases, the infants successfully recover from the hypoxic condition, but some patients develop HIE, leading to permanent neurological sequelae, such as seizure disorders, cerebral palsy, cognitive delays, and motor disabilities [6]. Furthermore, in addition to neurologic failure, asphyxia could lead to multiple organ impairment (central nervous system 28%, cardiovascular system 25%, kidneys 50%, and lungs 23%) [9,10] Clinical findings, laboratory examination, aEEG, and MRI in the present three cases showed severe perinatal asphyxia.…”

“…Some cases of perinatal asphyxia develop hypoxic ischemic encephalopathy (HIE) and multiple organ impairment, such as disseminated intravascular coagulation and respiratory, liver, heart, and renal failure [6]. Although perinatal asphyxia could potentially lead to CDI, CDI caused by severe asphyxia is very rare.…”

“…Perinatal asphyxia is associated with multi-organ hypoxia-ischemia and subsequent dysfunction, and it may be caused by perinatal events, such as maternal or fetal hemorrhage, intermittent or acute umbilical cord compression, uterine rupture, placental abruption, or shoulder dystocia, affecting the supply of oxygenated blood to the fetus [6]. Some cases of perinatal asphyxia develop hypoxic ischemic encephalopathy (HIE) and multiple organ impairment, such as disseminated intravascular coagulation and respiratory, liver, heart, and renal failure [6].…”