First intrapartum sonographic diagnosis of fetal hypoxic ischemic encephalopathy (FHIE).

Abstract

Novel Insights In presence of cardiotocographic features suspected for hypoxic insult, intrapartum ultrasound in the hands of experienced operators can demonstrate cerebral edema as an indirect sign of fetal hypoxia affecting the fetal CNS and exclude non-hypoxic conditions potentially leading to abnormalities of the fetal heart rate. Introduction Hypoxic-ischemic encephalopathy is a syndrome involving the fetal central nervous system as the result of a perinatal hypoxic-ischemic injury. To date, transfontanellar ultrasound represents the first line exam in neonates with clinical suspicion of HIE as it allows to show features indicating acute hypoxic injury and exclude potential non-hypoxic determinants of HIE, however there is no report concerning the sonographic assessment of the brain during labor. In this clinical case we report the intrapartum sonographic evaluation of the fetal brain as a tool for the differential diagnosis of cardiotocographic abnormalities. Case Presentation A 42-year-old para 2 woman underwent labor induction at 37+3 weeks due to preeclampsia. On admission cardiotocography was normal, as was umbilical artery Doppler. De novo changes of the CTG pattern prior to the onset of labor raised the suspicion of a supervening fetal cerebral insult leading to the decision to expedite delivery by emergency cesarean. During the preparation for delivery, intrapartum ultrasound allowed to demonstrate fetal cerebral edema representing an early sign of superimposed intrapartum acute hypoxic insult in the context of chronic antepartum hypoxia and exclude non-hypoxic conditions of cardiotocographic abnormalities. Conclusion This is the first intrapartum sonographic demonstration of imaging findings consistent with cerebral edema in a fetus at risk for in utero hypoxia, hence suspected for fetal hypoxic ischemic encephalopathy (FHIE). Intrapartum ultrasound can assist clinicians in the differential diagnosis of intrapartum fetal hypoxia as long as it does not delay any interventions required to prevent hypoxic injury.