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Fetal hypoxia‐ischaemia: wrong time, wrong place

Baxter has explored the question: how much is too much when it comes to perinatal hypoxia? As expected, the answer is complicated and relates to both the depth and duration of the ischemia as well as maternal and fetal factors. Broadly speaking, if the ischemia lasted less than 20 minutes, there was partial correlation with clinical severity —some infants were affected, and some were not—while if presumed ischemia extended beyond 20 minutes, most, but not all, were severely impaired. Some of the interest in this article involves understanding why a similar insult might lead to a different clinical outcome. Increasing recognition of other influences that affect neurodevelopment identify both infection and genetics as substantial contributors to clinical outcome. When minutes may make the difference in the clinical and radiographic outcome, determining when an injury began is imperative, but may not be practically possible. For decades, the medical and legal systems have worked to link scenarios with evidence of intrapartum hypoxia-ischemia. In some situations, the drive is determining causation for cerebral palsy (CP) in order to allocate blame. The other more critical motivator is to find markers that can allow preventative measures or to institute neuroprotective or restorative therapies for infants at risk. For intrapartum hypoxic-ischemic events to be considered as causative of CP, the traditional axiom requires a peripartum metabolic acidosis, early onset of severe or moderate neonatal encephalopathy in infants older than 34 weeks’ gestation, and CP of the spastic quadriparetic or dyskinetic type. Non-specific but supportive associations for an intrapartum injury include a sudden and sustained deterioration of preterm heart rate, Apgar scores of 0 to 6 of longer than 5 minutes, early evidence of multisystem involvement, and early imaging evidence of acute cerebral abnormality. As is the case with imaging, indirect proxies of hypoxia, such as pH levels, do not predict neurological damage in many cases. Clinically and legally, situations where damage has occurred without an obvious onset pose more of an issue. Chronic partial ischemia is a recognized pattern thought to explain this presentation. In a recent review, these types of injuries were considered to be less frequent than the basal ganglia type in term born neonates and are usually associated with a milder phenotype. To make the situation more complicated, survivors of such an insult may have long-term cognitive deficits even in the absence of motor problems. Conversely, outcomes from big data analysis suggest that for some, even an apparently minor insult may lead to an adverse outcome. However, a safe minimum duration of partial ischemia cannot be defined. Until we understand better the issues that may influence an individual’s resistance or susceptibility to a situation in which they may be exposed, it is unlikely that hard lines can be drawn. While magnetic resonance imaging can demonstrate patterns thought to support the timing of an injury again, the rules cannot be applied rigorously in every circumstance. We cannot rely on animal studies or soft biomarkers to define our clinical pathways. The search for an accurate and predictive marker of the outcome will hopefully provide the answer to the real question asked by obstetricians and pediatricians: What do I need to do now to help this child? Our obligation to personalize care will require accurate clinical databases, careful phenotyping, and correlation with emerging genomic information. Better understanding these factors will extend our capability of care beyond the minority who have intrapartum ischemia to the majority who are at risk for preventable neurodevelopmental disability.