Intrapartum recognition and management of fetal inflammation

Intra-amniotic inflammation and infection are common intrapartum conditions at term and represent a major cause of fetal and neonatal morbidity independent of hypoxia. These conditions trigger the fetal inflammatory response syndrome (FIRS), characterized by systemic cytokine activation, cardiovascular dysfunction, impaired thermoregulation, and neuroinflammation, which substantially increase the risk of early-onset neonatal sepsis, encephalopathy, and long-term neurological injury. The coexistence of inflammation and intrapartum hypoxic stress markedly amplifies fetal brain vulnerability. During labor, fetal inflammation is associated with specific cardiotocographic patterns that may precede metabolic acidemia. Early signs include unexplained fetal tachycardia or a progressive rise in baseline heart rate, often without preceding decelerations. With progression, loss of accelerations, abnormalities of baseline variability—including increased, reduced, or atypical sinusoidal patterns—and absence of sleep–wake cycling become evident. Decelerations may develop secondary to inflammation-related placental dysfunction, altered umbilical blood flow, and abnormal uterine contractility. Conclusion: Prompt recognition of these intrapartum features allows early intervention through maternal temperature control, antibiotic therapy, and timely delivery when indicated. Early identification and management of fetal inflammation are essential to mitigate inflammation-mediated neonatal morbidity and adverse neurological outcomes. Table presented.