Intrapartum fetal hypoxia is a rare event, although fetal intrapartum surveillance is discussed as a subject of major importance. This is mainly because of consequences of fetal hypoxia that may lead to cerebral palsy. A fetus suffering from hypoxia initially compensates by producing energy through anaerobic metabolism. At some stage, the fetus becomes decompensated and basic cellular functions fail, with risks of permanent morbidity or mortality. How long a fetus can survive on anaerobic metabolism differs because metabolic reserves differ, i.e., growth-restricted fetuses might deteriorate at an earlier stage. An increasing body of evidence has clarified brain-damaging mechanisms. Neuronal loss occurs in two phases: during the primary hypoxic event and later during the reperfusion/reoxygenation phase. Animal studies have suggested the possibility of prophylactic treatment to prevent neuronal loss after the hypoxic event. Intrapartum diagnostic tools should aim for detecting fetal hypoxemia/hypoxia when the fetus is still compensated. This may be achieved by assessment of biochemical data such as pH, lactate, and oxygen saturation, with the aim of prophylactic intervention before the fetus becomes decompensated. The measurement of cord blood levels of oxygen free radicals and excitatory amino acids at the time of birth may prove to be helpful in determining the risk of brain damage and evaluating the effect of prophylactic treatments to prevent or ameliorate brain injury from hypoxia.