Asphyxia describes any condition that results in oxygen deprivation and, in the unborn or soon-to-be-born infant, may occur prenatally in utero, during delivery or postnatally [1]. In cases of intrapartum asphyxia, the duration of oxygen deprivation may vary and is critical to the ensuing insult to the infant’s vital organs and, especially, to the brain. Oxygen deficiency at tissue level (hypoxia, see Box 60.1) is often accompanied by glucose and nutrient deprivation, and is further compounded by pre-existing or complicating factors in the mother, especially pyrexia, and in the infant such as sepsis or congenital anomalies, the concomitant degree of metabolic derangement (e.g. extent of hypoglycaemia or metabolic acidosis), and the time to delivery and effective resuscitation. All of these factors will potentially compound any hypoxic injury and the extent of any ensuing brain damage, described as hypoxic ischaemic encephalopathy (HIE, Box 60.1). Attempts to assign an HIE ‘grade’ may help to correlate early symptoms and signs with the degree and likelihood of long-term sequelae [2], although accurate prognostication of asphyxial brain damage remains difficult.