Cardiotocography, Hypoxia, and Feto-Neonatal Neurological Damage

Abstract

Complications occurring at any level of fetal oxygen supply can result in hypoxemia, which may ultimately lead to hypoxia/acidosis and neurological damage. Hypoxic-ischemic encephalopathy (HIE) is the short-term neurological dysfunction caused by intrapartum hypoxia/acidosis. This diagnosis requires the presence of several findings, including confirmation of newborn metabolic acidosis, low Apgar scores, early imaging evidence of cerebral edema, and the appearance of clinical signs of neurological dysfunction in the first 48 hours of life. Cerebral palsy (CP) comprises a heterogeneous group of nonprogressive movement and posture disorders, often accompanied by cognitive and sensory impairments, epilepsy, nutritional deficiencies, and secondary musculoskeletal lesions. Although CP is the most common long-term neurological complication associated with intrapartum hypoxia/acidosis, over 80% of cases are caused by other factors. Data on minor long-term neurological deficits are limited, but they suggest that less severe intellectual and motor impairments may result from intrapartum hypoxia/acidosis. Birth asphyxia is a broad term referring to intrapartum asphyxia severe enough to cause neurological damage in some newborns and, rarely, intrapartum or neonatal death. Cerebral palsy and long-term neurological complications such as learning difficulties and motor impairments may have causes other than birth asphyxia. Several intrapartum events can lead to asphyxia (i.e., hypoxia and metabolic acidosis), increasing the likelihood of neurological injury. The cardiotocograph (CTG) is a screening tool used to assess fetal well-being during labor and to identify the possibility of asphyxia. An abnormal CTG, sometimes severe enough to be described as a pathological trace, is commonly referred to as “fetal distress”, although many fetuses with such traces may not have hypoxia and metabolic acidosis. In current practice, these events are appropriately termed “pathological CTG trace” or “acidotic pH” rather than “fetal distress”. Accurate interpretation of the CTG is essential, and it is important to recognize a fetus displaying a pathological CTG in labor, which may imply possible hypoxia and birth asphyxia. Considering the broader clinical context when interpreting the CTG and taking timely and appropriate action based on the findings may help prevent birth asphyxia.