The role of lactate measurement in the prediction of fetal hypoxic-ischaemic brain injury during labour

Craig Pennell

Research output: ThesisDoctoral Thesis

303 Downloads (Pure)


[Truncated abstract] In this thesis the role of lactate measurement has been evaluated in intrapartum assessment of fetal wellbeing. Specifically, I have addressed the question of whether fetal lactate measurement is better than the assessment of fetal heart rate patterns or the measurement of pH at predicting fetal brain injury after intrapartum asphyxia. Using an ovine model of repeated umbilical cord occlusion designed to mimic events which may occur during human labour, I have shown that the measurement of fetal lactate levels after repeated cord occlusion is significantly associated with the severity of brain injury after the asphyxial insult. No significant associations were identified with fetal pH measurements or with the duration of decelerative or compound fetal heart rate patterns; however, this is the first study to describe an association between the duration of both increased fetal heart rate variability and fetal heart rate overshoot with the severity of subsequent brain injury. Although no significant association was identified between fetal arterial pressure measured between umbilical cord occlusions and the grade of brain injury, the studies performed in this thesis are the first to show a strong correlation between the duration of specific arterial pressure responses during cord occlusions and the grade of brain injury, accounting for approximately 90% of the variability seen in the severity of injury. The mechanism responsible for the improved ability of lactate measurement to predict fetal brain injury is unknown. It may be because fetal lactate levels are a more stable marker of anaerobic metabolism of glucose than fetal pH levels, which are influenced by both increasing levels of carbon dioxide and anaerobic metabolism of amino-acids and fatty acids. In addition fetal pH levels can be rapidly normalised through placental exchange of carbon dioxide whereas fetal lactate levels are slow to normalise across the placenta as they rely on facilitated diffusion.
Original languageEnglish
QualificationDoctor of Philosophy
Publication statusUnpublished - 2003


Cite this