Current monitoring techniques in neonates lack sensitivity for
hypoxia at cellular level. The recent introduction of the non-invasive Cellular
Oxygen METabolism (COMET) monitor enables measuring in vivo mitochondrial
oxygen tension (mitoPO2), based on
oxygen-dependent quenching of delayed fluorescence of 5-aminolevulinic
acid (ALA)-enhanced
protoporphyrin IX. The aim is to determine the feasibility and safety of non-invasive mitoPO2 monitoring in surgical newborns. MitoPO2 measurements were conducted in a tertiary pediatric center during surgical repair of
congenital diaphragmatic hernia or
esophageal atresia. Intraoperative mitoPO2 monitoring was performed with a COMET monitor in 11
congenital diaphragmatic hernia and four
esophageal atresia neonates with the median age at surgery being 2 days (IQR 1.25-5.75). Measurements were done at the skin and
oxygen-dependent delayed fluorescence was measurable after at least 4 h application of an ALA plaster. Pathophysiological disturbances led to perturbations in mitoPO2 and were not observed with standard monitoring modalities. The technique did not cause damage to the skin, and seemed safe in this respect in all patients, and in 12 cases intraoperative monitoring was successfully completed. Some external and potentially preventable factors-the measurement site being exposed to the
disinfectant chlorohexidine, purple skin marker, or infrared light-seemed responsible for the inability to detect an adequate delayed fluorescence signal. In conclusion, this is the first study showing it is possible to measure mitoPO2 in neonates and that the
cutaneous administration of ALA to neonates in the described situation can be safely applied. Preliminary data suggests that mitoPO2 in neonates responds to perturbations in physiological status.