Mark Wefers Bettink

Mitochondrial oxygen monitoring during surgical repair of congenital diaphragmatic hernia or esophageal atresia: 9 167 Introduction Major (non-cardiac) neonatal surgery is challenging for clinicians. The neonatal homeostasis is a frail equilibrium and is highly affected by general anesthesia and surgical manipulation (1,2). The anesthesiologist aims to monitor the physiology with the help of the heart rate, invasive blood pressure, saturation, end-tidal carbon dioxide, skin perfusion, urine output and serum lactate. These broad range of monitoring modalities are used as surrogate of end-organ perfusion with adequate oxygen transport as a prime goal. To date, the optimal blood pressure in neonates for adequate perfusion of peripheral and cerebral tissue is unknown. Invasive techniques available for effective monitoring of the circulation/cardiovascular system are seldom used due to technical restraints in neonates or are simply not feasible during neonatal surgery (3). Yet, the incidence of brain injury after (non-cardiac) neonatal surgery is increasingly reported (4)(5) as well as altered long–term neurodevelopmental outcomes (6–9). Several factors are thought to contribute to the postoperative brain injury, including alterations in the perioperative neonatal hemodynamics. Adequate oxygen supply to tissues is of pivotal importance. A non-invasive, bedside monitoring modality for cellular oxygenation could provide direct information about oxygen transport. This allows clinician to adjust their management on actual measurements of tissue perfusion and oxygenation instead of systemic circulatory measures. In this light, monitoring of cellular oxygenation has been suggested to be beneficial during neonatal-cardiac surgery due to the highly affected hemodynamics (10). Yet, major non-cardiac congenital anomalies which requires surgery within the first days causes alterations in the neonatal physiology as well (4)(7). The recent introduction of the non-invasive Cellular Oxygen METabolism (COMET) monitor (Photonics Healthcare B.V., Utrecht, The Netherlands) makes it possible to measure in vivo mitochondrial oxygen tension (mitoPO 2 ). Although mitochondrial oxygen sensing has been recognized as a promising technique for pediatric ICU and anesthesia (11,12), until now reported use has been limited to adults (13–16). The present study tests feasibility and safety of intraoperative use of COMET monitoring in infants for the first time. The COMET monitor measures mitoPO 2 by means of oxygen-dependent quenching of delayed fluorescence (17). Green pulsed laser excitation of protoporphyrin IX (PpIX) leads to a relatively long-lived red-light emission, called “delayed fluorescence”. The intensity of the delayed fluorescence decays with an oxygen-dependent lifetime, meaning more oxygen results in a shorter lifetime and vice versa. PpIX is the final precursor of heme