**2.4 Cerebral hypoxia**

10 Infrared Spectroscopy – Life and Biomedical Sciences

Fig. 1a. Example 1: Patient with loss of autoregulation and concordance of MAP and NIRS measurement of intravascular oxygenation (HbD). This patient had an unfavorable

Fig. 1b. Example 2: Maintenance of autoregulation (Tsuji, 2000)

outcome.

Cerebral hypoxia is a feared event as it translates to long-term morbidity and mortality*.* There is not enough data available linking a specific duration of hypoxia and levels of rSO2 or TOI while in the NICU with outcomes. There are no absolute numbers as reference in the human neonate. A piglet study from 2007 demonstrated changes seen on brain autopsy 72h after the animal spent 30 min. with rSO2-c of <40%. (Hou et al., 2007) It is not certain whether observations of concerning low levels of r-SO2/TOI in cardiac patients (Dullenkopf et al., 2003; Sorensen et al., 2008; van Bel et al., 2008; Wolf & Greisen, 2009) apply to infants with other diagnoses.

### **2.5 Cerebral hyperoxia**

Cerebral hyperoxia in the critically ill neonate may occur by 2 mechanisms: either as hyperoxygenation during the reperfusion phase of severe hypoxic ischemic encephalopathy most commonly occurring in neonates after perinatal birth depression or from decreased brain metabolism as seen in critical patients when blood flow is uncoupled from O2 (Toet, 2006; Wolf & Greisen, 2009). Either scenario is concerning for a poor long-term prognosis. The overall clinical situation needs to be taken into consideration as cerebral rSO2 in well preterm neonates has also been reported to be high in the first days of life. (Sorensen et al., 2009).
