Cerebral Oxygenation Monitoring

A Strategy to Detect Intraventricular Hemorrhage and Periventricular Leukomalacia

Heather E. Elser, MSN, RN, NNP-BC, CNS, PhD Student; Diane Holditch-Davis, PhD, RN, FAAN; Debra H. Brandon, PhD, RN, CCNS, FAAN


NAINR. 2011;11(3):153-159. 

In This Article

Current Knowledge About Cerebral Oxygenation

Although cerebral oximetry is not a standard instrument in the neonatal intensive care unit (NICU), several studies have examined cerebral oxygenation in infants. What we know thus far about cerebral oxygenation is limited to infants on extracorporeal membrane oxygenation;[42,61,62] infants undergoing cardiac surgery;[63,64] or during care activities such as suctioning,[65–67] surfactant administration,[65,68] indomethacin dosing,[69–71] and blood transfusions.[72,73]

Limited knowledge exists to identify IVH using cerebral oxygenation monitoring. Through the use of optical tomography, total hemoglobin levels, particularly, deoxygenated hemoglobin level, are higher on the ipsilateral side of an IVH.[74] As mentioned earlier, the simplistic formula for calculating cerebral oxygenation divides the amount of oxygenated hemoglobin level by the total hemoglobin level (see Table 1). If deoxygenated hemoglobin level increases in the vicinity of an IVH, then the amount of measurable cerebral oxygenation will decrease. As a result, cerebral oxygenation values will decrease compared with unaffected cerebral locations (see Table 3).

This logic is confirmed in a prospective study that examined 73 premature infants in the first day of life.[75] Results showed that infants without IVH ranged from 67.7% to 82.1%, and those with IVH, from 53.3% to 86.4%. As the severity in IVH increased, cerebral oxygenation was shown to decrease. From this one study during the first day of life, infants who develop an IVH appear to have lower cerebral oxygenation levels. To continue to confirm this assumption, infant age and cerebral oxygenation monitoring beyond the first day of life are needed.

Cerebral oxygenation monitoring related to PVL diagnosis is also unclear. Ischemic episodes are theorized to cause outcomes of PVL. Cells during an ischemic episode revert to anaerobic metabolism as the nutrients derived from blood flow is diminished or inhibited resulting in what some call an "energy failure."[54] Energy failure will show as lower tissue oxygenation values, and the amount of cerebral oxygenation available to be measured is reduced. Timing, however, is essential, as these ischemic events are not anticipated. The ability to identify these particular low cerebral oxygenation levels at the correct time and to know when an infant is at risk for PVL remains unknown. Further research will need to identify cerebral oxygenation probe placement to capture these lower levels of tissue oxygenation that are indicative of PVL.

Although infant cerebral oxygenation research is fragmented, it is important to begin to connect individual studies to the bigger picture in caring for premature infants. For example, when an anemic infant receives a blood transfusion, cerebral oxygenation values will increase because of the increase in oxygenated hemoglobin level. However, infants who receive an exchange transfusion will dilute their blood and show lower levels of cerebral oxygenation.[73] These notations will help scrutinize between an expected change in cerebral oxygenation and unexpected changes that may lead to neurologic complications. As a result, a better understanding can be extracted for how care activities and medical decisions effect health outcomes such as IVH or PVL that can be reduced in the future.


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