Sahoo S, Sheshadri V, Sriganesh K, Madhsudana Reddy KR, Radhakrishnan M, Umamaheswara Rao GS. World Neurosurg. 2016; 98: 211-216.
Affiliation
Senior Professor of Neuroanaesthesia, NIMHANS, Bangalore, Department of Neuroanaesthesia, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore. Electronic address: gsuma123@yahoo.com.
BACKGROUND: The effect of normobaric hyperoxia on brain oxygenation in the presence or absence of intact autoregulation has not been studied till now in acute traumatic brain injury (TBI).
METHODS: In this prospective clinical investigation in fifty patients operated for severe TBI, cerebral blood flow (CBF) velocity in the middle cerebral artery (MCA) was measured using transcranial doppler (TCD). Regional cerebral oxygen saturation (rSO2) using near infra-red spectroscopy (NIRS) at three different inspired oxygen fractions (FiO2 of 0.4, 0.6 and 1) was measured in the later 25 of these patients.
RESULTS: There was no difference in the hemodynamic and respiratory variables except for PaO2 which increased with increasing FiO2. The CBF velocities and pulsatility indices did not vary at different levels of FiO2 (0.4, 0.6 and 1) both on the operated and non-operated side. The rSO2 as evaluated by bifrontal NIRS sensors, increased with increasing FiO2 on the operated (pathological) side with impaired cerebral autoregulation and not with intact autoregulation.
CONCLUSIONS: In severe TBI, MCA CBF velocity is not affected by hyperoxia in both the pathological and normal side. The cerebral oxygen saturation increased with increasing arterial hyperoxia in the operated cerebral hemisphere while remaining within baseline range in the non-operated hemisphere. Impairment in the cerebral autoregulation in the pathological hemisphere contributes to this luxury oxygenation.