OBJECTIVE/AIM: To assess the impact of sevoflurane and anesthesia-induced hypotension on brain perfusion in children younger than 6 months. BACKGROUND: Safe lower limit of blood pressure during anesthesia in infant is unclear, and inadequate anesthesia can lead to hypotension, hypocapnia, and low cerebral perfusion. Insufficient cerebral perfusion in infant during anesthesia is an important factor of neurological morbidity. In two previous studies, we assessed the impact of sevoflurane anesthesia on cerebral blood flow (CBF) by transcranial Doppler (TCD) and on brain oxygenation by NIRS, in children ≤2 years. As knowledge about consequences of anesthesia-induced hypotension on cerebral perfusion in children ≤6 months is scarce, we conducted a retrospective analysis to compare the data of CBF and brain oxygenation, in this specific population. METHODS: We performed a retrospective analysis of data collected from our two previous studies. Baseline values of TCD or NIRS were recorded and then during sevoflurane anesthesia. From a database of 338 patients, we excluded all patients older than 6 months. Then, we compared physiological variables of TCD and NIRS population to ensure that the two groups were comparable. We compared rSO2 c and TCD measurements variation according to MAP value during sevoflurane anesthesia, using anova and Student-Newman-Keuls for posthoc analysis. RESULTS: One hundred and eighty patients were included in the analysis. TCD and NIRS groups were comparable. CBF velocities (CBFV) or rSO2 c reflects a good cerebral perfusion when MAP is above 45 mmHg. When MAP is between 35 and 45 mmHg, CBFV variation reflects a reduction of CBF, but rSO2 c increase is the consequence of a still positive balance between CMRO2 and O2 supply. Below 35 mmHg of MAP during anesthesia, CBFV decrease and rSO2 c variation from baseline is low. For each category of MAP and for the two groups, etCo2 and expired fraction of sevoflurane (FeSevo) were comparable (anova P > 0.05). CONCLUSION: In a healthy infant without dehydration, with normal PaCO2 and hemoglobin value, scheduled for short procedures, MAP is a good proxy of cerebral perfusion as we found that CBF assessed by CBFV and rSO2 c decreased proportionally with cerebral perfusion pressure. During 1 MAC sevoflurane anesthesia, maintaining MAP beyond 35 mmHg during anesthesia is probably safe and sufficient. But when MAP decreases below 35 mmHg, CBF decreases and rSO2 c variation from baseline is low despite CMRO2 reduction. In this situation, cerebral metabolic reserve is low and further changes of systemic conditions may be poorly tolerated by the brain.
OBJECTIVE/AIM: To assess the impact of sevoflurane and anesthesia-induced hypotension on brain perfusion in children younger than 6 months. BACKGROUND: Safe lower limit of blood pressure during anesthesia in infant is unclear, and inadequate anesthesia can lead to hypotension, hypocapnia, and low cerebral perfusion. Insufficient cerebral perfusion in infant during anesthesia is an important factor of neurological morbidity. In two previous studies, we assessed the impact of sevoflurane anesthesia on cerebral blood flow (CBF) by transcranial Doppler (TCD) and on brain oxygenation by NIRS, in children ≤2 years. As knowledge about consequences of anesthesia-induced hypotension on cerebral perfusion in children ≤6 months is scarce, we conducted a retrospective analysis to compare the data of CBF and brain oxygenation, in this specific population. METHODS: We performed a retrospective analysis of data collected from our two previous studies. Baseline values of TCD or NIRS were recorded and then during sevoflurane anesthesia. From a database of 338 patients, we excluded all patients older than 6 months. Then, we compared physiological variables of TCD and NIRS population to ensure that the two groups were comparable. We compared rSO2 c and TCD measurements variation according to MAP value during sevoflurane anesthesia, using anova and Student-Newman-Keuls for posthoc analysis. RESULTS: One hundred and eighty patients were included in the analysis. TCD and NIRS groups were comparable. CBF velocities (CBFV) or rSO2 c reflects a good cerebral perfusion when MAP is above 45 mmHg. When MAP is between 35 and 45 mmHg, CBFV variation reflects a reduction of CBF, but rSO2 c increase is the consequence of a still positive balance between CMRO2 and O2 supply. Below 35 mmHg of MAP during anesthesia, CBFV decrease and rSO2 c variation from baseline is low. For each category of MAP and for the two groups, etCo2 and expired fraction of sevoflurane (FeSevo) were comparable (anova P > 0.05). CONCLUSION: In a healthy infant without dehydration, with normal PaCO2 and hemoglobin value, scheduled for short procedures, MAP is a good proxy of cerebral perfusion as we found that CBF assessed by CBFV and rSO2 c decreased proportionally with cerebral perfusion pressure. During 1 MAC sevoflurane anesthesia, maintaining MAP beyond 35 mmHg during anesthesia is probably safe and sufficient. But when MAP decreases below 35 mmHg, CBF decreases and rSO2 c variation from baseline is low despite CMRO2 reduction. In this situation, cerebral metabolic reserve is low and further changes of systemic conditions may be poorly tolerated by the brain.
Authors: M E McCann; D E Withington; S J Arnup; A J Davidson; N Disma; G Frawley; N S Morton; G Bell; R W Hunt; D C Bellinger; D M Polaner; A Leo; A R Absalom; B S von Ungern-Sternberg; F Izzo; P Szmuk; V Young; S G Soriano; J C de Graaff Journal: Anesth Analg Date: 2017-09 Impact factor: 5.108