Sevoflurane anesthesia and brain perfusion.

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.

Impact of sevoflurane anesthesia on brain oxygenation in children younger than 2 years.

OBJECTIVE/AIM: To assess the impact of sevoflurane and anesthesia-induced hypotension on brain oxygenation in children younger than 2 years. BACKGROUND: Inhalational induction with sevoflurane is the most commonly used technique in young children. However, the effect of sevoflurane on cerebral perfusion has been only studied in adults and children older than 1 year. The purpose of this study was to assess the impact of sevoflurane anesthesia on brain oxygenation in neonates and infants, using near-infrared spectroscopy. METHODS: Children younger than 2 years, ASA I or II, scheduled for abdominal or orthopedic surgery were included. Induction of anesthesia was started by sevoflurane 6% and maintained with an expired fraction of sevoflurane 3%. Mechanical ventilation was adjusted to maintain an endtidal CO2 around 39 mmHg. Brain oxygenation was assessed measuring regional cerebral saturation of oxygen (rSO2 c), measured by NIRS while awake and 15 min after induction, under anesthesia. Mean arterial pressure (MAP) variation was recorded. RESULTS: Hundred and ninety-five children were included. Anesthesia induced a significant decrease in MAP (-27%). rSO2 c increased significantly after induction (+18%). Using children age for subgroup analysis, we found that despite MAP reduction, rSO2 c increase was significant but smaller in children ≤ 6 months than in children >6 months (≤ 6 months: rSO2 c = +13%, >6 months: rSO2 c = +22%; P < 0.0001). Interindividual comparison showed that, during anesthesia at steady-state with comparable CMRO2, rSO2 c values were significantly higher when MAP was above 36 mmHg. And the higher the absolute MAP value during anesthesia was, the higher the rSO2 c was. We observed a rSO2 c variation ≤ 0 in 21 patients among the 195 studied, and the majority of these patients were younger than 6 months (n = 19). No increase or decrease of rSO2 c during anesthesia despite reduction of CMRO2 can be explained by a reduction of oxygen supply. Using the ROC curves, we determined that the threshold value of MAP under anesthesia, associated with rSO2 c variation ≤ 0%, was 39 mmHg in all the studied population (AUC: 0.90 ± 0.02; P < 0.001). In children younger than 6 months, this value of MAP was 33 mmHg, and 43 mmHg in children older than 6 months. CONCLUSION: Despite a significant decrease of MAP, 1 MAC of sevoflurane induced a significant increase in regional brain oxygenation. But subgroup analysis showed that MAP decrease had a greater impact on brain oxygenation, in children younger than 6 months. According to our results, MAP value during anesthesia should not go under 33 mmHg in children ≤6 months and 43 mmHg in children >6 months, as further changes in MAP, PaCO2 or hemoglobin during anesthesia may be poorly tolerated by the brain.

Impact of sevoflurane anesthesia on cerebral blood flow in children younger than 2 years.

OBJECTIVE/AIM: To assess the impact of sevoflurane and anesthesia-induced hypotension on cerebral blood flow (CBF) in children younger than 2 years. BACKGROUND: Inhalational induction with sevoflurane is the most commonly used technique in young children. However, the effect of sevoflurane on cerebral perfusion has been only studied in adults and children older than 1 year. The purpose of this study is to assess the impact of sevoflurane anesthesia on CBF in neonates and infants, using transcranial Doppler (TCD) sonography. METHODS: Children younger than 2 years, ASA I or II, for abdominal or orthopedic surgery were included. Induction of anesthesia was started by sevoflurane 6% and maintained with an expired fraction of sevoflurane 3%. Mechanical ventilation was controlled to maintain an end tidal CO(2) around 39 mmHg. CBF was assessed by measuring the velocities (systolic velocity SVmca, diastolic velocity DVmca and mean velocity MVmca) in the proximal segment of the middle cerebral artery (mca) in children awake and then 15 min after induction. Mean arterial pressure (MAP) variation was noted. RESULTS: One hundred and thirteen children were included. We observed a significant decrease in MAP (-30%). DVmca decreased and pulsatility index increased significantly after induction. Subgroup analysis according to age showed that in infants older than 6 months, despite a significant reduction in MAP, there was no change in CBF velocity (CBFV) as measured by TCD sonography, until MAP dropped below 40% of baseline. In infants younger than 6 months, a significant decrease in MAP was observed which was associated with a significant variation in CBFV. In this population, when CBFV start to decrease, MAP under sevoflurane anesthesia was 38 mmHg or -20% from baseline value. CONCLUSION: Our results are in favor of a reduction in CBF after induction with sevoflurane in children younger than 6 months. This population is more sensitive to MAP decrease than older children because of a lower limit of cerebral autoregulation, and this limit may be 38 mmHg with sevoflurane anesthesia.