Pediatric Anesthesia ISSN 1155-5645
ORIGINAL ARTICLE
Sevoflurane anesthesia and brain perfusion s Pouyau1, Aure lie Mahr1, Simon Juhel1, Mathilde De Queiroz1, Ossam Rhondali1,2, Agne 1 Khalid Rhzioual-Berrada , Sylvain Mathews2 & Dominique Chassard1 ^pital Me re-Enfant, Lyon, France 1 Department of Pediatric Anesthesia, Ho ^pital Sainte Justine, Montre al, QC, Canada 2 Department of Pediatric Anesthesia, Ho
Keywords anesthesia; blood pressure; brain oxygenation; cerebrovascular circulation; drug effects; infant; inhalation; near-infrared spectroscopy; transcranial Doppler Correspondence partement Dr Ossam Rhondali, De sie Ho ^pital Me re Enfant, d’Anesthe Hospices Civils de Lyon, 59 boulevard Pinel, 69500 Bron, France Email: [email protected] Section Editor: Andrew Davidson Accepted 27 July 2014 doi:10.1111/pan.12512
180
Summary 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 rSO2c 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 rSO2c 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 rSO2c increase is the consequence of a still positive balance between CMRO2 and O2 supply. Below 35 mmHg of MAP during anesthesia, CBFV decrease and rSO2c 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 rSO2c 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 rSO2c 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.
© 2014 John Wiley & Sons Ltd Pediatric Anesthesia 25 (2015) 180–185
O. Rhondali et al.
Introduction Safe lower limit of blood pressure in an anesthetized infant is unclear, and inadequate anesthesia can lead to hypotension, hypocapnia, and low cerebral perfusion (1). Optimal cerebral perfusion is essential despite coexisting diseases, depressant effects of anesthetic drugs, fluid and blood losses, and surgical stimulation (2). Currently, the debate on neurological morbidity of anesthesia focuses on anesthetic-induced developmental neurotoxicity (3). But, it is important to emphasize that blood pressure and PaCO2 are potent regulating factors of cerebral blood flow (CBF) and insufficient cerebral perfusion in infant during anesthesia can lead to neurological morbidity (1,3–5). Rapid recognition of low cerebral perfusion and prompt correction of it is a challenge and a main goal of anesthesia in this vulnerable population. To achieve that, we must improve our knowledge about the relationship between cerebral perfusion pressure (CPP), CBF, and brain oxygen supply in children during anesthesia, especially in children ≤6 months, a more vulnerable population. As we recently studied the impact of sevoflurane anesthesia on CBF velocities (CBFV) by transcranial Doppler (TCD) and on brain oxygenation by NIRS in children ≤2 years (6,7), we conducted this retrospective study to compare the data of CBFV and brain oxygenation. The aim of this study is to understand consequences of anesthesia-induced hypotension on CBF and brain oxygenation in children ≤6 months. Materials and methods We included in this retrospective analysis data from our two previous studies, and we added 30 patient’s data collected after statistical analysis of NIRS study. These two studies were performed after approval of the Human Studies Committee and obtainment of informed written parental consent. These children required elective orthopedic abdominal or urological surgery, and they did not have any intracranial hypertension. Baseline values of TCD (systolic: SVmca, mean: MVmca, and diastolic: DVmca velocities in the middle cerebral artery) or regional saturation of oxygen (rSO2c) were recorded and then during sevoflurane anesthesia. Ventilation was adjusted to achieve an endtidal CO2 level between 35 and 40 mmHg. From a database of 338 patients, we excluded all patients older than 6 months. We analyzed variables of TCD and NIRS population to ensure that the two groups were comparable. We divided the patients into seven groups according to absolute MAP value during sevoflurane anesthesia (55 mmHg) to compare rSO2c or TCD measurements variation according to MAP value during sevoflurane anesthesia. Statistical analysis Continuous variables are expressed as mean SD. Patients were divided into two groups according to cerebral perfusion measurements (TCD or NIRS). As data were normally distributed (Kolmogorov–Smirnov test), we used unpaired Student’s t-test to compare physiological values between the two groups. We then compared rSO2c or TCD measurements variation from baseline according to MAP value during sevoflurane anesthesia, using ANOVA and Student–Newman–Keuls for posthoc analysis (MedCalc, Ostend, Belgium). A P < 0.05 was considered statistically significant. Results We analyzed the measurements of 180 patients (TCD group: n = 63, NIRS group: n = 117). There was no significant difference between variables of the TCD and the NIRS groups (Table 1). Mean age and weight of the children studied were, respectively, 2.2 1.4 months and 4.4 1.5 kg. Baseline MAP was 60 12 mmHg, and MAP during anesthesia was 39 10 mmHg (Table 2). Mean expired fraction of sevoflurane and etCO2 at steady state were, respectively, 3.1 0.5% and 38 5 mmHg (Table 3). Analyzing TCD measurements, we found that CBFV tend to increase when MAP is beyond 45 mmHg, and below this value, DVmca decreased significantly from baseline (Figure 1). rSO2c increase from baseline was significantly lower for a MAP during anesthesia ≤35 mmHg (Figure 2). For each category of MAP and for the two groups, etCo2 and expired fraction of sevoflurane were comparable (ANOVA, P > 0.05, Table 3).
Table 1 Comparison of physiological variables of the two populations
Age (months) Weight (kg) Baseline MAP (mmHg) MAP during anesthesia (mmHg) etCO2 (mmHg) FeSevo (%)
TCD group (N = 63)
NIRS group (n = 117)
P-value
2.1 1.5 4.4 1.6 62 14 39 9
2.2 1.3 4.5 1.5 59 11 40 11
0.84 0.53 0.10 0.63
38 6 3.1 1.4
38 4 3.2 0.4
0.49 0.41
Unpaired t-tests. Values are mean
SD.
181
O. Rhondali et al.
Sevoflurane anesthesia and brain perfusion
Table 2 Baseline variables and during sevoflurane anesthesia Baseline value
n = 180 Age (months) Weight (kg) MAP (mmHg) etCO2 (mmHg) FeSevo (%) rSO2c (%) SVmca (cms 1) MVmca (cms 1) DVmca (cms 1) PI
2.2 1.4 4.4 1.5 60 12
67 8 68 23 41 15 23 10 1.12 0.25
Value during anesthesia
39 10 38 5 3.1 0.5 77 12 68 24 33 15 16 11 1.67 0.59
P-value
ORIGINAL ARTICLE
Sevoflurane anesthesia and brain perfusion s Pouyau1, Aure lie Mahr1, Simon Juhel1, Mathilde De Queiroz1, Ossam Rhondali1,2, Agne 1 Khalid Rhzioual-Berrada , Sylvain Mathews2 & Dominique Chassard1 ^pital Me re-Enfant, Lyon, France 1 Department of Pediatric Anesthesia, Ho ^pital Sainte Justine, Montre al, QC, Canada 2 Department of Pediatric Anesthesia, Ho
Keywords anesthesia; blood pressure; brain oxygenation; cerebrovascular circulation; drug effects; infant; inhalation; near-infrared spectroscopy; transcranial Doppler Correspondence partement Dr Ossam Rhondali, De sie Ho ^pital Me re Enfant, d’Anesthe Hospices Civils de Lyon, 59 boulevard Pinel, 69500 Bron, France Email: [email protected] Section Editor: Andrew Davidson Accepted 27 July 2014 doi:10.1111/pan.12512
180
Summary 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 rSO2c 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 rSO2c 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 rSO2c increase is the consequence of a still positive balance between CMRO2 and O2 supply. Below 35 mmHg of MAP during anesthesia, CBFV decrease and rSO2c 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 rSO2c 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 rSO2c 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.
© 2014 John Wiley & Sons Ltd Pediatric Anesthesia 25 (2015) 180–185
O. Rhondali et al.
Introduction Safe lower limit of blood pressure in an anesthetized infant is unclear, and inadequate anesthesia can lead to hypotension, hypocapnia, and low cerebral perfusion (1). Optimal cerebral perfusion is essential despite coexisting diseases, depressant effects of anesthetic drugs, fluid and blood losses, and surgical stimulation (2). Currently, the debate on neurological morbidity of anesthesia focuses on anesthetic-induced developmental neurotoxicity (3). But, it is important to emphasize that blood pressure and PaCO2 are potent regulating factors of cerebral blood flow (CBF) and insufficient cerebral perfusion in infant during anesthesia can lead to neurological morbidity (1,3–5). Rapid recognition of low cerebral perfusion and prompt correction of it is a challenge and a main goal of anesthesia in this vulnerable population. To achieve that, we must improve our knowledge about the relationship between cerebral perfusion pressure (CPP), CBF, and brain oxygen supply in children during anesthesia, especially in children ≤6 months, a more vulnerable population. As we recently studied the impact of sevoflurane anesthesia on CBF velocities (CBFV) by transcranial Doppler (TCD) and on brain oxygenation by NIRS in children ≤2 years (6,7), we conducted this retrospective study to compare the data of CBFV and brain oxygenation. The aim of this study is to understand consequences of anesthesia-induced hypotension on CBF and brain oxygenation in children ≤6 months. Materials and methods We included in this retrospective analysis data from our two previous studies, and we added 30 patient’s data collected after statistical analysis of NIRS study. These two studies were performed after approval of the Human Studies Committee and obtainment of informed written parental consent. These children required elective orthopedic abdominal or urological surgery, and they did not have any intracranial hypertension. Baseline values of TCD (systolic: SVmca, mean: MVmca, and diastolic: DVmca velocities in the middle cerebral artery) or regional saturation of oxygen (rSO2c) were recorded and then during sevoflurane anesthesia. Ventilation was adjusted to achieve an endtidal CO2 level between 35 and 40 mmHg. From a database of 338 patients, we excluded all patients older than 6 months. We analyzed variables of TCD and NIRS population to ensure that the two groups were comparable. We divided the patients into seven groups according to absolute MAP value during sevoflurane anesthesia (55 mmHg) to compare rSO2c or TCD measurements variation according to MAP value during sevoflurane anesthesia. Statistical analysis Continuous variables are expressed as mean SD. Patients were divided into two groups according to cerebral perfusion measurements (TCD or NIRS). As data were normally distributed (Kolmogorov–Smirnov test), we used unpaired Student’s t-test to compare physiological values between the two groups. We then compared rSO2c or TCD measurements variation from baseline according to MAP value during sevoflurane anesthesia, using ANOVA and Student–Newman–Keuls for posthoc analysis (MedCalc, Ostend, Belgium). A P < 0.05 was considered statistically significant. Results We analyzed the measurements of 180 patients (TCD group: n = 63, NIRS group: n = 117). There was no significant difference between variables of the TCD and the NIRS groups (Table 1). Mean age and weight of the children studied were, respectively, 2.2 1.4 months and 4.4 1.5 kg. Baseline MAP was 60 12 mmHg, and MAP during anesthesia was 39 10 mmHg (Table 2). Mean expired fraction of sevoflurane and etCO2 at steady state were, respectively, 3.1 0.5% and 38 5 mmHg (Table 3). Analyzing TCD measurements, we found that CBFV tend to increase when MAP is beyond 45 mmHg, and below this value, DVmca decreased significantly from baseline (Figure 1). rSO2c increase from baseline was significantly lower for a MAP during anesthesia ≤35 mmHg (Figure 2). For each category of MAP and for the two groups, etCo2 and expired fraction of sevoflurane were comparable (ANOVA, P > 0.05, Table 3).
Table 1 Comparison of physiological variables of the two populations
Age (months) Weight (kg) Baseline MAP (mmHg) MAP during anesthesia (mmHg) etCO2 (mmHg) FeSevo (%)
TCD group (N = 63)
NIRS group (n = 117)
P-value
2.1 1.5 4.4 1.6 62 14 39 9
2.2 1.3 4.5 1.5 59 11 40 11
0.84 0.53 0.10 0.63
38 6 3.1 1.4
38 4 3.2 0.4
0.49 0.41
Unpaired t-tests. Values are mean
SD.
181
O. Rhondali et al.
Sevoflurane anesthesia and brain perfusion
Table 2 Baseline variables and during sevoflurane anesthesia Baseline value
n = 180 Age (months) Weight (kg) MAP (mmHg) etCO2 (mmHg) FeSevo (%) rSO2c (%) SVmca (cms 1) MVmca (cms 1) DVmca (cms 1) PI
2.2 1.4 4.4 1.5 60 12
67 8 68 23 41 15 23 10 1.12 0.25
Value during anesthesia
39 10 38 5 3.1 0.5 77 12 68 24 33 15 16 11 1.67 0.59
P-value
