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Fraction of Inspired Oxygen in Relation to Cerebrospinal Fluid Hyperintensity on FLAIR MR Imaging of the Brain in Children and Young Adults Undergoing Anesthesia

¹ Department of Anesthesiology, Box 359300, University of Washington, Seattle, WA 98195.
² Department of Epidemiology, Box 357236, University of Washington, Seattle, WA 98195.
³ Department of Radiology, CH-69, Children's Hospital and Regional Medical Center, 4800 Sand Point Way N. E., Seattle, WA 98105.

Received September 26, 2001; accepted after revision March 12, 2002.

 
Address correspondence to D. W. W. Shaw.

Abstract

Top Abstract Introduction Materials and Methods Results Discussion References

 
OBJECTIVE. Cerebrospinal fluid (CSF) hyperintensity has been described on fluid-attenuated inversion recovery (FLAIR) imaging in anesthetized patients who underwent MR imaging without apparent subarachnoid abnormality. The purpose of our study was to delineate likely causes for this hyperintensity. Specifically, we sought to determine whether a high inspired oxygen fraction given as part of the anesthetic was responsible for the CSF hyperintensity seen on FLAIR imaging.

MATERIALS AND METHODS. A retrospective study was conducted using anesthetic records and brain MR images of 70 children and young adults who had a FLAIR sequence while undergoing general anesthesia. Information about inspired oxygen fraction, oxygen saturation, and type of anesthetic agents preceding the FLAIR sequence was obtained from the anesthetic record. A pediatric neuroradiologist who was unaware of the inspired oxygen fraction and anesthetic agent ascertained the presence of CSF hyperintensity in the basilar cisterns and cerebral sulcal subarachnoid space.

RESULTS. Twenty-one patients received an inspired oxygen fraction less than or equal to 0.60, and 49 received an inspired oxygen fraction greater than 0.60. Inspired oxygen fraction greater than 0.60 was significantly associated with the presence of CSF hyperintensity in the basilar cisterns (p < 0.001) and in the cerebral sulcal subarachnoid space (p = 0.03). The type of anesthetic agent, patient's sex, or status (based on the American Society of Anesthesiology physical status and classification system), and presence of cardiopulmonary disease or seizure disorder were not associated with CSF hyperintensity.

CONCLUSION. High inspired oxygen fraction during anesthesia is associated with CSF hyperintensity in the basilar cisterns and the cerebral sulcal subarachnoid space on FLAIR imaging in children and young adults. Physicians should be aware of this finding to avoid misinterpreting this artifact as an abnormality.

Introduction

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By nulling the signal of cerebrospinal fluid (CSF), fluid-attenuated inversion recovery (FLAIR) imaging is a sensitive MR imaging technique in the evaluation of parenchymal lesions adjacent to CSF [1, 2]. Subtle changes in the composition of CSF will result in its incomplete nulling. Therefore, this technique is also sensitive in the evaluation of CSF diseases and abnormalities such as meningitis and subarachnoid hemorrhage, by showing a hyperintense signal that may not be apparent on other sequences [3, 4]. Recently, however, the presence of CSF hyperintensity has been observed in some patients with no apparent subarachnoid abnormality [5]. General anesthesia (Ketonen K et al., presented at the American Society of Neuroradiology meeting, May 1999) and specifically propofol [6] have been implicated as a potential cause of CSF hyperintensity. Other investigators have proposed this hyperintensity is related to increased oxygen tension [7].

General anesthesia is necessary to obtain good quality MR images in children who are not candidates for other types of sedation. The purpose of this study was to investigate the possible causes of CSF hyperintensity. More specifically, we sought to determine whether a high fraction of inspired oxygen given as part of the anesthetic, which would result in elevated oxygen tension in the blood and CSF, is associated with CSF hyperintensity. An association between inspired oxygen fraction and CSF hyperintensity would support the hypothesis that increased partial pressure of oxygen in the CSF induces increased signal in the subarachnoid CSF on the FLAIR sequence. Understanding the cause of this phenomenon could prevent misinterpretation of this finding as an abnormality or a disease and might allow modification of the anesthetic technique to avoid producing CSF hyperintensity.

Materials and Methods

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We conducted a retrospective cohort study using the anesthetic records and brain MR images of 94 consecutive patients who had a FLAIR sequence as part of their brain MR examination while they were undergoing general anesthesia from February 1997 to May 2000 at our pediatric institution. Four patients had more than one MR examination during the study period; only the first MR examination was included in our analysis. Institutional review board approval was obtained for our study.

Imaging studies were performed on a 1.5-T MR imaging system (Signa; General Electric Medical Systems, Milwaukee, WI). Imaging parameters for the FLAIR sequence were as follows: TR/TE_eff, 10,000/149; inversion time, 2200; axial slice thickness, 5 mm; skip, 2 mm; and number of excitations, 1. A pediatric neuroradiologist, who was unaware of the inspired oxygen fraction and anesthetic agent, ascertained the presence of CSF hyperintensity at the basilar cisterns and cerebral sulcal subarachnoid space. An ordinal scale was used to quantify the hyperintensity in each location: 0, hypointense to brain (normal CSF signal on FLAIR); 1, isointense to brain (mild abnormality of CSF signal); and 2, hyperintense to brain (marked abnormality of CSF signal) (Fig. 1A,1B,1C,1D). The FLAIR images were reviewed with the associated axial T1- and T2-weighted sequences to more carefully judge the signal intensity in the cerebral sulci. Inspired oxygen fraction, blood oxygen saturation, and type and concentration of anesthetic agents in the 15 min preceding the FLAIR sequence were determined from anesthetic records. The inspired oxygen fraction was calculated in cases in which the patient's airway was instrumented and the inspired oxygen fraction was missing from the anesthetic record, but the total amount of fresh gas flow delivered was recorded (inspired oxygen fraction = [flow rate_air x 0.21 + flow rate_oxygen] / [flow rate_air + flow rate_oxygen + flow rate_{nitrous oxide}]).

View larger version (136K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1A. —Fluid-attenuated inversion recovery (FLAIR) MR images in 5-year-old boy undergoing anesthesia with halothane who received supplemental oxygen during two separate MR imaging examinations. FLAIR images obtained at level of basilar cisterns (A) and cerebral sulci (B) while patient was receiving inspired oxygen fraction of 1.0 show hyperintensity of cerebrospinal fluid (CSF) compared with brain (grade 2).

View larger version (120K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1B. —Fluid-attenuated inversion recovery (FLAIR) MR images in 5-year-old boy undergoing anesthesia with halothane who received supplemental oxygen during two separate MR imaging examinations. FLAIR images obtained at level of basilar cisterns (A) and cerebral sulci (B) while patient was receiving inspired oxygen fraction of 1.0 show hyperintensity of cerebrospinal fluid (CSF) compared with brain (grade 2).

View larger version (138K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1C. —Fluid-attenuated inversion recovery (FLAIR) MR images in 5-year-old boy undergoing anesthesia with halothane who received supplemental oxygen during two separate MR imaging examinations. FLAIR images obtained at same levels as A and B during subsequent MR imaging examination when inspired oxygen fraction was 0.5. CSF is dark (grade 0). (Because only first examination for any patient was entered into this study, images C and D were excluded from analysis.)

View larger version (118K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1D. —Fluid-attenuated inversion recovery (FLAIR) MR images in 5-year-old boy undergoing anesthesia with halothane who received supplemental oxygen during two separate MR imaging examinations. FLAIR images obtained at same levels as A and B during subsequent MR imaging examination when inspired oxygen fraction was 0.5. CSF is dark (grade 0). (Because only first examination for any patient was entered into this study, images C and D were excluded from analysis.)

Twenty-four of the 94 patients were excluded from our final analysis for the following reasons: We included only those patients who had their airway secured with either an endotracheal tube or a laryngeal mask. Eight patients were excluded in whom supplemental oxygen was provided with nasal cannula or face mask because nasal cannula and face mask administration of oxygen does not allow accurate determination of the level of oxygen reaching the lungs. (One child did not have his airway instrumented but was retained in the analysis because he was breathing room air; therefore, his inspired oxygen fraction could be determined accurately.) Thirteen children were excluded in whom the inspired oxygen fraction preceding the FLAIR sequence was not recorded. Three children were excluded with documented CSF abnormalities (subarachnoid metastatic disease and meningitis) known to produce a hyperintense signal on the FLAIR sequence. Our analysis thus consisted of the MR imaging studies of 70 patients (age range, 1 month-20 years; mean age, 7.1 years).

Analysis of patient characteristics according to inspired oxygen fraction was conducted using the chi-square test for categoric variables or the Fisher's exact test when the expected number of subjects in any cell was less than 5. Wilcoxon's rank sum test was used to test differences in continuous variables because some variables were not normally distributed. We also used Wilcoxon's rank sum test to analyze the association between inspired oxygen fraction and the degree of CSF hyperintensity in the basilar cisterns and the cerebral sulcal subarachnoid space during the FLAIR sequence. In additional analyses, we dichotomized inspired oxygen fraction into high inspired oxygen fraction (>0.60) and low inspired oxygen fraction (0.60) because all the inspired oxygen fractions were either greater than or equal to 0.95 or less than or equal to 0.60 (Fig. 2). To estimate the magnitude of the association, we also dichotomized the CSF hyperintensity (mild or marked vs absent) to calculate the relative risk of CSF hyperintensity associated with inspired oxygen fraction level. Using the Mantel-Haenszel stratified analysis, we assessed the following clinical characteristics for their effects on the association between inspired oxygen fraction and CSF hyperintensity: anesthetic agents (propofol alone, halothane alone, isoflurane alone, and a combination of agents), sex, status (based on the American Society of Anesthesiology [ASA] physical status and classification system), cardiopulmonary disease (presence or absence), and seizure disorder (presence or absence). A factor was considered a confounder if adjustment for the factor significantly changed the relative risk of CSF hyperintensity in relation to inspired oxygen fraction.

View larger version (8K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2. —Bar graph shows distribution of inspired oxygen fraction levels among 70 patients.

Results

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Twenty-one patients received an inspired oxygen fraction less than or equal to 0.60, and 49 received an inspired oxygen fraction of greater than 0.60. Patients in the high inspired oxygen fraction group were similar to the patients in the low inspired oxygen fraction group with respect to age, weight, sex, presence of cardiopulmonary or seizure disorders, ASA status, and blood oxygen saturation (Table 1). Anesthesia was maintained with halothane, isoflurane, or propofol for 63 patients, and seven patients received a combination of propofol and either halothane or isoflurane. Halothane was distributed evenly between the two inspired oxygen fraction groups (Table 1). Propofol was the anesthetic agent in 57% of patients in the high inspired oxygen fraction group and in 33% of patients in the low inspired oxygen fraction group, but this difference was not statistically significant. Isoflurane was used more commonly in patients from the low inspired oxygen fraction group (24%) than in patients from the high inspired oxygen fraction group (6%), and nitrous oxide was exclusively present in patients from the low inspired oxygen fraction group.

Inspired oxygen fraction greater than 0.60 preceding the FLAIR sequence was significantly associated with the presence of CSF hyperintensity in the basilar cisterns (p < 0.001) and in the cerebral sulcal subarachnoid space (p = 0.03) (Fig. 3A,3B). In the basilar cisterns, 71.4% of patients in the high inspired oxygen fraction group showed some degree of CSF hyperintensity compared with 23.8% of patients in the low inspired oxygen fraction group. In the cerebral sulcal subarachnoid space, 83.7% of patients in the high inspired oxygen fraction group showed some degree of CSF hyperintensity compared with 66.7% of patients in the low inspired oxygen fraction group, with marked CSF hyperintensity noted in 71.4% of patients in the high inspired oxygen fraction group and in 42.9% of patients in the low inspired oxygen fraction group. The administration of a high inspired oxygen fraction was associated with a threefold greater risk of CSF hyperintensity in the basilar cisterns (95% confidence interval [CI]: 1.4-6.6) and with a 1.3-fold greater risk of CSF hyperintensity in the cerebral sulcal subarachnoid space (95% CI: 0.9-1.7).

View larger version (32K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3A. —Bar graphs of cerebrospinal fluid hyperintensity (grading: = none [0], [UNK] = mild [1], = marked [2]) among 70 patients. Bar graphs show patients who received low (0.6) and high (>0.6) inspired oxygen fraction in basilar cisterns (A) and sulcar subarachnoid space (B). Most subjects in low inspired oxygen fraction group had no hyperintensity in basilar cisterns (A); however, in sulcal subarachnoid space (B) many had sufficient oxygen pressure to show hyperintensity even with this lesser degree of supplementation. In both regions, total percentage of mild and marked hyperintensity increased in patients with higher level of oxygen supplementation. (Basilar cisterns, p < 0.001; sulcal subarachnoid space, p = 0.03.)

View larger version (46K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3B. —Bar graphs of cerebrospinal fluid hyperintensity (grading: = none [0], [UNK] = mild [1], = marked [2]) among 70 patients. Bar graphs show patients who received low (0.6) and high (>0.6) inspired oxygen fraction in basilar cisterns (A) and sulcar subarachnoid space (B). Most subjects in low inspired oxygen fraction group had no hyperintensity in basilar cisterns (A); however, in sulcal subarachnoid space (B) many had sufficient oxygen pressure to show hyperintensity even with this lesser degree of supplementation. In both regions, total percentage of mild and marked hyperintensity increased in patients with higher level of oxygen supplementation. (Basilar cisterns, p < 0.001; sulcal subarachnoid space, p = 0.03.)

The type of anesthetic agent (except nitrous oxide), sex, ASA status, and presence of cardiopulmonary disease or seizure disorder were not associated with CSF hyperintensity (Tables 2 and 3) and did not confound or modify the association between the inspired oxygen fraction level and the presence of CSF hyperintensity on the basis of the stratified analysis. Thus, the risk estimates are presented without adjustment for these characteristics. Nitrous oxide, which was used only in the low inspired oxygen fraction group, was negatively associated with the presence of CSF hyperintensity. Children with CSF hyperintensity tended to be older than children without, and this association was statistically significant for the cerebral sulcal subarachnoid space. The median age of children with hyperintensity in the cerebral sulcal subarachnoid space was 7.8 years, compared with 1.4 years for children without (p = 0.004).

Discussion

Top Abstract Introduction Materials and Methods Results Discussion References

 
We found that a high inspired oxygen fraction level administered to patients undergoing general anesthesia is associated with the presence of CSF hyperintensity on the FLAIR sequence in the basilar cisterns and in the cerebral sulcal subarachnoid space. Most of our patients received either propofol or halothane, and no statistically significant difference was seen in these groups with respect to patients with CSF hyperintensity and those without. Nitrous oxide was the only anesthetic agent that showed statistical significance in being more frequently identified in the group showing no CSF hyperintensity. This finding is not surprising, however, because all 13 of our patients who received nitrous oxide were in the low inspired oxygen fraction group.

Ketonen et al. (ASNR meeting, May 1999) found CSF hyperintensity on FLAIR sequences in 12 of 14 patients who underwent general anesthesia compared to none of 20 patients who did not undergo general anesthesia. That study, however, did not account for the amount of oxygen administered to the patients, which could be important because higher levels of inspired oxygen fraction are often used with general anesthesia. Filippi et al. [6] reported a retrospective analysis of 55 brain MR studies in children. In their analysis, all 13 children given propofol (11 of whom received supplemental oxygen) showed CSF hyperintensity, whereas none of the 42 children given chloral hydrate (and presumably not receiving supplemental oxygen) had this finding. They concluded that propofol was more likely than oxygen to be the primary cause of CSF hyperintensity. In our study, however, propofol was similarly distributed between patients who did and those who did not show CSF hyperintensity, suggesting that propofol is not a significant cause of CSF hyperintensity shown on the FLAIR sequence. Our findings best support the results of a recent study [7] involving eight adult patients that ascribed the CSF hyperintensity to increased inspired oxygen fraction. That study also advanced in vitro data showing a similar degree of T1 shortening when both saline and various anesthetic agents were admixed in glass tubes with 100% oxygen as compared to room air.

By nulling the CSF, FLAIR maximizes the sensitivity for parenchymal lesions adjacent to CSF, as well as abnormalities of CSF. Failure to null or suppress the CSF signal results in CSF hyperintensity on FLAIR. This phenomenon can be observed in patients with CSF abnormalities and is caused by T1 shortening usually due to blood or other elevated protein concentration in the CSF [3, 4]. In our study, the mechanism underlying the presence of CSF hyperintensity in patients without CSF abnormality is likely related to the fact that oxygen, being slightly paramagnetic, also produces a mild shortening in T1.

The alveolar gas equation indicates that the partial pressure of oxygen in the alveolus may range from 102 mm Hg while breathing room air (21% oxygen) to 673 mm Hg while breathing 100% oxygen [8]. The arterial oxygen partial pressure is almost identical to the alveolar oxygen partial pressure because the difference in oxygen pressure between the alveolus and the arterial blood is less than 6 mm Hg in young healthy patients [9]. These findings indicate that the partial pressure of oxygen in the arterial blood in the brain can vary greatly depending on the fraction of inspired oxygen.

Oxygen diffuses rapidly through the blood—CSF barriers [10]. Oxygen transfer from the arterial blood to the CSF is presumed to take place at the pial vessels and also directly through the choroid plexus [11, 12]. Kazemi et al. [11] observed a substantial elevation of oxygen pressure in the cisternal and ventricular CSF in dogs when the inspired oxygen concentration was increased from 21% to 100%. They found that, after 10 min, arterial oxygen pressure rose to 585 mm Hg and the cisternal CSF oxygen pressure rose to about 155 mm Hg. Deliganis et al. [7] proposed that the difference in signal intensity observed in different areas of the CSF might be explained by the diffusion of oxygen into the subarachnoid CSF directly from vessels on the pia—arachnoid surface of the brain, so that the hyperintensity is mainly noticed in the sulci and the basilar cisterns and much less in the ventricles, which do not have a comparable network of vessels relative to the volume of CSF. Similarly, we suggest that differences in observations of hyperintensity between the basilar cisterns and the sulcal subarachnoid space relate to the relative greater volume of CSF per unit of pia—arachnoid vascularity in the basilar cisterns, resulting in greater dilution of the oxygen and therefore higher oxygen levels in the sulcal subarachnoid space.

It is not known why young patients were less likely to show CSF hyperintensity than older patients in our study, but this may be the result of age-related differences in physiology. Alternatively, this may be the result of the relative inability to appreciate the CSF hyperintensity because of lesser differences compared to the relative signal intensity associated with immature myelination of the brain. In addition, smaller CSF spaces in a young child make it difficult to see normal CSF in subarachnoid convexities. Our sample size for younger patients was small, with only 15 patients younger than 2 years old.

Some limitations of our study must be mentioned. Being nonrandomized, this study was subject to biases. However, by study design, our sample was unselected (we looked at all MR images for a defined period); the radiologist assessing the MR images was unaware of the inspired oxygen fraction level and anesthetic agent; and we accounted in our statistical analysis for the fact that age, type of anesthetic agents, ASA status, and sex could potentially bias our findings. We cannot exclude that propofol may play a role in the hyperintensity; however, on the basis of the statistical analysis, the effect of propofol would be very small compared with that of oxygen. CSF abnormalities such as subarachnoid hemorrhage and abnormal protein content might have caused some cases of CSF hyperintensity, but we attempted to exclude those patients clinically.

In our study, the relative risk between inspired oxygen fraction and CSF hyperintensity was derived by dichotomizing our patients into low and high inspired oxygen fraction groups. All except one patient in the low inspired oxygen fraction group received some supplemental oxygen, and a significant percentage of these patients showed some degree of CSF hyperintensity (especially in the cerebral sulcal subarachnoid space). The difference in the relative risk of CSF hyperintensity would likely have been even more striking if one compared a high inspired oxygen fraction group to a group receiving no supplemental oxygen, in which we would expect the incidence of the finding of CSF hyperintensity, in the absence of abnormalities or diseases, to be much lower than that in our low inspired oxygen fraction group.

In conclusion, a high inspired oxygen fraction level during anesthesia is associated with CSF hyperintensity in the basilar cisterns and the cerebral sulcal subarachnoid space on the FLAIR MR sequence in children and young adults. Anesthetic agents did not appear to explain this finding in our study population. Knowledge of this phenomenon is important for the correct interpretation of FLAIR MR images in patients receiving supplemental oxygen.

References

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