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Neuroradiology |
1 From the Department of Radiology, University of Washington, Box 357115, 1959 NE Pacific St, Seattle, WA 98195-7115 (A.V.D., D.J.F., K.R.M.); and the Department of Anesthesiology, Harborview Medical Center, Seattle, Wash (A.M.L.). Received February 2, 2000; revision requested March 16; revision received May 16; accepted June 1. Address correspondence to K.R.M. (e-mail: kmarav@u.washington.edu).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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MATERIALS AND METHODS: MR images from nine examinations performed in eight patients under general anesthesia were reviewed retrospectively. In phantom experiments, T1 measurements obtained with several inhaled anesthetic agents and propofol dissolved in saline were compared with those obtained with either 100% O2 or room air. To confirm phantom experiment results, a healthy volunteer underwent sequential FLAIR imaging while breathing high-flow 100% O2.
RESULTS: Of the nine examinations performed with patients under general anesthesia, eight had resultant images that showed increased CSF signal intensity within the basal cisterns and sulci over the cerebral convexities. Anesthetic phantom measurements showed T1 shortening only when the agent was administered with high concentrations of oxygen. In the healthy volunteer, images obtained before and during administration of 100% O2 demonstrated increased CSF signal intensity after O2 administration; this was identical to the changes observed in patients under anesthesia.
CONCLUSION: The paramagnetic effects of supplemental O2 administration result in shortened CSF T1. Radiologists should be aware of this phenomenon to avoid attributing increased CSF signal intensity on FLAIR images to abnormal CSF properties such as hemorrhage or elevated protein content.
Index terms: Anesthesia • Brain, MR, 10.121411, 10.121413, 10.121415 • Cerebrospinal fluid, MR, 167.121411, 167.121413, 167.121415 • Magnetic resonance (MR), contrast enhancement, 10.12143, 167.121413 • Oxygen • Phantoms
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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We recently observed increased cerebrospinal fluid (CSF) signal intensity in a patient who underwent fluid-attenuated inversion recovery (FLAIR) imaging under general anesthesia. Initially, this finding was interpreted as indicating that the CSF was abnormal, possibly as a result of hemorrhage or increased protein content. Over several months, it was noted that several other patients undergoing brain MR imaging with general anesthesia had similar CSF findings. The purpose of this study was to determine whether increased CSF signal intensity is seen on FLAIR MR images in patients under general anesthesia and to investigate the cause of these changes. We hypothesized that either the inhaled anesthetic agent or supplemental O2 caused the high CSF signal intensity seen on the FLAIR images.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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All examinations consisted of nonenhanced T1- (500/9–12 [repetition time msec/echo time msec], one signal acquired) and T2-weighted fast spin-echo ([2,700/85–102], one signal acquired) MR imaging. In seven patients, fast FLAIR images (10,000/140/2,200 [inversion time msec]) were obtained. All images were obtained by using a 1.5-T system (Signa; GE Medical Systems, Waukesha, Wis). Images were analyzed for abnormalities in the appearance of the brain parenchyma and for CSF signal intensity characteristics within the ventricles and subarachnoid spaces. On FLAIR images, CSF signal intensity was graded as normal or mildly, moderately, or markedly increased relative to the normally dark CSF appearance on images obtained with this pulse sequence. Parenchymal signal intensity was evaluated for abnormality and noted as being either absent or present.
Phantom Imaging
To determine whether the elevated CSF signal intensity on FLAIR images was the result of CSF T1 changes that were induced by the anesthetic agent or supplemental O2, a phantom experiment was conducted. The phantoms consisted of 15-mL glass tubes containing normal saline. Normal saline was chosen as the substrate because it closely simulates normal CSF fluid. Test solutions were equilibrated by bubbling the anesthetic gases at known concentration, mixed with either 100% O2 or air (21% O2), through a spinal needle that had been inserted into the depth of the saline-filled tubes. The anesthetic gas–O2 mixture was vented through a second short needle that had been inserted into the rubber top of the tube; the vented gas was observed continuously by using an end-tidal anesthetic agent monitor (POET; Criticare, Waukesha, Wis). Equilibration was considered complete when the anesthetic concentration of the vented gas stabilized at the desired level for at least 2 minutes.
Two sets of tubes containing saline were equilibrated at room temperature for three different concentrations of isoflurane. Each set of tubes was equilibrated with either 100% O2 or room air at concentrations of 0.5%, 1.0%, and 2.0% isoflurane in saline solution; these concentrations respectively were consistent with low, normal, and high dose levels used for clinical anesthesia in neurodiagnostic procedures. In a similar manner, additional tubes equilibrated with either 100% O2 or room air were equilibrated with concentrations of 1.0%, 2.0%, and 4.0% sevoflurane, which again represented the commonly used clinical concentrations of this agent. Thus, a total of 12 tubes were analyzed. An additional tube containing 30 µg/mL of propofol (Diprivan; Zeneca, Wilmington, Del) in saline (equal to a clinical high-dose anesthetic serum concentration) was equilibrated by using room air. A second additional tube contained saline that was equilibrated with 100% O2, and a third additional tube contained saline that was equilibrated with room air.
Tubes were imaged with fast spin-echo inversion recovery using varying inversion times, from which T1 was calculated. Imaging parameters were 4,000/15, with inversion times of 500, 1,000, 1,500, 2,000, 2,500, and 3,000 msec and one signal acquired. An echo train length of eight was used, with a flip angle of 90° and a section thickness of 5 mm. T1-weighted imaging (500/9) also was performed in the phantoms. Regions of interest (ROIs) were traced within each of the tubes, and mean signal intensity values were obtained for each tube at each inversion time by one of the authors (A.V.D.). The mean ROI size encompassed approximately 80% of the diameter of the tube. The T1s for the various solutions were computed by using customized software that had been developed in IDL programming language (Research Systems, Boulder, Colo). ROI data were fit to a three-parameter model by using a nonlinear least squares curve-fitting algorithm (1).
Healthy Volunteer Imaging
A healthy volunteer underwent brain imaging before and during administration of 100% O2 through a nonrebreathing face mask at a rate of 10 L/min. Imaging was performed by using the FLAIR sequence, with parameters identical to those described for patient imaging. After the acquisition of a baseline image, images were acquired sequentially every 5 minutes during O2 administration for a total of 35 minutes. Informed written consent was obtained for this portion of the study, and the healthy volunteer underwent imaging in concordance with approval granted by our institutional review board. The volunteer’s images were analyzed visually by three radiologists (K.R.M., A.V.D., D.J.F.) who were not blinded to the fact that the subject received O2. Quantitative data were collected by a single radiologist (A.V.D.), who measured mean CSF signal intensity in the suprasellar and quadrigeminal plate cisterns. To assess whether there were subtle changes in parenchymal signal intensity after O2 administration, ROI data were also collected for gray and white matter. The mean ROI size for CSF and parenchymal signal intensity measurement was 4–5 mm2.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Similar to us, other investigators also have observed these CSF signal intensity changes on FLAIR images obtained in patients receiving propofol (2,3). The cause of these changes, however, is unclear. Filippi et al (2) suggested that they may have been artifacts that resulted from the inherent T1 with propofol, because propofol has a T1 close to but slightly shorter than that of CSF. Results of our phantom studies, however, showed that significant alteration of signal intensity does not occur at clinically administered dose levels of propofol. As is the case with the inhaled anesthetic agents examined in our study, propofol is typically administered in conjunction with supplemental O2. Results of our phantom experiments confirmed that it is supplemental O2, rather than propofol, that causes a reduction in CSF T1 and subsequent high signal intensity on FLAIR images.
The phenomenon of O2-related T1 shortening has great clinical importance. In some of the patients involved in our retrospective review, the increased CSF signal intensity on FLAIR images had been attributed initially to an underlying CSF abnormality, such as abnormal protein content or subarachnoid hemorrhage. It was only after increased signal intensity was seen in additional patients at imaging; laboratory (normal CSF analysis in one patient) and computed tomographic findings (normal in two patients) and clinical history did not support the MR imaging findings that this diagnosis was reassessed.
We find it interesting that, as is shown in the Table, MR images from eight of the nine examinations performed with the patient under general anesthesia showed abnormal CSF signal intensity. The case in which CSF signal intensity characteristics were judged to be normal corresponded to the only case in which 50% O2 was used during anesthesia.
Results of the phantom experiments confirmed what we have seen clinically: CSF signal intensity on FLAIR images is most likely influenced by the partial pressure of O2 within the blood and probably is not affected by the concentration of inhaled anesthetic agent. The phenomenon was reproduced by performing imaging in a healthy volunteer; again, increased CSF signal intensity was seen on FLAIR images. Although our subject was not intubated, high-flow O2 administration through a nonrebreathing face mask would be expected to increase the partial pressure of arterial blood O2 levels from approximately 100 to as high as 600 mm Hg (4).
O2 with two unpaired electrons is weakly paramagnetic and has been documented as causing a mild increase in T1 (5–8). In healthy individuals at sea level, the resting saturation of hemoglobin is close to 100%. Oxyhemoglobin is diamagnetic, and a slight increase in saturation to 100% would not be expected to cause substantial change in the T1 of blood or surrounding tissues. Dissolved free O2 in blood normally is less than 0.3% (0.3 mL/100 mL) but may increase by approximately 0.003 mL/100 mL of blood per millimeter of mercury with large increases in inhaled concentration of O2. (4). Thus, the level of O2 can be as high as 1.8 mL/100 mL of blood at a partial pressure of 600 mm Hg. Diffusion from this increased pool of free O2 in the blood is the most likely explanation for the O2 increase in the CSF.
In considering the increased signal intensity of CSF with O2 administration, one question that arises relates to the anatomic site of O2 transportation into the CSF. The fact that all cases showed lower degrees of T1 shortening or no effect at all in the intraventricular CSF suggests that the primary source of supplemental O2 entry into the CSF was not through the choroid plexus. One hypothesis to account for our observations is that O2 diffuses into the cisternal subarachnoid CSF compartment directly from the arterial vascular space through the walls of arteries and arterioles on the piaarachnoid surface of the brain. The differential amount of O2 effect in the basal cisterns relative to the intraventricular space could be further explained by the relative lack of major arterial vessels that line the ventricles, since most of the vessels in this region are subependymal veins.
In our examination of a healthy volunteer, we observed also a mild delay in equilibration of the T1 in the quadrigeminal plate cistern, which lagged slightly behind that in the suprasellar cistern (Fig 4). Again, this might be accounted for by the increased number and size of arterial vessels within the suprasellar region. Of note, there was no measurable change in parenchymal brain signal intensity with increased O2 inhalation in the healthy volunteer, in whom we were able to measure signal intensity on FLAIR images obtained before and after administration of O2. This correlates with the absence of observable signal intensity changes in the brain parenchyma at a single time point in the group of patients that underwent imaging under anesthesia. We did, however, observe enhancement in the nasal and sinus mucosa on nonenhanced T1-weighted images in most of our patients (Fig 1b), which provides additional indirect evidence of the paramagnetic effect of O2 as the cause of the increased CSF signal intensity.
Patients undergoing MR imaging with supplemental O2 may demonstrate abnormal CSF signal intensity on T1-weighted and, most prominently, FLAIR images. The changes on FLAIR images mimic those described in patients with subarachnoid hemorrhage (9) or markedly increased CSF protein (10) and can easily lead to confusion with these entities and potential misdiagnosis. To avoid misdiagnosis, awareness of the potential for abnormal CSF signal intensity in patients undergoing MR imaging with general anesthesia or intravenous sedation must be recognized by physicians who interpret brain MR images. In addition, one should be aware that similar changes may be observed in any patient receiving supplemental O2, including those receiving it through a face mask or nasal cannula, as demonstrated in our healthy volunteer. Thus, supplemental O2 administration should be considered in the differential diagnosis when abnormally increased signal intensity of the CSF is encountered on FLAIR images.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Author contributions: Guarantors of integrity of entire study, K.R.M., A.V.D.; study concepts, all authors; study design, all authors; definition of intellectual content, all authors; literature research, all authors; clinical studies, K.R.M., A.V.D.; experimental studies, all authors; data acquisition, K.R.M., A.V.D.; data analysis, all authors; statistical analysis, A.V.D., D.J.F.; manuscript preparation, all authors; manuscript editing, K.R.M., D.J.F., A.V.D.; manuscript review, all authors.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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