Hyperintense signal abnormality in subarachnoid spaces and basal cisterns on MR images of children anesthetized with propofol: new fluid-attenuated inversion recovery finding.
Academic Article
Overview
abstract
BACKGROUND AND PURPOSE: MR imaging is the method of choice for pediatric neuroimaging. Sedation is often needed to suppress patient motion and ensure diagnostic image quality, and propofol is rapidly becoming the preferred anesthetic. The purpose of this study was to document a new finding on fast fluid-attenuated inversion recovery (fast-FLAIR) MR images of children anesthetized with propofol that can be mistaken for subarachnoid space pathologic abnormality. METHODS: A retrospective analysis was conducted of 55 MR images of the brain for children who ranged in age from 1 week to 12 years. Forty-two patients received chloral hydrate, and 13 received propofol anesthetic. Multiplanar MR images were studied to detect the presence or absence of hyperintense signal (artifact) in the subarachnoid spaces and basal cisterns. The T1 values and null times of chloral hydrate, propofol, and CSF were determined in vitro at room temperature by using an inversion recovery pulse sequence at 1.5 T. RESULTS: The fast-FLAIR images of all 13 patients who received propofol had hyperintense signal abnormality. For 10 (77%) of 13 patients, this artifact was in the basal cisterns and subarachnoid spaces overlying the brain convexity. For three (23%) of 13 patients, this artifact was in the convexity region only. Two patients underwent follow-up MR imaging with a nonpropofol anesthetic agent, and the artifact resolved. None of the images of the children who received chloral hydrate had this artifact. The T1 value of chloral hydrate was 0.2 s, of propofol was 1.86 s, and of CSF was 2.32 s at room temperature. CONCLUSION: The fast-FLAIR images of children anesthetized with propofol have artifactual hyperintense signal in the basal cisterns and subarachnoid spaces, and this artifact mimics disease of the subarachnoid space. The T1 value of propofol approaches that of CSF. Depending on the chosen null time, there may be incomplete nulling of signal coming from propofol. To account for this observation, other possible causes include increased CSF pulsation in children creating motion artifact, changes in arterial oxygen concentration intrinsic to propofol or related to the supplemental oxygen normally administered, or changes in CSF protein levels related to propofol binding to proteins for uptake into CSF.
