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Temple University School of Medicine Philadelphia, PA 19140
Lev and Schafer [1] described gadolinium diffusion into the subarachnoid space in patients with renal failure. In this article, we discuss the phenomenon of progressive gadolinium diffusion into the vitreous and aqueous humors of the ocular globes, perivascular (Virchow-Robin) spaces, and the ventricles of the brain seen on fluid-attenuated inversion-recovery (FLAIR) MR imaging in patients with chronic renal failure.
Three patients with end-stage renal disease—two men (ages, 57 and 65 years) and one woman (age, 66 years)—who were receiving dialysis treatments underwent MR imaging for evaluation of an altered mental state. None of the patients had undergone lumbar puncture, nor did any of them have a history of a recent subarachnoid hemorrhage. On the day of the MR imaging, the patients' creatinine levels ranged from 2.5 to 5.5 mg/dL (normal range, 0.6-1.2 mg/dL), and the blood urea nitrogen ranged from 39 to 77 mg/dL (normal range, 20-40 mg/dL).
Spin-echo T1-weighted, fast spin-echo T2-weighted, and fast FLAIR sequences were used in both the initial and follow-up MR imaging. During the initial examination, gadolinium (0.1 mmol/kg) was administered before axial T1-weighted MR imaging was performed; after a delay of approximately 3 min, fast FLAIR MR imaging was performed. Unenhanced follow-up MR imaging was performed twice during a period of 1-96 hr after the initial MR examination. In addition, two patients underwent CT to confirm the absence of an acute intracranial or vitreous hemorrhage.
On delayed FLAIR imaging of all three patients, gadolinium diffusion into the vitreous and aqueous humors of the ocular globes (Fig. 1A,1B) and ventricles of the brain (Fig. 1B) was seen. In one patient, gadolinium diffusion into a prominent perivascular space was also identified (Fig. 2). Diffusion into the ocular globes and brain ventricles was not evident on the initial follow-up FLAIR images (acquired < 6 hr after the first examination) when gadolinium was visible in subarachnoid space. This finding is likely related to the dilutional effect of the vitreous and aqueous humors and the cerebrospinal fluid (CSF) in the ventricles. In the only patient who underwent follow-up MR imaging 96 hr after the first examination, the gadolinium had completely cleared from the subarachnoid and ventricular CSF but not from the vitreous humor, in which a hyperintense fluid signal continued to be observed on FLAIR imaging. Perhaps this finding resulted from the CSF turning over more rapidly than the vitreous humor.
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Although gadolinium leakage into the globes and ventricles was clearly evident on FLAIR MR images of all patients as hyperintense fluid signal, leakage was seen on T1-weighted MR images in only one patient, revealed as mildly increased intensity. The greater sensitivity of FLAIR MR imaging to such leakage is related to the long inversion time, resulting in T1 contrast weighting and, therefore, the capability to depict small concentrations of gadolinium more clearly [2].
The theoretic clinical concern regarding gadolinium diffusion into the vitreous humor and CSF-filled spaces in the brain is neurotoxicity. The findings of thorough neurologic and ophthalmologic examinations of our patients were unremarkable. One of the three patients also underwent electroencephalography, which showed no abnormal electrical activity. Because none of our patients had a lumbar puncture, we do not have evidence regarding the presence or absence of CSF changes. However, Lev and Schafer [1] detected no CSF abnormality in the patients in their study.
In conclusion, gadolinium contrast material can diffuse across semipermeable membranes such as the meninges, choroid plexus, or uveochoroid membrane in patients with impaired renal function. The finding of gadolinium diffusion, however, appears to represent a radiologic pitfall only for the diagnosis of disorders that produce high protein levels, such as an infection or hemorrhage. The clinical correlation in our three patients shows that diffused gadolinium appears not to be associated with clinical neurotoxicity.
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