On February 7, 2018, researchers from the National Institutes of Health (NIH) reported on the unexpected finding of gadolinium leakage into ocular structures (GLOS) in acute stroke patients after administration of a gadolinium-based contrast agent (GBCA). “Blood-ocular barrier disruption in acute stroke patients” by Hitomi et al. is published in the journal Neurology. Blood-ocular barriers (BOBS) protect the compartments of the eye.
NIH researchers performed baseline MRI scans with a gadolinium-based contrast agent on 167 stroke patients upon admission to the hospital and compared them to scans performed 2 and/or 24 hours later with fluid-attenuated inversion recovery (FLAIR) imaging. The study found that gadolinium leakage was evident on post-contrast FLAIR images in 127/167 (76%) patients. At 2 hours after administration of the GBCA, GLOS was more common in the aqueous chamber alone. At 24 hours, GLOS was present in 121/162 (75%) patients, always involving the vitreous chamber, but also affecting the aqueous chamber in 6% of cases.
The authors concluded that GLOS is common in patients with acute stroke, and delayed GLOS was a marker for chronic vascular disease. They noted that the mechanism for acute GLOS remains uncertain but may be a remote effect of acute cerebral injury on the blood-ocular barrier.
It remains unclear whether gadolinium can enter the eye in healthy people.
Gadolinium has been detected in eyes before
There is other evidence of gadolinium entering the compartments of the eye. A 2002 article by Kanamalla and Boyko described gadolinium diffusion into the vitreous and aqueous humors of the ocular globes, perivascular space, and brain ventricles in patients with chronic renal disease. One patient underwent a follow-up MRI at 96 hours after contrast administration and gadolinium had not cleared the vitreous humor as observed on FLAIR imaging.
A 2011 small case series, “Ocular Pathologic Features and Gadolinium Deposition in Nephrogenic Systemic Fibrosis” reported on 2 autopsy cases of NSF. Case 1 had significant ocular histopathologic findings including 2 large scleral plaques, a posterior scleral deposit near the macula, and a large episcleral bony plaque. Gadolinium was detected in and around blood vessel of the choriocapillaris, but not in the scleral plaques. Case 2 had conjunctival plaques in the eye that were seen clinically and scanning electron microscopy with energy-dispersive x-ray spectroscopy (SEM-EDS) demonstrated calcium-phosphate content, but no gadolinium. Scleral plaques are associated with NSF.
While much of the earlier research related to gadolinium deposition is centered around NSF and renally-impaired patients, it appears that many of the findings could happen to anyone who undergoes an MRI with a gadolinium-based contrast agent. Just like gadolinium retention is not limited to renally-impaired patients, perhaps “gadolinium leakage into ocular structures” is not limited to acute stroke patients.
Hitomi, E., Simpkins, A. N., Luby, M., Latour, L. L., Leigh, R. J., & Leigh, R. (2018). Blood–ocular barrier disruption in acute stroke patients. Neurology. JOUR. Retrieved from http://n.neurology.org/content/early/2018/02/07/WNL.0000000000005123.abstract
Kanamalla, U. S., & Boyko, O. B. (2002). Gadolinium Diffusion into Orbital Vitreous and Aqueous Humor, Perivascular Space, and Ventricles in Patients with Chronic Renal Disease American Journal of Roentgenology , 179(5), 1350–1352. JOUR. Retrieved from http://www.ajronline.org/content/179/5/1350.short
Barker-Griffith, A., Goldberg, J., & Abraham, J. L. (2011). Ocular pathologic features and gadolinium deposition in nephrogenic systemic fibrosis. Archives of Ophthalmology, 129(5), 661–3. Retrieved from http://archopht.jamanetwork.com/article.aspx?articleid=427337