Vitrectomy involves the removal of vitreous humor and its replacement with intraocular tamponade agents, such as intraocular gas, silicone oil and/or perfluorocarbon liquid (PFCL). These agents play crucial roles in managing conditions such as retinal detachment, diabetic retinopathy and ocular trauma, promoting retinal adhesion to the retinal pigment epithelium and aiding hemostasis.^{Reference Foster1} This article describes two cases of subarachnoid migration of intraocular tamponade agents following vitrectomy.

A 68-year-old woman with severe myopia presented with retinal detachment in the right eye. She underwent vitrectomy with intravitreal gas and PFCL injection. Two days after surgery, she developed complete amaurosis. Brain CT revealed gas and hyperattenuating material within the right eye, due to PFCL, as well as along the optic nerve, which did not shift following ventral decubitus (Figure 1).

Figure 1.

Intravitreal tamponade agent migration to the optic nerve. Brain CT in the supine position demonstrated a gas bubble floating within the right vitreous cavity (white arrow in A) and hyperattenuating material in the ipsilateral optic nerve due to perfluorocarbon liquid migration (black arrow in A). Brain CT, performed in the prone position, demonstrated that the gas bubble shifted to the posterior compartment of the globe (white arrow in B); however, there was no displacement of the hyperattenuating material within the optic nerve (black arrow in B). Also note that the perfluorocarbon inside the ocular globe changed position according to the decubitus position, remaining in the most inferior region of the eye. A schematic representation illustrating the expected distribution of perfluorocarbon liquid and intraocular gas within the ocular globe in the prone position, without extension to the optic nerve, is shown in (C).

An 82-year-old man with diabetic retinopathy underwent vitrectomy for retinal detachment, receiving intravitreal injection of silicone oil and PFCL. One week later, he experienced complete vision loss in the right eye. Brain CT and MRI revealed tamponade material migration into the subarachnoid space and ventricles via the optic nerve sheath (Figure 2).

Figure 2.

Intravitreal tamponade agent migration to the optic nerve and lateral ventricles. Brain CT revealed the presence of hyperattenuating intravitreal tamponade material, corresponding to silicone oil, in the right eye, associated with inappropriate migration along the optic nerve sheath (arrows in A), as well as to the lateral ventricles (arrows in B), exhibiting a floating appearance. Brain MRI demonstrated that the material had a hyperintense signal in the ocular globe and optic nerve (arrows in C) on T1-weighted imaging. The tamponade material presented isointense signal on T2-weighted imaging (arrows in D), as well as in the lateral ventricles, with a floating appearance (arrows in E). Fluid attenuated inversion recovery (FLAIR) with fat saturation revealed signal suppression of the tamponade material in the right eye and optic nerve (arrows in F). Also note the chemical shift artifacts at the interfaces of the tamponade material with the vitreous chamber and cerebrospinal fluid, visualized as fine curvilinear bands on C, D and E. A schematic representation depicting the expected distribution of silicone oil, which naturally floats within the ocular globe in the supine position, without extension to the optic nerve (G).

Intravitreal tamponade agents have specific properties on imaging studies:

Intraocular gas is usually composed of sulfur hexafluoride and perfluoropropane. It appears markedly hypoattenuating, with or without air-fluid levels, on CT and hypointense on all MRI sequences.^{Reference Reiter, Schwope, Kini, York and Suhr2,Reference Herrick, Hayman, Maturi, Diaz-Marchan, Tang and Lambert3} Typically, gas stays in the uppermost portion of the eyeball, requiring the patient to remain in specific positions, such as facedown, for at least a week after surgery.

PFCLs are fluorochemicals in which hydrogen is replaced by fluorine, with perfluoro-octane most commonly used. They appear hyperattenuating on CT and generally hypointense on all MRI sequences.^{Reference Herrick, Hayman, Maturi, Diaz-Marchan, Tang and Lambert3,Reference Williams, Williams, Winegar, Carmody and Christoforidis4} PFCLs accumulate in the most dependent eyeball regions. Removal is necessary after treatment to prevent retinal toxicity.^{Reference Herrick, Hayman, Maturi, Diaz-Marchan, Tang and Lambert3}

Silicone oil is a viscous hydrophobic polymer, commonly composed of polydimethylsiloxane.^{Reference Herrick, Hayman, Maturi, Diaz-Marchan, Tang and Lambert3} It appears hyperattenuating on CT, hyperintense on T1-weighted imaging and usually iso- to hypointense on T2-weighted imaging, demonstrating signal loss on fat-saturation sequences.^{Reference Reiter, Schwope, Kini, York and Suhr2,Reference Herrick, Hayman, Maturi, Diaz-Marchan, Tang and Lambert3} After treatment, removal is necessary due to possible adverse effects, such as glaucoma and corneal changes. Although hyperattenuating on CT, it is less dense than cerebrospinal fluid and tends to float in the frontal/temporal horns in the supine position (“floating” appearance), in intraventricular extension cases.

These agents do not present contrast enhancement or surrounding edema. Although rare, intracranial migration can simulate conditions such as hemorrhage and neoplasms. In addition to vision loss, long-term neurological adverse effects of tamponade agent migration are still undetermined and should be avoided.^{Reference Naseripour, Ghasempour, Falavarjani, Sanjari and Yousefi5}

The most likely mechanism underlying the migration of intraocular tamponade agents from the vitreous cavity to the subarachnoid space is through the pial layer surrounding the optic nerve, entering the perineural subarachnoid space, which remains continuous with the intracranial subarachnoid space. This continuity facilitates the potential migration of these agents into the ventricular system via the foramina of Luschka and Magendie, providing a plausible route for their accumulation within the cerebral ventricles.^{Reference Sarohia, Javan and Aziz6,Reference Cao, Zhao, Wang, He, Xia and Xu7}

Several predisposing factors have been identified as contributing to this process. Increased intraocular pressure may force the tamponade material through microdefects in the lamina cribrosa, allowing it to penetrate the pia mater of the optic nerve or directly enter the subarachnoid space through an atrophic optic disc.^{Reference Cao, Zhao, Wang, He, Xia and Xu7} Additionally, congenital anomalies, such as optic disc pits and morning glory syndrome, may create abnormal connections between the vitreous cavity and the subarachnoid space, facilitating migration.^{Reference Naseripour, Ghasempour, Falavarjani, Sanjari and Yousefi5}

Therefore, imaging features of these agents assist physicians in identifying inadvertent migration and differentiating it from hemorrhages and tumors. Postoperative control of intraocular pressure is essential to minimize unintended complications.