Silicone oil is used as a long term intraocular tamponade in vitreoretinal surgery for conditions such as rhegmatogenous retinal detachments. Complications such as silicone oil associated keratopathy, cataract formation, or emulsification with secondary glaucoma have been reported.¹ We report the unusual case of intracranial silicone oil migration with subsequent visual field defect in the fellow eye and the results of neurosurgical intervention

Case report

A 66 year old male patient had undergone cataract surgery and lens implantation on both eyes 20 months earlier. Six months after cataract surgery a retinal detachment was seen in the left eye which was first treated with pars plana vitrectomy and gas tamponade (15% C₂F₆). After a period of 4 months, a redetachment occurred and silicone oil (Acri.Sil-ol 5000, 5000 cps, Acri.Tec, Hennigsdorf, Germany) was used as a permanent tamponade. Postoperative visual acuity was 20/500 in the left eye. Twelve months later, the patient was referred to our institution for further evaluation of a temporal hemianopia of sudden onset in the right eye (fig 1A) and for treatment of elevated intraocular pressure in the left eye. At presentation, visual acuity was 20/20 in the right eye and light perception in the left eye. Intraocular pressure was in a normal range in the right eye and elevated to 35 mm Hg in the left eye despite local antiglaucomatous monotherapy using latanoprost (Xalatan). Emulsified silicone oil was detected in the anterior chamber angle during gonioscopy of the left eye. Funduscopy revealed a glaucomatous excavation and atrophy of the optic nerve in the left eye with a cup-disc ratio of 1.0 (fig 1B); the retina was attached, with the silicone oil filling of the globe being incomplete. Magnetic resonance imaging (MRI) of the brain was then performed for further evaluation. T1 weighted MRI scan revealed a hyperintensive signal in the left vitreous cavity characteristic for silicone oil.² An identical hyperintensive signal was also observed in the left optic nerve and the left half of the optic chiasm (fig 1C); in contrast, in T2 weighted sections the silicone located in the optical system and in the vitreous cavity appeared hypointensive (fig 1D). In order to prevent a further progression of the visual field defect of the right eye, a decompression of the optic nerve seemed prudent. After informed consent, the patient underwent left subfrontal craniotomy and the left optic nerve and the optic chiasm were explored. No oil was found in the subarachnoid space or in the brain tissue. Therefore, the left optic nerve at the transition to the optic chiasma was slit open and the intrachiasmatic and intranerval silicone oil was removed by smooth suction and irrigation. The nerve was completely hollowed out by the oil with only thin perineural structures remaining (fig 2A, B, C). At the end the small opening in the nerve was covered with a collagen fleece coated with fibrin glue (Tachocomb H, Nycomed Pharma GmbH, Unterschleissheim, Germany). The neurosurgical intervention was performed without intraoperative or postoperative complications. In addition, a re-vitrectomy with gas tamponade was performed to remove the silicone oil from the vitreous cavity of the left eye. One month later, a regression of the visual field defect in the right eye was observed (fig 2D) and best corrected visual acuity was 20/32. Intraocular pressure in the left eye was normal without treatment after surgery.

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Figure 1

 (A) Temporal hemianopia of the right eye. Visual acuity was 20/20. (B) The optic disc of the left eye shows atrophy and glaucomatous damage, the cup-disc ratio is 1.0. Note the reflex on the retinal surface, caused by the silicone oil tamponade. (C) Axial T1 weighted MRI scans demonstrate intraocular silicone oil (S) which is hyperintensive compared to the normal vitreous (V). Note the hyperintensive signal in the area of the intracranial portion of the optic nerve and the chiasm (arrow). (D) T2 weighted scans demonstrate hypointensive signals in the silicone filled eye (S) as well as in the area of the optic nerve and chiasm.

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Figure 2

 (A) Left optic nerve (ON) before incision. Arrows point at translucent thinned perineural sheath with silicone oil beneath. OC, entrance to optic canal; ICA, internal carotid artery. (B) Silicone oil (arrow) evading from left optic nerve after incision of perineural sheath. (C) View into left optic nerve after complete removal of the silicone oil. The nerve has been hollowed out by the oil with just thin nerve walls remaining. (D) After intracranial surgery, a regression of the visual field defect was observed.

Comment

This case indicates that silicone oil can migrate intracranially under certain, yet unknown, conditions. Referring to the literature, there is only one case by Eller and co-authors³ describing the intracranial migration of silicone oil in a patient with AIDS who had undergone vitrectomy with silicone oil tamponade for treatment of retinal detachment secondary to cytomegalovirus infection of the retina. As in our patient, there was a coincidence of uncontrolled high intraocular pressure associated with atrophy and glaucomatous damage of the optic nerve. It seems likely that elevated intraocular pressure and optic nerve atrophy allowed intraocular silicone oil to migrate intracranially, although a definite conclusion cannot be drawn from two case reports. However, a histopathological study⁴ previously demonstrated silicone cavities posterior to the lamina cribrosa in an silicone filled eye with glaucomatous nerve damage. The case presented in this report is unique because of the additional affection of the fellow eye as a result of optic nerve compression caused by silicone oil within the optic nerve sheath and its close proximity to the chiasm and the regression of the visual field defect after neurosurgical intervention.