Unexplained visual loss after silicone oil removal (UVLASOR) is a visual dysfunction that occurs after vitreoretinal surgery for silicone oil (SO) removal. It was first reported in 2004.
SO is used in the treatment of refractory retinal detachment to provide long-term tamponade as a vitreous substitute. Unlike gas, it is not absorbed for a long period, and its high transparency allows postoperative fundus observation. According to the SO package insert, it should be removed at an appropriate time within one year after the retina has stabilized.
Incidence varies among studies; in the 421-eye series by Moya et al., it was 3.3%, and in the 46-eye series by Oliveira-Ferreira et al., it was 10.9% 1, 2). High rates of visual loss have been reported in retinal detachment due to giant retinal tear with foveal sparing 1).
Before diagnosing UVLASOR, the following causes of postoperative visual loss must be excluded:
Additionally, confirming the absence of structural abnormalities through OCT evaluation is also a diagnostic requirement.
Long-term retention of SO is associated with various complications including corneal endothelial damage, cataract progression, secondary glaucoma due to elevated intraocular pressure, and oil migration into the optic nerve head. According to the package insert, it should be removed at an appropriate time within one year after retinal stabilization. In cases where removal is difficult, such as those with a high risk of re-detachment, decisions are made on an individual basis.
The most prominent feature of ULVASOR is a sudden and significant decrease in visual acuity after SO removal surgery.
Fundus and anterior segment findings
Fundus examination: Often appears normal, with no retinal detachment, macular edema, or other obvious lesions.
OCT findings: Subtle findings such as thinning of the ganglion cell layer (GCC) may be observed.
Fundus autofluorescence findings: A prominent leopard-spot pattern may be seen on fundus autofluorescence imaging.
Functional test findings
PERG findings: Pattern electroretinography shows reduced amplitude, indicating macular dysfunction.
mfERG findings: Multifocal electroretinography may show a selective damage pattern in the central macula.
Visual field findings: Automated perimetry detects a deep central scotoma with reduced foveal sensitivity.
In UVLASOR, the fundus often appears normal on routine examination, which is one factor that makes diagnosis difficult. High-resolution OCT analysis and electrophysiological tests (PERG, mfERG) can detect macular dysfunction and subtle changes in the ganglion cell layer that are not visible to the naked eye. For details, see the “Pathophysiology and detailed pathogenesis” section.
The exact cause of UVLASOR remains unknown, but several contributing factors have been identified or suspected.
Oliveira-Ferreira et al. reported that high intraocular pressure and SO emulsification during SO tamponade were associated with unexplained vision loss2).
The diagnosis of UVLASOR is primarily a clinical diagnosis of exclusion, confirmed when vision loss after SO removal is present and no identifiable cause is found through other tests or diagnostic procedures.
In patients with vision loss after SO removal, it is essential to systematically rule out the following treatable causes.
| Diagnosis | Key differentiating features |
|---|---|
| Posterior ischemic optic neuropathy (PION) | Visual field defect, elevated inflammatory markers |
| Recurrent retinal detachment | Visual field defect, retinal tear |
| Cystoid macular edema (CME) | Late petaloid leakage on IVFA, thickening on OCT |
| Epiretinal membrane | Metamorphopsia, surface membrane on OCT |
| Glaucoma | Visual field defect, enlarged optic cup |
| SO adhesion to IOL | Micropsia, glare |
Since the pathophysiology is unknown, management of UVLASOR is primarily supportive care.
In some cases, vision may improve spontaneously over time. Close monitoring with regular follow-up examinations is recommended.
Long-term SO tamponade may be associated with an increased risk of complications including UVLASOR. Early removal of SO is considered to reduce risk, but there is no consensus on optimal timing. SO removal may be considered in cases with elevated intraocular pressure, but it is not effective in all cases and may increase the risk of retinal detachment. 1)
Steroid Therapy
Intensive steroid therapy: Limited evidence suggests it may be beneficial in some cases.
One study reported significant visual improvement after 4 weeks of oral prednisone and three periocular triamcinolone injections over 9 weeks.
However, further research is needed to confirm efficacy.
Intraocular Pressure Management
Topical and systemic intraocular pressure-lowering medications: Used for elevated intraocular pressure due to SO 2).
Anti-inflammatory treatment: Considered as adjunctive therapy in cases with inflammation.
The efficacy of immunomodulatory therapies such as intravitreal methotrexate is currently unknown.
Surgery is not typically the first-line treatment for vision loss after SO removal. However, surgery may be necessary for recurrent retinal detachment, visual disturbances due to SO droplets, epiretinal membrane, or other complications.
The prognosis varies; some patients experience spontaneous improvement in vision, but many others have permanent visual impairment. Studies suggest that longer SO tamponade duration may lead to worse visual prognosis. The severity of initial vision loss and underlying retinal or optic nerve damage are also factors affecting prognosis.
The exact pathophysiology of UVLASOR remains unclear and is likely a multifactorial disease process. Proposed mechanisms all suggest damage to the inner retinal layers, particularly the ganglion cell complex (GCC), as a common final pathway.
Intense light from the surgical microscope interacts with the SO and micro-bubbles within the SO, inducing uneven macular illumination. This can significantly amplify light exposure to the macula, potentially causing direct phototoxicity. Avoiding prolonged use of intraocular illumination near the macula is considered important in vitreous surgery.
Longer SO tamponade duration leads to progressive thinning of the inner retinal layers and loss of retinal neurons. Tamponade duration is a known risk factor for UVLASOR and is thought to reflect cumulative damage to the inner retina.
A decrease in amplitude on PERG indicates that the visual impairment is primarily due to macular dysfunction. mfERG shows a selective damage pattern in the central macula, supporting that foveal dysfunction is predominant.
Rapid changes in local potassium, calcium (Ca²⁺), and magnesium (Mg²⁺) concentrations in the retro-oil fluid, as well as accumulation of cytokines and inflammatory substances, may induce apoptosis of photoreceptors and ganglion cells.
The distribution volume in an eye filled with silicone oil is very small (< 0.5 mL), creating an environment where inflammatory substances are highly concentrated compared to eyes filled with vitreous or saline (approximately 5 mL).
High concentrations of basic fibroblast growth factor (bFGF) and inflammatory cytokines such as interleukin-6 (IL-6) are present in the retro-oil fluid. Elevated levels of these growth factors contribute to the formation of fibrocellular membranes that lead to changes in retinal layers affecting vision.
After vitrectomy, the blood-retinal barrier and blood-aqueous barrier temporarily become compromised, altering the transport of substances into and out of the eye. This is also thought to contribute to changes in the biochemical environment of the retro-oil fluid.
Thinning of the ganglion cell layer is one finding suggestive of ULVASOR, but it alone does not establish a definitive diagnosis. Similar findings can occur in glaucoma, optic nerve diseases, and other retinal degenerations, so a process of exclusion is necessary. To date, no pathological findings have been reported in eyes that developed ULVASOR.
To date, no pathological findings have been reported in eyes that developed ULVASOR. This is one factor that has significantly delayed the elucidation of the pathology of this disease.
Associations have been reported with the duration of silicone oil tamponade, silicone oil emulsification, and elevated intraocular pressure during the tamponade period 1, 2). However, further research is awaited to clarify the details of the mechanism.
In cases where unexplained vision loss, optic atrophy, and vascular narrowing during long-term use of the Boston type I keratoprosthesis (Boston Kpro Type I) are attributed to chronic uveitis reactions, immunomodulatory therapy is recommended. Whether this phenomenon contributes to the understanding of UVLASOR pathology awaits future clarification.
Moya R, Chandra A, Banerjee PJ, Tsouris D, Ahmad N, Charteris DG. The incidence of unexplained visual loss following removal of silicone oil. Eye (Lond). 2015;29(11):1477-1482. doi:10.1038/eye.2015.135.
Oliveira-Ferreira C, Azevedo M, Silva M, Roca A, Rocha-Sousa A. Unexplained visual loss after silicone oil removal: a 7-year retrospective study. Ophthalmol Ther. 2020;9(3):1-13. doi:10.1007/s40123-020-00259-5.
Scheerlinck LM, Schellekens PA, Liem AT, Steijns D, van Leeuwen R. Incidence, risk factors, and clinical characteristics of unexplained visual loss after intraocular silicone oil for macula-on retinal detachment. Retina. 2016;36(2):342-350. doi:10.1097/IAE.0000000000000711.
