Silicone oil keratopathy is corneal decompensation caused by contact, deposition, or emulsification of silicone oil (SO) used as an intraocular tamponade agent in vitrectomy. It is also called emulsified oil keratopathy.
SO is a colorless, transparent hydrophobic liquid with a viscosity of 900–1,250 mm²/s. It is chemically and biologically inert, allowing long-term intraocular tamponade. It is used to treat proliferative vitreoretinopathy, macular hole retinal detachment, and refractory retinal detachment. However, when SO contacts the corneal endothelium, endothelial damage occurs, initially causing band keratopathy, and as endothelial damage progresses, it leads to bullous keratopathy 1).
The incidence of SO keratopathy is reported to be 6–9.4%. Some reports indicate it reaches 28% in patients who underwent SO tamponade after open globe injury.
When SO migrates into the anterior chamber and directly contacts the corneal endothelium, it causes mechanical trauma to endothelial cells. Additionally, when aqueous humor is replaced by SO, oxygen and nutrient supply to the endothelium is blocked. Furthermore, emulsification of SO causes micro-oil droplets to penetrate the corneal stroma, leading to tissue damage.
Caused by SO tamponade after vitreous surgery. The direct cause is the migration of SO into the anterior chamber and contact with the corneal endothelium. Emulsification of SO is also an important pathogenesis, with emulsified micro-oil droplets penetrating the corneal stroma.
| Risk Factor | Mechanism |
|---|---|
| Aphakic eye | Lack of lens barrier facilitates SO migration into the anterior chamber |
| Long-term retention (6 months or more) | Prolonged contact time with the endothelium |
| Excessive SO injection volume | Increased risk of SO migration into the anterior chamber |
| Open globe injury (zone III) | Increased risk of keratopathy due to extensive tissue damage |
In phakic eyes, SO frequently causes cataracts. In aphakic eyes, SO can cause pupillary block leading to increased intraocular pressure; therefore, prophylactic peripheral iridectomy at the 6 o’clock position is performed. Emulsified SO can also clog the trabecular meshwork, increasing intraocular pressure 2).
Migration of SO into the anterior chamber can obstruct the trabecular meshwork, and emulsified SO is phagocytosed by macrophages and accumulates in the trabecular meshwork, inducing trabeculitis 2). Long-term contact between SO and the trabecular meshwork can cause permanent structural changes 2).
According to the package insert, silicone oil should be removed at an appropriate time within one year after the retina has stabilized following tamponade. However, in cases with a high risk of redetachment or risk of phthisis bulbi due to hypotony, removal may not be possible. The benefits and risks of removal should be carefully considered on a case-by-case basis.
Clinical Diagnosis
History taking: Confirm history of vitrectomy, SO tamponade, and duration of SO retention.
Slit-lamp examination: Observe band keratopathy, corneal edema, opacity of the endothelial surface, and SO droplets in the anterior chamber. SO is recognized as a cause of corneal edema 1).
Imaging and Special Tests
Anterior segment OCT (AS-OCT): Depicts corneal thickening, hyperreflective dots in the stroma, and round/oval hyporeflective spaces.
In vivo confocal microscopy: Confirms fibrotic changes in the basal epithelium, decreased keratocyte density, increased pleomorphism and anisocytosis of endothelial cells, and inflammatory cells.
Other causes of band keratopathy (e.g., chronic uveitis, hypercalcemia, phthisis bulbi) must be excluded.
Asymptomatic and mild cases can be observed. Since keratopathy can be progressive, monitoring for secondary infection is necessary.
For mild ocular irritation or foreign body sensation, bandage contact lenses or hypertonic saline eye drops are used. This is similar to general conservative management for endothelial decompensation.
Penetrating keratoplasty is performed for corneal decompensation, but the average graft survival is limited to 21–25 months. Removal of silicone oil before or simultaneously with keratoplasty improves graft prognosis. Transplantation with silicone oil left in place tends to have a poor prognosis.
When silicone oil migrates into the anterior chamber and directly contacts the corneal endothelium, mechanical trauma occurs. The risk of contact increases especially in the supine position as the oil rises to the endothelial surface. In aphakic eyes, the absence of a lens barrier facilitates oil migration into the anterior chamber. Contact over weeks to months reduces endothelial cell count.
The corneal endothelium lacks blood supply and obtains oxygen and glucose from aqueous humor production and circulation. When the aqueous humor is completely replaced by silicone oil, endothelial cells become oxygen-deprived. Reduced aqueous flow may alter fluid pH and promote silicone oil emulsification.
Silicone oil emulsification is a multifactorial phenomenon. In addition to the oil’s interfacial tension and viscosity, shear forces from eye movements promote emulsification. Microdroplets of emulsified oil penetrate the corneal stroma and are observed histopathologically as localized intrastromal silicone oil vacuoles surrounded by macrophages. Irregularities of Descemet’s membrane and formation of a retrocorneal membrane are also noted.
Corneal resistance factor (CRF) and corneal hysteresis (CH) significantly decrease postoperatively in eyes that underwent SO tamponade. This finding suggests that SO affects the biomechanical properties of the cornea.
SO emulsification is a phenomenon in which SO separates into tiny droplets due to shear forces from eye movements and changes in interfacial tension. Emulsified SO can clog the trabecular meshwork, causing increased intraocular pressure, or penetrate the corneal stroma, leading to tissue damage. Emulsification is promoted by long-term retention and surgical manipulation.
