Central Vision Loss Associated with Silicone Oil in the
Treatment of Retinal Detachment
Nicholas B Grissom1*, Vishak J. John*, Timothy Martin1
1Wake Forest School of Medicine, Medical Center Boulevard Winston-Salem, N.C
Vishak J. John, MD, Medical Center Boulevard, Winston-Salem, N.C. 27157, Tel No: 333-716-8666; E-mail:
Nicholas Grissom, Wake Forest School of Medicine, Medical Center Boulevard Winston-Salem, N.C. 27103, Tel No: 9197607704; E-mail:
Received: 12 August, 2016; Accepted: 19 September, 2016; Published: 29 September, 2016
Grissom NB, John VJ, Martin T (2016) Central Vision Loss Associated with Silicone Oil in the Treatment of Retinal
Detachment. Int J Open Access Ophthal 1(2): 4. DOI: 10.15226/2474-9249/1/2/00104
Purpose: We present four patients that experienced vision
loss associated with the use and removal of silicone oil as part of
treatment for retinal detachment. Though silicone oil has been
previously reported to cause vision loss, we believe these cases
represent a distinct pathological mechanism.
Methods: Patients underwent evaluation with a complete
ophthalmic examination, optical coherence tomography of the
macula, magnetic resonance imaging of the orbits, electroretinogram,
and other tests as deemed clinically necessary.
Patients: Four patients were diagnosed with rhegmatogenous
retinal detachments and underwent vitrectomy with silicone oil
placement as part of their treatment. These patients later developed
severe central scotomata, and retained poor central visual acuity
after refraction and treatment of identifiable causes of decreased
Conclusion: These four patients experienced significant loss of
visual acuity associated with the use or removal of silicone oil in the
treatment of retinal detachment.
Visual loss has been previously reported with the use of silicone
oil, but in prior literature characteristic changes on optical coherence
tomography were noted.
Imaging and other diagnostic modalities performed on these
patients did not identify the cause for these patients vision loss and
we believe these four cases represent a novel pathologic entity.
Silicone oil is a commonly used adjunctive treatment
in vitreoretinal surgery . One setting in which the use of
silicone oil tamponade has been prominent is the treatment and
management of Rhegmatogenous retinal detachment (RRD).
The introduction of silicone oil has proven to be beneficial, as
few agents match the effectiveness of silicone oil as an ocular
tamponade agent. However, studies over the past decade have
reported the incidence of vision loss as a complication associated
with the use of silicone oil [1–8]. Most reports suggest that a
central scotoma is the most common severe complication seen in this setting, suggesting foveal injury or an optic neuropathy .
Initially, it was thought that the inciting event for the development
of vision loss was the removal of the silicone oil, though patients
have also experienced loss of visual acuity prior to removal of
the oil. It remains unclear why the retina is affected by silicone
oil, and specifically why the fovea in particular is preferentially
Some studies suggest that pre-existing risk factors such
as glaucoma and optic nerve abnormalities define the patient
population at risk for severe vision loss . Additionally, multiple
studies have assessed the ability of Spectral Domain Optical
Coherence Tomography (SD-OCT) as a tool to objectively assess
the changes associated with silicone oil associated vision loss
. We present four patients that experienced severe vision loss
following use of silicone oil as part of their treatment for retinal
detachment, and discuss how our findings relate to the current
body of research.
A 53-year-oldman presented with a macula-on retinal
detachment of the right eye with a giant retinal tear in 2009. The
visual acuity on presentation was 20/20-1 in the right eye. He
underwent a Pars-Plana Vitrectomy (PPV) with a scleral buckle,
external cryopexy and injection of silicone oil. At one month post
op, the Best-Corrected Visual Acuity (BCVA) was 20/50. Three
months post-operatively he reported that his vision was much
worse, and the visual acuity was 20/200, but he had developed
a dense posterior sub capsular cataract. Phacoemulsification
with IOL at post op month four did not improve his vision as
anticipated. Nine months following the initial retinal detachment
repair, the silicone oil was removed, and his BCVA remained
at 20/200 postoperatively. Further evaluation revealed a 0.7
log unit relative afferent pupillary defect in the right eye and
Humphrey threshold perimetry demonstrated a discrete central
scotoma in the right eye (Figure 1). Intraocular Pressure (IOP)
was within normal limits. SD-OCT showed a normal foveal
contour and thickness with no epiretinal membrane or cystoid macular edema. At 15 months post-operatively, the patient's
BCVA had improved minimally to 20/125 in the right eye with
unremarkable macular OCT. Three years later, the acuity and
visual field was unchanged, and OCT of the macula remained
normal (Figure 2).
A 60-year-oldman with history of ocular hypertension
presented with an RRD of the left eye in 2014. He underwent
vitrectomy with scleral buckle placement and silicone oil
injection one week later due to failure of a pneumatic procedure.
The choice of oil as tamponade, as opposed to gas, in his surgery
was due to his desire to fly back to his home in Colorado. His
postoperative BCVA was 20/30 in the left eye initially. He
later underwent cataract surgery with silicone oil removal at a
different facility three months later and noted a sudden loss of
vision resulting in central scotoma in the early postoperative
period. His BCVA decreased to CF@ 3', and IOP was elevated at
24 mm Hg. The slit lamp exam was unremarkable. Funduscopic
exam revealed mild inferior retinal thinning and questionable
temporal pallor of the optic disc. OCT showed a mild epiretinal
membrane and central thickness of 295 um (Figure 3). Full-field
Electroretinogram (ERG) revealed lower amplitudes in the left
eye from all scotopic and photopic stimuli, but a multifocal ERG
did not reveal any abnormalities, and the optic disc was graded
as normal by two different neuro ophthalmologists. An MRI of
the orbits with and without contrast did not demonstrate any
evidence of a retrobulbar optic neuropathy. At four months after
oil removal, his vision remained CF.
A 44 year old woman with history of pathologic myopia
presented in 2014 with two retinal tears in the left eye with
resultant vitreous hemorrhage. She was initially treated with
pneumatic cryopexy with success in the left eye. Two months
post-operatively, the patient presented with bilateral RRDs, and
was treated with scleral buckle placement and cryopexy in both
eyes. Four weeks following the surgery, the patient had a PPV
with silicone oil injection in the left eye for recurrent detachment.
The patient's BCVA improved from 20/100 pre-op to 20/25 in
the left eye after four weeks. Three months after the procedure,
the silicone oil was removed from the left eye, after which
patient noticed severe loss of central vision and color vision loss,
with BCVA of CF@3'. Intraocular pressures remained normal
throughout. Slit lamp examination was notable for trace nuclear
sclerosis with 3+ posterior subcapsular cataract. Fundus exam
revealed a flat macula with lacquer cracks and no subretinal fluid
or fibrosis of the retina. OCT was obtained and central foveal
thickness was 278, with normal foveal profile and no CME or
SRF were noted (Figure 4). An MRI obtained two months after oil
removal revealed no retrobulbar abnormality and the optic nerve
was normal in appearance. An RNFL OCT was also obtained,
which was unremarkable. At this time, BCVA was 20/400, with
E Card @ 6'. Eight months post-operatively the patient's BCVA
Figure 1: Humphrey threshold 30-2 perimetry shows a discrete central
scotoma and decreased foveal threshold
Figure 2: OCT imaging of right eye demonstrates mild epiretinal membrane
with normal appearance of the outer retina. We have included
his left normal OCT for comparison.
Figure 3: OCT of left macula highlighting normal retinal architecture.
A 46 year old female with history of high myopia presented in
2014 with bilateral inferior macula-involving, fovea-threatening
retinal detachments that appeared chronic in nature. She had
a BCVA of 20/25 on presentation. She underwent cryopexy
and scleral buckle placement in the right eye one week after
presentation. Following the procedure, persistent sub-retinal
fluid was noted in the periphery, so a PPV was performed with
placement of silicone oil. Two months postoperatively, BCVA
was 20/30 under oil. One year later, the patient presented again
with BCVA of CF @ 3' and was found to have a severe posterior
subcapsular cataract. Both the cataract and silicone oil were
removed at this time. These procedures failed to improve the
patient's visual acuity, and at one month post-op the BCVA
remained CF @ 6' in the right eye. Funduscopic exam and fundus
photography were remarkable for small area of RPE atrophy
on inferior peripheral retina.OCT of macula at one month postop
revealed a normal myopic foveal contour (Figure 5). An OCT
of RNFL was performed, which was normal (Figure 6). An MRI
of the orbits was obtained and did not reveal any retrobulbar
abnormality and the optic nerve was normal in appearance. Two
months post-operatively, the patient's BCVA remained CF @ 6'.
All four of the patients had acute central visual loss following
removal of silicone oil, which was a component of their treatment
for retinal detachment. In these patients the diagnostic workup
was unable to identify a cause for the decreased vision. In
published literature, Errera et al  were consistently able to
identify abnormalities in patients with visual loss due to silicone
oil tamponade on SD-OCT; typically hyper reflective areas
adjacent to the retina that they believe represent bubbles of
emulsified silicone oil. Shalchi et al  also identified microcystic
macular changes in the inner nuclear layer of affected eyes on
SD-OCT, in addition to noting a focal loss of the papillofoveal
projection. This is significant because no such findings were
noted in our four patients. Notably, only one of the patients
included in this case report had an IOP spike at any point during
the workup, and the only evidence of any optic neuropathy was
the RAPD seen in Patient 1
Figure 4: OCT of left eye demonstrating a myopic fundus. The retinal
layers are normal and intact.
Figure 5: OCT of right macula demonstrating myopic fundus with normal
Figure 6: Normal OCT of retinal nerve fiber layer in the right eye.
Several theories have been proposed about the mechanism
by which silicone oil results in visual loss. Animal studies were
the first to demonstrate that silicone oil penetrated the internal
limiting membrane and caused loss of horizontal and bipolar
cell processes . A study performed by Williams et al. 
delineated the modern theories about how silicone oil causes
injury. Perhaps the most prominent idea in current literature
is the "vitreous potassium sink" theory, which suggests that the
silicone oil tamponade disrupts the natural potassium reservoir
provided by the vitreous, allowing intraretinal potassium spikes
that can injure the outer layers of the fovea. An alternative
idea suggests that the silicone oil droplets themselves migrate
subretinally, which can result in optic neuropathy that is similar in phenotype to that caused by multiple sclerosis and Leber's
optic neuropathy . Nicholson et al suggest that accumulation
of oil droplets in the prefoveal region is not the likely mechanism
of injury, a conclusion that is consistent with many other studies
that have not found a clear correlation between the length of
time silicone oil tamponade was in place with the injury rate or
severity . Most modern data suggests that the end result of the
silicone oil tamponade is neuronal cell loss in the macula. This
results in a measureable reduction in inner retinal thickness,
and is the physiologic defect that results in the visual changes we
observed . The cases we present here are significant because
previous reports of silicone oil toxicity have demonstrated
characteristic OCT findings, while these four patients do not
have OCT abnormalities that explain their visual loss. We believe
these patients represent a different pathologic entity from those
reported in the literature, and with current imaging modalities
we do not have an explanation of the etiology.
Though the techniques needed to establish how silicone
oil results in visual loss are well-described, currently the
pathophysiology of the condition is not well-reported in
literature. It is unclear if the microcystic macular changes that
have been observed are also present in unaffected eyes but are
asymptomatic, or if they are an integral part of the pathogenesis
of the visual loss. The rarity of this complication makes studies
with significant power difficult to create, so a larger sample size
may be necessary to adequately study this phenomenon.
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