These notes summarise the management of
common or serious retinal conditions. To navigate to a particular
condition click on the link below:
If you have questions about a condition not listed on this page please do get in touch (contact details)
Age-related macular degeneration (AMD) There have been important advances in the treatment of AMD in recent
years, most notably the introduction of agents that inhibit vascular endothelial
growth factor. Anti-VEGF agents target the new vessels responsible for
exudative (wet) AMD and the results of large radomised clinical trials (ANCHOR and MARINA)
as an effective treatment. Many patients with active wet AMD have
Lucentis available on the NHS if they meet certain criteria outlined
by NICE, such as a VA of 6/12 to 6/96, new onset disease, and lack
of foveal scarring. Lucenits treatment is available privately but drug costs are extremely high.
For this reason self-paying patients are often given Avastin
off-label, a much cheaper agent that is chemically related to Lucentis.
Although Avastin has not been subject to a large trial like Lucentis,
many clinicians feel it has a similar clinical effect. I am currently a principal investigator for a new surgical treatmentof
wet AMD that delivers a focal dose of radiation to the macular
via vitrectomy. Surgery has commenced recently at King's College
Hospital, and it is anticipated that centres in Southampton and Belfast
will soon follow. The potential advantage of
radiation is that it can eradicate the new vessels that
cause leakage in a one off procedure, unlike Lucentis which
requires regular injections for life. The study is called CABERNET, and the sponsors are Neovista, a US biotechnology
company. Preliminary results from America look encouraging,
with visual outcome similar or better than Lucentis treatment, but
until the CABERNET study is completed a firm conclusion on
efficacy cannot be drawn. Patients wishing to be involved in this
study should click here
for more information.
Sadly, for atrophic (dry)
AMD there are no breakthrough medical or surgical treatments on the
horizon - low vision aids remain the mainstay of treatment. There
is some interest in implantable telescopic lenses for dry AMD and a
trial of these is underway at King's College Hospital and other
centres. Contact details are available by clicking here. A
guide to AMD referral is available by
clicking here. A patient information sheet is available here.
Severe, exudative, age-related macular degeneration
Diabetic retinopathy The
treatment of diabetic retinopathy has remained much the same for over a
decade. Those with mild disease (no abnormality or background
retinopathy) continue to require regular screening, such as annual
photographs via DECS (diabetic eye complications screening).
DECS refers cases with signficant maculopathy
or unexplained visual loss to clinic, and these patients may then
remain under regular review by an ophthalmologist. More severe
disease (proliferative retinopathy or vision threatening maculopathy)
is usually treated
with laser - pan retinal photocoagulation (PRP) to treat proliferating
new vessels, or macular grid laser to reduce macular oedema.
Severe proliferative disease not responding to treatment, or
vitreous haemorrhage from new vessels, may require vitrectomy and laser
in a small proportion of patients. Tight glucose control has been
proven to slow the progression of diabetic retinopathy so encourage
patients to keep under regular review by their GP or endocrinologist.
of hypertension is also important. For referral guidelines click here. A patient information sheet is available here.
Retinal vein occlusion Retinal
vein occlusion can be divided into branch retinal vein occlusion
(BRVO) or central retinal vein occlusion (CRVO), depending on which
vessels are involved. CRVO produces haemorrhage throughout the
retina, whereas BRVO produces a branch distribution. A hemivein
occlusion produces involvement of either the superior or inferior
retina and is managed as for a CRVO. BRVO is
initially managed by observation alone, but if macular oedema develops
a macular grid laser is usually required. Intravitreal steroid
injections or intravitreal Avastin or also available although the
studies of these new treatments are still in progress. BRVO and
CRVO may lead
to neavascularisation of the retina or iris. Iris new vessels can
produce neovascular glaucoma, typically about 3 months after occlusion
(100 day glaucoma). New vessels are usually treated by panretinal
photocoagulation (PRP), although anti-VEGF agents are increasingly
used in this setting. CRVO macular oedema
is more difficult to treat but anti-VEGF agents may have a role to
play. Novel surgical techniques
such as radial optic neurotomy (RON) are available for select patients.
Patients diagnosed with vein occlusion should have their
cardiovascular risk factors carefully managed by their GP, to reduce
the chance of
recurrence and systemic disease. Most patients with acute onset retinal
vein occlusion should be seen by an ophthalmologist within
approximately 1-2 weeks.
Vitreous floaters and posterior vitreous detachment A sudden onset
of floaters, field defect or photopsia should be considered a
retinal detachment until proven otherwise. As same-day
dilated fundus examination by an ophthalmologist is essential it could
be argued that dilated fundoscopy by an optometrist is not
necessary. Patients can be reassured that greater than 90% of
those with floaters will not have a retinal detachment -
most have a posterior vitreous detachment alone.
longstanding floaters, or occasional
photopsia can be investigated by an optometrist. Maximal dilation
essential to gain an adequate view of the retinal periphery where
breaks tend to occur - use a combination of tropicamide 1% and
phenylephrine 2.5% after excluding narrow angles, drop allergies, a
history of unstable cardiac
disease, or iris clip intraocular lenses. Serious adverse reactions to
eyedrops are extremely uncommon.
Explain that patients should not to drive until the drops
have worn off. Note if Shafer's sign is positive or negative.
This is tested by shining a bright slit-beam across the lens and
focussing into the anterior vitreous. The presence of anterior vitreous
pigment cells (Shafer positive) makes a retinal break likely and
warrants urgent ophthalmology review, even if no break can be detected.
Anterior vitreous pigment (Shafer's sign positive) due to a retinal break
No referral is required for posterior vitreous
detachment or lattice degeneration if these occur in isolation.
For patients who present with floaters, always provide a retinal
detachment warning, advising the patient to present immediately if they
develop flashes, increasing floaters, or a visual field
defect. Document that a retinal detachment warning was given and that
the dilating drops were used to examine the retinal periphery.
Patient information sheet for those with floaters is available here.
Retinal tears and holes Retinal
tears usually occur during posterior vitreous detachment, when an
abnormally strong vitreoretinal adhesion pulls a
break in the retina. These typically have a U-shaped or
horseshoe configuration and acute tears usually require treatment
(retinopexy) with laser or cryotherapy, to reduce the risk
of retinal detachment. Longstanding tears sometimes lead to
a healing response that creates an adhesion between the retina and the
underlying RPE, creating much the same
effect as retinopexy - in this setting retinopexy may not be
An acute U-shaped, horseshoe tear surrounded by laser retinopexy
Retinal holes have a different pathogenesis - they are round atrophic defects in the retina that can occur without
posterior vitreous detachment. They often occur within areas of lattice
Round holes can lead to retinal detachment but it is not proven that
retinopexy reduces this risk and so treatment is seldom advised. Hence an asymptomatic,
flat, small round hole in lattice does not routinely require referral.
If there are several holes or
the view is poor then routine ophthalmology review is justified. A hole
with subretinal fluid should be seen by an
ophthalmologist the same day, as should symptomatic retinal
tears. Asymptomatic retinal tears with signs of chronicity
(pigment change at their border), and no subretinal fluid, can be
seen by an ophthalmologist semi-urgently (1-2 weeks).
Retinal detachment Retinal
detachment is usually occurs when a posterior vitreous detachment pulls
a break in the retina, and vitreous fluid passes into the potential
space between retina and RPE. Detached
retina does not see so the patient experiences an enlarging visual
field defect. If the detachment extends to involve the macular (a
macular-off retinal detachment), then visual acuity drops
Occasionally, chronic retinal detachments are asymptomatic.
retinal detachment include high myopia, complicated cataract
surgery, trauma, a postitive family history, and previous retinal detachment in either
A superior and nasal macular-on retinal detachment
involves one of three strategies: pneumatic
retinopexy, cryobuckle surgery, or vitrectomy/laser/gas. Pneumatic
retinopexy is reserved for a small number of straightforward
detachments; it has the advantage that it is a simple procedure, but it
has a fairly high failure rate, with about 30% of cases going on to
require cryobuckle or vitrectomy. Cryobuckle involves the use of
scleral explants to indent the sclera/RPE in apposition to the retina.
The retina-RPE are then sealed together with a laser
or cryoprobe. Vitrectomy involves removal of the vitreous gel,
and a gas bubble to push the retina onto the RPE from within the eye,
and again, laser or cryoprobes are used to seal the break.
Because of the gas bubble patients have certain restrictions
after surgery and these are outlined in the patient information sheets
posted elsewhere on this website. Occasionally,
retinal detachments are detected during routine optometry examination,
and these can be referred to an opthalmologist semi-urgently (1-2
weeks), however in all other situations patients require same-day
ophthalmology review and shoud be kept nil by mouth. Refer to a
with a Vitreoretinal Service, such as King's College Hospital.
Macular hole The exact
pathogenesis of macular holes is not known but the end result is a
full-thickness defect centred on the fovea. As expected this
produces a central visual defect with blurred vision and distortion. Macular holes are divided into four groups
Stage 1. Impending
Stage 2. Small slit-like break
Stage 3. Full thickness hole
Stage 4. Full thickness hole combined with a posterior vitreous detachment
Macular holes seen on OCT (left) and a fundus photograph (right).
treatment only a small
minority of macular holes resolve and surgery is usually recommended,
unless the macular hole has been present for a very long time (2 years
of more), when the visual prognosis is guarded. Surgery involves
vitrectomy and gas, and leads to hole closure in 80-90% of eyes. Not
all eyes with closure of the hole have visual
improvement but most have an appreciable improvement. Fully normal
vision is seldom achieved. Patients should be referred to a
Vitreoretinal Surgeon, on a routine basis. A patient
information sheet is
Epiretinal membrane An epiretinal
membrane is a thin layer of scar tissue on inner surface of the
retina. It usually occurs at the macula. Contraction of the
membrane causes corrugations in the fovea that distort the patient's
vision, with straight lines appearing bent or bowed. It can occur in
isolation or in association with other eye disease such as
peripheral retinal breaks, posterior uveitis, and trauma.
Treatment involves surgical removal with vitrectomy and membrane
peel. This usually, but not always, improves the distortion.
The effect on visual acuity may be less marked but some benefit
is common. Sometimes the membanes recur and repeat surgery is
required. Patients should be referred to a Vitreoretinal Surgeon, on a routine basis.