These notes summarise the management of common or serious retinal conditions. To navigate to a particular condition click on the link below:
- Age-related macular degeneration
- Diabetic retinopathy
- Retinal vein occlusion
- Vitreous floaters
- Posterior vitreous detachment
- Retinal tears and holes (lattice degeration)
- Retinal detachment
- Macular hole
- Epiretinal membrane
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) established ranibizumab (Lucentis) 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 immediate 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 diabetic 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. Control 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. Non-acute, longstanding floaters, or occasional photopsia can be investigated by an optometrist. Maximal dilation is 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 required.
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 degeneration. 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 precipitously. Occasionally, chronic retinal detachments are asymptomatic. Risk factors for retinal detachment include high myopia, complicated cataract surgery, trauma, a postitive family history, and previous retinal detachment in either eye.
A superior and nasal macular-on retinal detachment
Treatment 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, asymptomatic, chronic 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 centre 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).
Without 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 available here.
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.