01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Age-related macular degeneration is a disorder of the macula involving the photoreceptors, retinal pigment epithelium and supporting tissues. Its consequences are often task-specific: letters disappear in the centre of a word, a face becomes difficult to recognise, or a straight edge looks bent. Asking how sight has changed can be more informative than asking only whether the patient can still walk around the room.
Clinical classification should distinguish early or intermediate changes, late atrophic disease, active neovascular disease and inactive scar. The familiar terms dry and wet are useful shorthand but can conceal change. An eye previously described as dry may develop new neovascularisation, and a scarred treated eye may reactivate at its margin. Referral and retreatment therefore respond to current symptoms and imaging rather than an old diagnostic label.
Key points
- AMD primarily affects central vision used for reading and recognising faces; peripheral vision may remain useful.
- Drusen and pigment change establish a risk context, while fluid, haemorrhage and new symptoms raise concern for active neovascularisation.
- Examine and test each eye separately, because a better fellow eye can conceal unilateral deterioration.
- NICE recommends referral for suspected active wet AMD normally within one working day and treatment within fourteen days of referral when indicated.
- Anti-VEGF treatment targets active neovascular leakage; established atrophy or scar may limit how much vision can improve.
- Ophthalmic bevacizumab gamma has a current UK licence and NICE appraisal, so its status differs from repackaged oncology bevacizumab.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Age and susceptibility
Ageing is central to risk, with inherited susceptibility and environmental exposures influencing the course. A family history can inform discussion but does not predict an individual's exact progression.
Modifiable influences
Smoking and broader vascular or nutritional factors contribute to risk and overall health. Smoking cessation is therefore relevant even after AMD is diagnosed and even when an eye already requires injections.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Outer-retinal support failure
Dysfunction of the retinal pigment epithelium and its supporting tissues affects photoreceptor maintenance and waste handling. Drusen and pigment abnormalities can precede clinically important loss of central function.
- 2Atrophic tissue loss
Progressive loss of pigment epithelium and overlying photoreceptors creates areas unable to support normal central vision. The location and expansion of these areas determine the impact on reading and fixation.
- 3Neovascular leakage
Abnormal vessels grow in or beneath the retinal layers and may leak fluid or blood. Persistent activity can disrupt photoreceptors and culminate in fibrosis, explaining the importance of recognising new activity promptly.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Ask about distortion, difficulty reading in ordinary lighting, reduced contrast, missing letters and a central grey patch. Test each eye alone and establish when the change began. The absence of ocular pain is typical and should not reduce concern about newly active macular disease.
Deposits beneath the retinal pigment epithelium and associated pigment changes support AMD in the right clinical setting. Their presence does not mean every new symptom is due to the same mechanism; other macular and optic-nerve disorders may coexist.
Macular haemorrhage, fluid or pigment-epithelial changes with new central symptoms suggest neovascular activity. Some patients report little impairment because the other eye dominates. Imaging can therefore identify activity that is clinically important before the patient describes marked disability.
Atrophy removes functioning outer-retinal tissue, while fibrosis after neovascular disease can produce an enduring central defect. A poor baseline acuity does not by itself establish inactivity; identify any treatable lesion and consider the patient's remaining useful vision and goals.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Monocular acuity and symptom mappingFirst step - Why
- Document the change in central visual function and its effect on daily activities.
- Interpretation and limitations
- Use appropriate correction and ask the patient to describe distortion in each eye separately. Amsler-type assessment can illustrate symptoms but neither a normal grid nor acceptable acuity rules out neovascular activity.
- 02
Dilated macular examination - Why
- Identify drusen, atrophy, blood, scar and competing retinal pathology.
- Interpretation and limitations
- Compare both eyes and previous imaging if available. A new haemorrhage may be a strong clue, but the lack of visible blood does not exclude leakage. Peripheral symptoms or a field curtain require a wider retinal assessment.
- 03
Optical coherence tomography - Why
- Assess retinal and subretinal fluid, pigment-epithelial morphology and structural damage.
- Interpretation and limitations
- NICE recommends OCT for suspected active wet AMD. Interpret apparent cysts with the retinal architecture because degenerative spaces can occur without active leakage. Serial OCT should be assessed alongside vision and examination rather than using thickness as the only outcome.
- 04
Fluorescein angiography when necessary - Why
- Clarify neovascular disease when clinical examination and OCT do not exclude it.
- Interpretation and limitations
- NICE recommends FFA to confirm suspected wet activity when OCT has not excluded neovascularisation, but not when examination and OCT already exclude it. The clinician selects further imaging to resolve uncertainty rather than ordering every test routinely.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Diabetic or venous macular oedema
Intraretinal fluid can arise from diabetic vascular leakage or retinal vein occlusion. The wider retinal pattern and systemic history help distinguish these causes from AMD-related neovascularisation.
Vitreomacular interface disease
An epiretinal membrane or vitreomacular traction may bend retinal architecture and cause distortion. OCT shows the mechanical relationship, which requires a different management discussion from active vascular leakage.
Other central retinal disorders
Central serous disease, macular dystrophy and inflammatory lesions can mimic aspects of AMD. Age, medication exposure, bilaterality and multimodal imaging guide reconsideration when the presentation is atypical.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01ReferralAct on suspected active wet diseaseFirst stepNew central symptoms or examination findings raise suspicion of neovascular AMD.+
- 1Refer directly to the macula service through the urgent route, normally within one working day, even if visual impairment is not yet reported.
- 2Include onset, each eye's acuity, prior AMD and treatment history, examination findings and available OCT without delaying the referral to obtain extra images.
- 3When the diagnosis and treatment indication are confirmed, offer treatment as soon as possible and within fourteen days of referral to the macula service.
02Active treatmentControl neovascular leakage and reassess benefitA specialist confirms active wet AMD with potentially useful benefit from anti-VEGF therapy.+
- 1Discuss available anti-VEGF options, likely injection frequency, procedural risks and the possibility of stabilisation rather than a large visual gain.
- 2Use the selected product's loading and maintenance schedule, adjusting intervals according to disease activity and its licensed regimen.
- 3Investigate unexpected deterioration for recurrent leakage, haemorrhage, atrophy, scar, another ocular diagnosis or a treatment complication.
- 4Discuss stopping when treatment offers no useful benefit or the lesion is inactive with no prospect of functional improvement, and specify the subsequent monitoring plan.
03Atrophic and supportive carePreserve function beyond injection decisionsThe eye has non-neovascular AMD, established atrophy or residual impairment despite treatment.+
- 1Support smoking cessation, a balanced diet and vascular risk management, and explain how to report a new change in either eye.
- 2Assess whether stage-specific discussion of AREDS2 supplementation is relevant, including other medicines, smoking history and the limitations of the evidence.
- 3Offer low-vision assessment, lighting and magnification strategies, reading adaptations and support for emotional and practical difficulties.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Bevacizumab gamma, Lytenava 25 mg/mL
For adult neovascular AMD, administer 1.25 mg in 0.05 mL by intravitreal injection every four weeks initially. Continue monthly until maximum acuity and/or no disease activity; three or more consecutive monthly injections may be needed. Thereafter individualise intervals using visual and anatomical activity. Discontinue if continued treatment gives no benefit and withhold for the product's specified safety triggers.Do not use with ocular or periocular infection or active intraocular inflammation. Withhold for pressure at least 30 mmHg, a retinal break, specified substantial visual loss or subretinal haemorrhage, thromboembolic events, or intraocular surgery in the preceding or planned next 28 days. Do not resume before the next scheduled treatment. Discontinue for rhegmatogenous detachment or stage 3 or 4 macular holes. Review pregnancy individually; effective contraception is needed through treatment and for at least three months afterwards, and breastfeeding requires a specific treatment-versus-feeding decision.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Central visual disability
Reading, recognising people, cooking and medication administration may become difficult while peripheral navigation remains relatively preserved. Functional assessment should capture this pattern rather than equating mobility with adequate vision.
Haemorrhage and fibrosis
Fragile neovascular tissue can bleed and later scar, leaving an enduring central defect. A sudden large deterioration warrants prompt reassessment of lesion activity and other retinal emergencies.
Treatment-related injury
Intravitreal procedures carry risks including infection, inflammation, pressure rise and retinal tears. Reliable post-treatment advice is necessary because early assessment can change the outcome of a complication.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Review each treated eye with acuity, symptoms and OCT at the agreed interval. A patient who reports new deterioration between appointments needs earlier assessment rather than waiting for the next injection slot.
- After an injection, provide a direct urgent contact route for increasing pain, redness, photophobia, floaters or reduced sight. Mild transient irritation should not be used to dismiss a worsening course.
- Monitor the fellow eye and discuss simple monocular self-checks using a familiar task or grid. These checks support symptom awareness but do not replace the prescribed clinical visits.
- Revisit reading, falls, medication management, transport and emotional wellbeing. Consider certification of visual impairment and an eye clinic liaison officer when appropriate; support need not wait until every treatment option is exhausted.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Supplement evidence is stage specific
The NEI AREDS studies support a risk-reduction role for selected people with intermediate AMD or advanced disease in one eye. Supplements do not restore an atrophic macula or treat active leakage, and their benefit should not be assumed in people with no AMD or only early changes.
Smoking changes supplement safety
The original AREDS formulation included beta-carotene, which increases lung-cancer risk in current or former smokers. A discussion of supplementation should distinguish an AREDS2 formulation from an unspecified high-dose eye vitamin and review the total intake from other products.
Licensing is formulation specific
Lytenava is an ophthalmic bevacizumab gamma product with a wet-AMD indication and NICE TA1022 recommendation. This does not convert every bevacizumab preparation into a licensed ocular product or establish a licence for every retinal indication. Identify the exact medicine and indication during consent and prescribing.
Visual hallucinations and adaptation
People with reduced sight may describe formed visual experiences with retained insight. Explore the history sensitively and assess other causes when there is altered cognition or wider neurological change. Clear explanation, visual support and appropriate referral can reduce fear without assuming a psychiatric diagnosis.
11Common pitfallsFrequent interpretation and management errors.
- 01
Do not allow the phrase dry AMD in an old letter to delay assessment of new distortion or macular bleeding.
- 02
Do not wait for vision to fall below a driving threshold before referring suspected active wet AMD.
- 03
Avoid interpreting a single OCT number as a complete activity or prognosis assessment; fluid pattern, tissue integrity and visual change all matter.
- 04
Do not promise that a supplement or injection will reverse established atrophy or fibrosis, and do not omit practical support while treatment continues.