How to diagnose and treat exudative macular degeneration?

Diagnosis and Treatment of Exudative (Wet) Macular Degeneration

Diagnostic Approach

Exudative AMD requires multimodal imaging with optical coherence tomography (OCT) as the primary diagnostic tool, supplemented by fluorescein angiography (FA) to confirm choroidal neovascularization (CNV) and guide immediate treatment decisions. 1

Essential Imaging Modalities

• OCT is the cornerstone diagnostic tool that detects subretinal fluid, intraretinal fluid, and highly reflective subretinal lesions corresponding to CNV before clinical examination or FA shows changes 1, 2, 3
• OCT identifies characteristic features including thickening and fragmentation of the retinal pigment epithelium layer, subretinal fluid accumulation, and the presence of CNV as highly reflective subretinal lesions above and separate from the RPE 4, 3
• Fluorescein angiography remains the gold standard for confirming active leakage from CNV and should be performed at baseline and selected follow-up visits to guide treatment decisions 5, 6
• Indocyanine green angiography (ICG-A) may be considered at baseline under certain conditions, particularly for differentiating CNV types 5

Advanced Imaging Technologies

• OCT angiography (OCT-A) is emerging as a powerful non-invasive tool that demonstrates 94.9% correspondence with traditional multimodal imaging for identifying active CNV requiring treatment, though FA remains necessary for detecting leakage 5, 6, 7
• OCT-A enables depth-resolved visualization of CNV without dye injection and can detect non-exudative type 1 neovascularization earlier than conventional methods 5, 7
• Color fundus photography (CFP), confocal fundus autofluorescence (FAF), and near-infrared reflectance (NIR) imaging should be included in comprehensive baseline assessment 5

Clinical Presentation

• Patients present with blurred central vision, metamorphopsia (distorted vision detected by Amsler grid testing), and progressive central vision loss 1
• Wet AMD represents 10-15% of AMD cases but causes faster progression and greater vision loss than dry AMD due to abnormal choroidal blood vessel growth 1

Treatment Algorithm

Initiate intravitreal anti-VEGF therapy immediately upon diagnosis with three loading doses at exactly 4-week intervals, as early treatment within 2 years significantly reduces legal blindness and visual impairment. 1, 8

Initial Treatment Protocol

• Administer three loading doses at 4-week intervals using aflibercept, ranibizumab, or bevacizumab as first-line agents 1, 9
• Perform OCT imaging at each visit to assess for persistent subretinal or intraretinal fluid and guide ongoing treatment decisions 1
• Biomicroscopic fundus examination must accompany each injection visit to monitor for complications 1

Maintenance Regimens

• Aflibercept every 8 weeks after loading phase is an evidence-based maintenance option 1
• Treat-and-extend protocol adjusts injection intervals based on disease activity, extending by 2-week increments when no fluid is present 1
• PRN (as-needed) regimen administers injections only when OCT shows recurrent fluid, though this requires more frequent monitoring 1
• Monthly injections provide the most intensive treatment but increase treatment burden 1

Adjunctive Therapy

• Prescribe AREDS2 supplementation (vitamin C, vitamin E, zinc 25mg, copper, lutein 10mg, zeaxanthin 2mg) to all patients with wet AMD to reduce progression risk in the fellow eye by up to 36% over 10 years 1, 8
• Enforce mandatory smoking cessation as cigarette smoking is the key modifiable risk factor that increases AMD progression proportional to pack-years smoked 1, 8

Monitoring and Follow-Up

• Perform OCT at every treatment visit to detect subretinal or intraretinal fluid requiring continued anti-VEGF therapy 1, 8
• Monitor the fellow eye aggressively every 6-12 months even without symptoms, as patients with wet AMD in one eye remain at exceptionally high risk for bilateral disease 8, 1
• Fluorescein angiography may be necessary at any follow-up visit to evaluate for recurrent or persistent CNV activity 5

Critical Management Considerations

When to Stop Anti-VEGF Therapy

• Discontinue anti-VEGF injections immediately when OCT confirms absence of subretinal or intraretinal fluid and backshadowing represents fibrotic scarring or geographic atrophy, as continued injections provide no benefit 8
• Transition to AREDS2 supplementation and vision rehabilitation services when exudative disease converts to dry atrophy 8

Complications and Adverse Events

• Intravitreal anti-VEGF injections carry risks of endophthalmitis (requiring immediate reporting of symptoms), retinal detachment, and ocular hemorrhage, though these occur at similar rates to sham treatment 1
• Patients must report symptoms of endophthalmitis, retinal detachment, or decreased vision immediately after injection 1

Patient Counseling

• Reassure patients that central vision loss is common but total blindness is extremely rare as peripheral vision remains preserved 1, 8
• Set realistic expectations that vision rehabilitation optimizes existing function rather than restoring lost vision 8, 1
• Screen for depression and Charles Bonnet syndrome (visual hallucinations), which frequently accompany severe central vision loss but do not represent psychosis 1
• Refer immediately to vision rehabilitation services for optical/electronic magnifying devices, bright lights, and reading aids 1, 8

Common Pitfalls to Avoid

• Do not delay treatment initiation while awaiting additional testing, as early treatment within 2 years of diagnosis significantly improves outcomes 1
• Do not rely solely on clinical examination to detect CNV, as OCT identifies disease progression before examination or FA shows changes in 87% of cases 2
• Do not continue anti-VEGF therapy indefinitely without OCT confirmation of active exudation, as fibrotic scarring and geographic atrophy do not respond to anti-VEGF treatment 8