Age-Related Macular Degeneration (AMD)

Pathophysiology & Types

Dry AMD (Non-Exudative)

• Pathophysiology: Characterised by retinal pigment epithelial (RPE) degeneration and the accumulation of drusen (yellowish deposits) beneath the retina. Progression can lead to geographic atrophy, where areas of the RPE and overlying photoreceptors become atrophic.

• Clinical Course: Typically gradual decline in central vision over months to years.

• Signs:

  • Drusen deposits on fundoscopy

  • Macular atrophy in later stages

  • Generally slower progression than wet AMD

Wet AMD (Exudative)

• Pathophysiology: Choroidal neovascularisation develops beneath the retina; new vessels leak fluid and blood, leading to subretinal haemorrhage, exudation, and eventual scar formation.

• Clinical Course: Often rapid and more severe loss of central vision.

• Signs:

  • Metamorphopsia (distortion of straight lines) detectable with an Amsler grid

  • Subretinal fluid or haemorrhages on ophthalmoscopic or OCT (Optical Coherence Tomography) exam

Prevalence

• Dry AMD: Accounts for ~90% of cases, though 2% per year can progress to wet AMD.

• Wet AMD: Although less common, it causes the majority of severe vision loss in AMD.

Risk Factors

1. Non-Modifiable

   • Age >60 (most significant factor)

   • Genetic predisposition (family history)

   • Caucasian ethnicity

2. Modifiable

   • Smoking (strongest modifiable risk factor)

   • Obesity (BMI >30)

   • Hypertension

   • Diet low in omega-3 fatty acids and leafy greens

   • Cardiovascular disease (CVD)

Presentation

• Central Vision Loss

  • Gradual onset in dry AMD

  • Sudden or rapid worsening in wet AMD

• Metamorphopsia

  • Early sign of wet AMD

  • Detected via Amsler grid self-checks

• Functional Impact

  • Difficulty with reading, recognising faces, and fine detail tasks (e.g. driving, crafts)

Management

Shared Measures for Both Dry & Wet AMD

1. Lifestyle Modifications

   • Smoking cessation: Greatest potential to reduce disease progression in smokers

   • Healthy diet: Increase intake of omega-3 (fatty fish) and leafy green vegetables; maintain a BMI <25

   • Blood pressure control and management of cardiovascular risk factors

2. Nutritional Supplements

   • AREDS2 formulation (Age-Related Eye Disease Study 2):

     • Typically contains vitamin C, vitamin E, zinc, copper, lutein, and zeaxanthin

     • Can reduce progression in intermediate and advanced AMD, although not a cure

3. Monitoring

   • Self-check with Amsler grid (ideally daily or weekly) to detect early changes in vision

   • Routine eye reviews:

     • At least every 1–2 years for patients with dry AMD or those at risk

     • More frequent if there is evidence of progression

Additional Management for Wet AMD

1. Intravitreal Anti-VEGF Injections

   • Medications such as ranibizumab, aflibercept, or bevacizumab (off-label)

   • Aim to reduce neovascularisation and stabilise or improve vision

   • Typically administered every 4–8 weeks depending on clinical response

2. Urgent Referral

   • Sudden vision loss or signs of active wet AMD (new metamorphopsia, subretinal fluid/bleeding) warrant urgent ophthalmology assessment

   • Early treatment significantly improves outcomes

Notes:

• Early Identification: Patients with dry AMD should be vigilant for signs of progression (metamorphopsia, acute vision change) and know how to use an Amsler grid.

• Smoking Cessation: Strong recommendation to quit smoking to slow disease progression.

• Anti-VEGF Therapy: A mainstay for wet AMD; can stabilise or improve vision if started promptly.

• Comprehensive Management: Control blood pressure, maintain healthy weight, and optimise diet and exercise to reduce progression risk.