Age related Macular Degeneration Flashcards

1
Q

EPIDEMIOLOGY

A

Commonest cause of untreatable blindness in people over 60 years of age in the Western world.

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2
Q

CLASSIFICATION

A
  1. Atrophic or dry type: avascular degenerative changes.

2. Exudative or wet type: subretinal neovascularisation.

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3
Q

CLINICAL FEATURES

A

SYMPTOMS
1. Painless < in VA to 6/60 or worse in a comfortable white eye:
Dry: gradual decrease over many years.
Wet: sudden visual loss may occur due to haemorrhage or exudation.
2. Metamorphopsia: image distortion due to retinal distortion occurs mainly in the wet type.
3. Symptoms of a central or paracentral scotoma.
4. symptoms or signs of subretinal neovascularisation: sudden loss of vision, metamorphopsia, haemorrhage, exudation or scarring

SIGNS
1. Decreased visual acuity.
2. Metamorphopsia or a central scotoma on Amsler grid.
3. Fundoscopy
Dry type
(i)Drusen: round yellowish spots of various sizes visible subretinally.
(ii) Pigmentchangesinthemaculararea.
Wet type
(i) Drusen
(ii) Consequences of subretinal neovascularisation:
-Leakage under the RPE and/or neuroretina
-Haemorrhage under the RPE and/or neuroretina
-Scar formation under and in the neuroretina

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4
Q

SPECIAL INVESTIGATIONS

A

fluorescein angiography if subretinal neovascularisation –> confirm neovascular membrane and define its position and size.

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5
Q

TREATMENT

A

General:

  1. Optimal spectacles
  2. Inform patients: total blindness never occurs. Some functional vision is always retained as the peripheral visual field always remains unaffected.
  3. Low vision aids such as magnifiers, telescopes and illumination devices are available, but patients need to be well educated and motivated to work with them.
  4. Patients motivated to maintain independence.
  5. Patients must be made aware of the services available in the community such as large print books and books on tape.

SPECIFIC MANAGEMENT
DRY TYPE
There is no specific treatment which affects the natural progression of the disease.

WET TYPE

  1. Neovascularisation–>urgent referral: within days to weeks.
  2. Self monitoring with an Amsler grid for early signs of progression.
  3. Laser photocoagulation (hot laser): thermal destruction of accessible parts of the neovascular membrane.
  4. Photodynamic therapy: photosensitising drug–> attaches to the neovascular membrane–> “cool” laser activate the drug in the eye–> produce oxygen free radicals which selectively destroy the neovascular membrane with minimal collateral damage.
  5. Intravitreal injection of anti-VEGF agents: target the subretinal neovascular process selectively and so produce minimal collateral damage.
  • tend to slow, but do not stop, the progression of the disease.
  • efficacy of all these therapies is dramatically < if > haemorrhage and scarring occurs, making early recognition of the condition and appropriate referral crucial.
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6
Q

Cause

A
  1. increasing age–> it is rare <50 years.
  2. Strong familial associations.
  3. Genes involved in inflammation.
  4. Environmental factors also appear to be important.
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