6.1.9 Manages patients presenting with macular degeneration. Flashcards

1
Q

Distinguising between Wet & Dry AMD

Dry vs wet: Symptoms

A

DRY:

Initially asymptomatic, then…
Gradual reduction in VA
Metamorphopsia
Central scotoma (when advanced)

WET:

Sudden reduction in VA (<6/12)
Metamorphopsia
Central scotoma

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2
Q

Dry vs wet: Signs

A

DRY:

Drusen
Focal hyper/hypopigmentation
Geographic atrophy

WET:

Drusen & pigment abnormalities
Haemorrhage
Hard exudates
Retinal elevation
Pigment epithelial detachment (PED) leads to disciform scarring

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3
Q

Complications of AMD

A
  • Serous fluid leaks from the choriocapillaris passing through Bruch’s membrane, leading to an RPE detachment.
  • Must understand difference between Occult & Classic & Combination!
    • Occult happens below RPE
    • Classic happens above RPE after getting through chroid so worse prognosis!
    • Both generally have a green-greyish lesion on the macula and generally haemorrhaging. Occult will look less distinct but classic is more well defined and delineated
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4
Q

Establishes Patient Needs & Visual Function with AMD

A
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5
Q

Risk factors

A
  • Age ^
  • Race - late AMD more common in Caucasians
  • Gender – females > males
    o Greater risk possibly due to longevity
  • Heredity – risk of AMD is up to 3 times as high if first-degree relative has the disease
  • Smoking - doubles risk (2-3x) of AMD
    o Tar of cigarettes = hydroquinine = oxidative stress = DRY
    o Nicotine = induces capillary formation = WET
  • Hypertension & other cardio-vascular risk factors (vascular disease > ischaemia/accumulation of waste products > degeneration of RPE)
  • Dietary factors
    o Low in omega 3 & 6, vitamins, carotenoids, and minerals
    o High fat intake, obesity, excessive alcohol consumption
    o BMI of 30 = higher risk
  • Aspirin – evidence is limited
  • Females – greater risk possibly due to longevity
  • Cataract surgery – can speed up progression from dry to wet
  • No evidence for increased risk of AMD due to light exposure
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6
Q

Stages of Dry AMD and their defininition

A

No apparent ageing changes: No drusen, No AMD, pigmernaty changces
Normal ageing chancges: only druplets, no AMD pigmentory changes
Ealry AMD: Medium drusen (63um-125um), no amd pig changes
Intermediate AMD: Large drusen 125> um
Late AMD : Neovasc or geographic atrophy

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7
Q

Stages of wet AMD

A

 Late AMD (wet active)
o CNV
o Ocular (fibrovascular PED / serous PED with neovascularisation
o Mixed predominantly or minimally classic CNV with occult CNV)
o Retinal angiomatous proliferation (RAP)
o Polypoidal choroidal vasculopathy (PCV); macular neovasc, occurs more in African Americans & Asians

 Late AMD (wet inactive)
o Fibrous scar
o Sub-fovea; atrophy or fibrosis secondary to an RPE tear
o Atrophy
o Cystic degeneration
o Eyes still may develop of have recurrence of late wet active AMD

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8
Q

Management: Dry

A

 No treatment available - prophylaxis only
 Address risk factors – first you would advise to modify = smoking
 Other risk factors to address dietary/alcohol
o Encourage diet rich in leafy greens / omega 3 & omega 6/fatty acids
o Diet rich in vitamin C and E
Antioxidants are also availble!

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9
Q

Antioxidants

A

 Antioxidants to reduce free radical damage by giving an electron to a free radical to prevent the chain reaction and stop them from causing damage
 Lutein, zeaxanthin and meso-zeaxanthin and xanthophylls – 3 main macular pigments = act as antioxidants
 Carotenoids = antioxidant
 Macushield - contains 3 carotenoids including zeaxanthin
 Optihealth - contains lutein and zeaxanthin; vitamin A; manganese also helps protect against free radicals
o Some evidence that Vitamin A supplements should not be given to smokers as it may increase the risk of lung cancer

 Amsler to monitor progression from dry to wet
 Low vision aids if necessary
 Glasgow and great Clyde guidance
o AMD/VA/amsler stable no referral
o Reduced VA/amsler distortion – routine

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10
Q

Wet referral?

A

 Wet AMD fast-track referral on SCI gateway (1-2 weeks)
Anti-VEGF
 Most used treatment
 Criteria – 6/12 or worse
 Avoids the proliferation of new & unhealthy blood vessels
 Visual prognosis
o 25% cases VA improves
o 90% VA remains stable
 Ranibizumab (lucentis) – approved by NHS Scotland & NICE - £742
o Initial loading dose – 3 injections, every 4 weeks
o Maintenance injections usually 1-3 months, for as long as necessary
o Effective for all lesion types
 New drug – Brolucizumab (Beovu) – now approved by NHS Scotland & NCE, can increase time between appointments to 12 weeks – minimize treatment burden for patients

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11
Q

Other historical treatments

A

 Laser photocoagulation – few cases suitable, not usually justified
o Laser destroys new choroidal vessels at the cost of destroying nearby retinal cells – does not prevent recurrences
o Immediate reduction in VA, but better VA in long term
o Benefit only significant after 6 months of treatment
o Still approved but basically been abandoned for anti-VEGF
o
 Photodynamic treatment to occlude new blood vessels in CNV
o Uses verteporfin – highly-reactive oxygen molecules damage the choroidal neovascular endothelium = thrombosis of subretinal choroidal network
o Reduces chance of significant visual loss – no improvement in VA
o Cost-Ineffective

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12
Q
A
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