6.1.9 Macular degeneration Flashcards

1
Q

What are the 5 stages of AMD?

A
  1. Early AMD
  2. Late AMD (dry)
  3. Late AMD (intermediate)
  4. Late AMD (wet active)
  5. Late AMD (wet inactive)
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2
Q

How does NICE classify AMD?

A
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3
Q

What are the 9 risk factors for AMD?

A

Age: 65 and over more at risk of AMD, with risk increasing with age

Genetics: FOH AMD are 4-6 x more likely to develop late AMD

Smoking: smokers are 2-3 times more likely to develop late AMD. In females 2.5 x more likely to develop wet AMD, in males 3.2 x

Hypertension: some evidence in association with late AMD

BMI and exercise: overweight/obese increases risk of late AMD, active lifestyle also has proactive effect against wet AMD development

Light: no evidence for increased risk of AMD due to light exposure but College says it is good to advise sunglasses with 100% UVA UVB protection in bright light environments

Gender: More recent evidence shows no evidence for more risk but previously it was thought women more than men (may be because women have longer life)

Race: previous studies said caucasians more at risk but recent evidence is inconclusive and NICE doesn’t say

Nutrition: diet low in omega 3 and 6, vitamins, carotenoid and minerals is a risk factor for AMD. eat a balanced diet with coloured fruit and vegetables and dark leafy veg, increase intake of oily fish, Evidence it can improve depending on the stage:

  • No AMD or early AMD: no evidence for reduced risk with nutritional suppplements
  • Intermediate and/or late AMD: mod quality evidence for reduced risk of progression in px taking AREDS (vitamin C/E, beta-carotene, zinc, copper) or AREDS2 ( AREDS without beta-carotene, with omega 3 fatty acids, lutein and zeaxanthin) formulation (no difference between both in delaying but ARERDS is contraindicated in smokers as beta-carotene increases risk of lung cancer) or antioxident supplements.
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4
Q

What are the layers of the retina, starting from the vitreous cavity?

A
vitreous cavity
inner limiting membrane
nerve fiber layer
ganglion cell layer
inner plexifrom layer
inner nuclear layer
outer plexiform layer
outer nuclear layer
outer limiting membrane
photoreceptor layer
retinal pigment epithelium
Bruch's membrane
choroid
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5
Q

Where is the choroid and what is the function?

A

The choroid is beteen the sclera and retina, it sits below Bruch’s membrane and is made up of choroidal vessels that supply the outer retina- it is important at the macula where retinal circulation is absent

provides 2/3 nutrition to the retina and RPE

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6
Q

What is the purpose of the macula and what is the anatomy?

A

It has the highest concentration of photoreceptors and gives high resolution central and colour vision

horizontally oval and 5 mm in diameter. The foveola is the central floor with a diameter of 0.35mm and is the thinnest part of the retina- thickness is only cone photoreceptors (outer plexiform layer containing Henle fibrrs, cytoplasmic extensions of foveal cones)

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7
Q

What is the purpose of the RPE and the anatomy?

A

The RPE maintains the photoreceptors- it absorbs stray light and forms the outer blood retinal barrier, it also regenerates the visual pigment

It is the highly pigmented layer of the retina which sits between Bruch’s membrane and the neurosensory retina

It is the most metabolically active at the macula (as this is where there is the highest concentration of photoreceptors and retinal circulation is absent); this is also the area where it is most likely to suffer consequence of RPE failue due to the accumulation of metabolic debris and lipofuscin

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8
Q

Where is Bruch’s membrane and what is the purpose?

A

It lies between the choroid and RPE

It controls the exchange of nutrients and waste products

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9
Q

Where is the neurosensory retina and what is it?

A

It is a collection of retinal layers including the retinal nerve fiber layer down to the photorecepto layers- it includes all retinal layers about the RPE

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10
Q

What is the foveal pit?

A

It is the centre of the macula and enables detailed colour vision
It has a large number of cone photoreceptors and no ganglion cells overlying them

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11
Q

How does AMD develop?

A

Undigested metabolic debris and lipofuscin accumulates beneath the retina between Bruch’s membrane and the RPE

In older eyes the debris are not removed and they form drusen (it is thought there may be an inflammatory response element to this)

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12
Q

What is dry AMD?

A
  • It is the early and intermediate stages of the disease
  • Debri build up causes drusen formation and degeneration of RPE
  • Slow and progressive thinning and degerenation of the photoreceptors and RPE leads to failure of central vision
  • 90% only mild to mod gradual visual loss
  • Less aggressive but causes about 20% of AMD related severe visual loss
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13
Q

What are dry AMD clinical features?

A

Drusen:
-many large soft drusen= more likely to develop atrophy and severe visual loss= greater risk of developing wet AMD

Pigmentary abnormalities:
-Hypopigmentation: lighter area of retina compared to rest, this in combination with drusen increases risk of progression to late AMD

-Hyperpigmentation: darker areas of retina compared to surround, this in combincation with drusen increases risk of progression to late AMD

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14
Q

What are the two types of drusen?

A

soft and hard drusen

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15
Q

What is geographic atrophy and what do px experience?

A
  • One or more areas of RPE hypopigmentation
  • loss of overlying photoreceptors with clearly visible choroidal vessels and large area of retinal dysfunction
  • 10% people with dry AMD develop GA
  • bilateral in 50%
  • severe visual loss- especially if at or near the fovea (blank patch in centre of vision))
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16
Q

What is the pathology of wet AMD?

A

It is caused by the growth of new vessels from the choroidal circulation

A choroidal neovascular membrane develops intra-choroidally and then actively proliferates and spreads through Bruch’s membrane to the RPE and subretinal space

The end stage is loss of overlying photoreceptors and fibrosis (disciform scar)

The new vessels leak fluid and bleed causing sub-RPE, sub-retinal or intra-retinal fluid and/or haemorrhages

17
Q

How does a px with wetAMD present?

A
  • Distortion and rapid visual loss, although in early cases vision can be preserved
  • The most extreme and devastating vision loss is usually due to large haemorrhages covering the macula
18
Q

What are fundal features of wetAMD?

A

Fluid on OCT
raised area with indirect ophthalmoscopy
Haemorrhages and/or exudates sometimes
Disciform scar

19
Q

How does a disciform scar develop in wetAMD and how is it classified?

A
  • wet AMD that is untreated or not treated soon enough can lead to fibrous scar formation due to repeated leakage of fluid and blood
  • It is a large elevated patch of scar tissue in the central macular area and causes significant visual loss
  • It is classified by NICE as Late AMD (wet inactive)
20
Q

When would you dilate for px with AMD?

A

All px who have sx of sudden onset recent visual distortion or blurring
All px with dry AMD who have a deterioration in their vision
- use slit lamp VOLK

21
Q

How to investigate a px with AMD?

A

Sx check:
wetAMD px complain of sudden onset reduced vision or distortion- but this can also develop slowly over a few months

those with dry AMD may describe significant change in visual ability if they go on to develop wet AMD

OH: previous signs of AMD or changes at macula, previous VA, previous HES

GH: smoker or ex-smoker? Diabtes, hypertension?

FOH: FHx AMD?

other info: Driver? registered as SI? Impact on life? support from LV services/social services/voluntary organisations

22
Q

What preliminary investigations would you do for AMD px?

A

VA: D+N monoc and binoc VA (if near VA is less than expected from the distance VA then further investigation needed

Refraction: to rule out refractive change as the cause of reduced vision (wetAMD can cause hyperopic shift due to fluid at macula)

Pupil responses: check for RAPS to rule out other causes such as artery and vein occlusions

Amsler: optional as value in detecting treatable AMD is in doubt (30% of cases who went on to have treatment for sub-retinal membranes were detected using Amsler in The West London Survey in 2004

23
Q

What wet AMD px does NICE say is treatable?

A

VA between 6/12 and 6/96
No structural damage to the fovea
Evidence of progressive wet AMD

24
Q

In a dilated fundus exam what would you record presence/absence of?

A
  • Macular drusen
  • Pigmentary changes -hypo/hyper
  • Retinal thickening (oedema and exudates)
  • Any fluid
  • Any haemorrhages
  • Fibrosis
25
Q

How to manage wetAMD?

A

urgent referral

wetAMD rapis access referral form

26
Q

How to manage dry AMD?

A

not generally referred

  • routine may be required if: px requests an opthalmological opinion, a certificate of visual impairment registrstion, no community low vision services available
  • provide information and advice and minimum yearly review
  • can refer to low vision services: will give low vision assessment and loan low vision aids free
  • can refer to social services: urgent- if at risk to themselves or others (e.g. falls/burns/taking meds/crossig rd), soon- at risk of losing independence (e.g. needs kitchen skills training or mobility training), routine-gadgets and advice
27
Q

Would you prescribe glasses for a px getting wetAMD treatment?

A

Rx often changes following and during anti VEGF treatment due to changes in retinal thickness

Preferable not to give new glasses untila fter 3 loading doses and the HES considers macular stable

28
Q

What px information/advice/education would you give?

A
  • Give verbal and written advice (write name and type of condition): Leaflets: macular society, college of optom
  • tell the px how common the condition is and how it will affect them

Treatment: benefits and risk of treatments, suspected wetAMD- explain to px that antiVEGF treatment is intravitreal injection but details will be discussed at HES first

SOS warning: px with dryAMD you need to explain sx of wetAMD e.g. sudde onset distortion or reduction in vision- seek out optometric examination as soon as possible

Smoking: give advise to quit smoking for px who smoke and haves signs of AMD- can go to their GP for support

Nutrition: no evidence supplements help in those with no sign/early AMD, but healthy balanced diet with an increased intake of leafy green veg and oily fish can still be recommended. In those with intermediate or late AMD there is some evidence of delayed progression if ARED or AREDS2 formulation used

Driving: Inform px if you suspect vision is below the legal requirements for driving, advise them to check their vision on a car number plate at 20m

28
Q

What px information/advice/education would you give?

A
  • Give verbal and written advice (write name and type of condition): Leaflets: macular society, college of optom
  • tell the px how common the condition is and how it will affect them

Treatment: benefits and risk of treatments, suspected wetAMD- explain to px that antiVEGF treatment is intravitreal injection but details will be discussed at HES first

SOS warning: px with dryAMD you need to explain sx of wetAMD e.g. sudde onset distortion or reduction in vision- seek out optometric examination as soon as possible

Smoking: give advise to quit smoking for px who smoke and haves signs of AMD- can go to their GP for support

Nutrition: no evidence supplements help in those with no sign/early AMD, but healthy balanced diet with an increased intake of leafy green veg and oily fish can still be recommended. In those with intermediate or late AMD there is some evidence of delayed progression if ARED or AREDS2 formulation used

Driving: Inform px if you suspect vision is below the legal requirements for driving, advise them to check their vision on a car number plate at 20m

29
Q

What are the current treatments for AMD?

A

only for wet AMD

NICE approves treatments are anti-VEGF drugs and Photodynamic therapy (PDT

30
Q

How do anti VEGF drugs work?

A

Vascular Endothelial Growth Factor (VEGF) is a proteing that triggers the formation of new blood vessels- anti VEGF drugs bind to these factors to prevent this- hence preventing leakage
Administered via intravitreal injection

31
Q

How do anti VEGF drugs work?

A

Vascular Endothelial Growth Factor (VEGF) is a proteing that triggers the formation of new blood vessels- anti VEGF drugs bind to these factors to prevent this- hence preventing leakage
Administered via intravitreal injection

32
Q

What are the three antiVEGF treatments available and when does NICE recommend the treatment for them?

A

Ranibizumab (Lucentis)- subfoveal lesions with 0.5mg, after loading dose, every 4 weeks
Aflibercept (Eylea)- subfoveal lesions with 2mg, after loading dose is complete, every 8 weeks
Bevacizumab (Avastin)- not currently licensed for use in the eye but is used ‘off label’ in some units, royal college of ophthalmologists changed guidance to include in 2018

33
Q

What is the treatment regime for antiVEGF?

A

Treat and extend is most widely used regime: px recieves 3 loading doses of the chosen drug separated by 1 month. Then recieve treatment every visit but the separation of the treatments is decided based upon OCT (no fluid on OCT means the time between injection would be extended and if lots of fluid then shortened)

PRN (pro re nata) regime is used but less frequently: px recieves initial 3 loading doses but reviewed monthly and only recieve injection when there is fluid visible on OCT scan

34
Q

When is photodynamic therapy used?

A

PDT with verteporfin has largely been replaced by anti VEGF for more px

used for px with idiopathic polypoidal choroidal vasculopathy (IPCV) either combined with anti-VEGF or PDT alone

May be used for chronic central serous chorioretinopathy

35
Q

How does PDT work?

A
  • Intravenous injection of verteporfin (visudyne)
  • Verteporfin preferentially taken up by the CNV membrane, not the retina so no retinal damage
  • Drug is activated by low powered laser causing damage to proliferating cells and seals/regresses leaking vessels
  • Painless for px
36
Q

Post PDT (photodynamic therapy) what advice would you give px?

A
  • Explain that they will be sensitive to light and to advise that they werar a hat and cover their arms for 48hrs after PDT
  • Will be given tinted glasses to wear for the rest of the day
  • Warn px may experience blurred vision and flashing lights