Gradual visual loss

Question 1

What is dry AMD?

Answer 1

Usually bilateral
Dry is more common and less severe than wet AMD and causes gradual central vision loss due to macula death (issue with faces/ reading).
In mild Dry AMD you see soft drusen that are focal degenerative changes (partic thickening) in Brusch’s membrane which separates the choroid from the RPE. Pigmentation spots in the macula are also visible. Usually sight is unaffected by these changes.
As AMD progresses, RPE + choroidal capillaries atrophy which causes secondary atrophy of the photoreceptor cells. (RPE provide metabolic support for photoreceptors).
Accounts for 90% AMD but only 10-20% of severe visual loss.

Question 2

What is wet AMD?

Answer 2

Usually bilateral
Due to subretinal proliferation of new blood vessels (neovascularization) which are from the inner choroid. The vessels proliferate under Bruch’s membrane before penetrating the membrane via breaks that are a consequence of soft diffuse drusen. These breaks may provide sites through which new blood vessels grow and proliferate from the choroid into the RPE/ photoreceptor layer. These blood vessels are fenestrated and cause a puddle of plasma to lift the retina and create a “blister”/ oedema under the retina. This results in a curved retina. Photoreceptors die due to “dangling” in toxic plasma. These vessels are also prone to bleed cause sub/retinal haemorrhage. A fibrovascular scar will develop.
First sign- distorted vision e.g. curved lamppost
Relatively rapid onset and severe sudden central vision loss can occur if untx.

Question 3

What are the RF for either type of AMD?

Answer 3

smoking, age >50, CVD disease (HT, Hyperlipidaemia), low antioxidant levels in the blood.

Question 4

What are the effects of Macular Degeneration on a patient?

Answer 4

loss of independence due to difficulty with shopping, reading, use of the telephone, prepping meals, managing money and increased risk of falling. These individuals are more likely to suffer from emotional distress and depression.

Question 5

How might a person with poor vision resulting from AMD be assisted in coping with this problem?

Answer 5

“Visual rehabilitation” i.e. by an OT who assesses and trains patients to continue with activities at home with modifications e.g. lighting or with adaptive devices (for measuring things)
Registration as visually impaired to enable access to social services.
Support groups and societies.
Low vision aids: magnifiers, audio tools,
mobility services

Question 6

How do you investigate/evaluate AMD? How is wet AMD characterised?

Answer 6

Visual Acuities (near and distant)
Central visual field
Reading speed
Contrast sensitivity (Bright is not always better, must be sig contrast)
Fundus pics
OCT optical coherent tomography (shows layers of retina)
Angiogram (shows leaks)

extrafoveal (far from fovea)
subfoveal (under fovea)
juxtafovea (close to fovea)
leakage of vessels (obvious/ not/ mixed)

Question 7

How is AMD managed?

Answer 7

NO Tx for Dry AMD

1. Anti-VEGF injections First line
   injected into vitreous at 4/52 intervals interrupting factors stimulating neovascularization
   e.g. Pegaptanib sodium, Ranibizumab
2. Focal Laser Photocoagulation
   non-selective laser + destruction of abnormal blood vessels but also damage overlying retina. recurrence in 50%. Only used in extrafoveal lesions (far from fovea) and those with obvious leakage. Can cause loss of acuity and absolute scotoma.
3. Photodynamic therapy (PDT)
   inject dye into eye which travels through Retinal layers into choroid and absorbed by vessels. Non thermal light activates dye to causes localised endothelial damage thrombosing and occluding the abnormal vessels. 3/12 repetition.

Question 8

What are the types of cataracts?

Answer 8

1. congenital due to

2.