Gradual Loss of Vision

Question 1

What commonly causes gradual loss of vision?

Answer 1

Cataracts
Macular Degeneration 
Glaucoma 
Diabetic Neuropathy 
Hypertension 
Slow retinal detachment

Question 2

What are the cut off definitions for partial sighted registration and severe visual impairment or blind?

Answer 2

Partial sighted registration criteria - <6/60 or >6/60 but with visual field restrictions
Severe visual impairment (blind) - <3/60 or >3/60 but with substantial visual field defects

Question 3

What is AMD or age related macular degeneration?

Answer 3

Most common cause of irreversible blindness in the developed world. Most common in the elderly. AMD occurs as a result of drusen (calcified mitochondria) and bleeding into the macula. Over time this progresses to optic atrophy (pale well demarcated disc) and central retinal degeneration bilaterally.

Question 4

What are the risk factors for age related macular degneration?

Answer 4

Increasing age 
Family history 
Smoking 
Cardiovascular disease, HTN etc. 
Cataract surgery 
Ethnicity – Caucasian

Question 5

How does AMD present?

Answer 5

Deteriorating central vision
At first no loss in vision just difficulty making out images
Especially problems with faces and reading
Particular difficulty with low light or changing light conditions
Fluctuation in vision
Photopsia (flickering/flashing lights)
Glare around objects

Question 6

How should suspected AMD be investigated?

Answer 6

Slit lamp microscopy and fundoscopy is investigation of choice – drusen (yellow areas of pigment deposition) or red patches representing intra or sub retinal fluid leakage or haemorrhage
Acuity and visual fields
OCT to reveal areas of disease not visible to microscopy
Fluorescein angiography to guide treatment with anti-VEGF if neovascularisation excluded from OCT and clinical investigations

Question 7

What is different about wet AMD?

Answer 7

Wet AMD/exudative – Early and Late
This occurs as a result of the development of choroidal neovascular membranes under the retina. These can leak blood causing a central disciform scar. Vision will decrease rapidly. Ophthalmoscopy and OCT shows fluid exudation under the retina. Rapid treatment is required.

Question 8

How is wet AMD managed?

Answer 8

Stop smoking
Diet rich in green vegetables
Fluorescein angiogram then 4-6week reviews with retinal imaging and OCT
Anti-VEGF injections such as bevacizumab, pegaptanib and ranibizumab - within 2 months and 4, weekly injections
Photocoagulation may be useful in some specific cases

Question 9

How is dry AMD managed?

Answer 9

Dry AMD/non-exudative – Early and Late

Much slower (over decades) visual loss. Unclear aetiology. Prevention is the best treatment for this disease and much of the evidence suggest it is genetic. Particularly antioxidant vitamin and mineral supplements are recommended.

Zinc oxide and antioxidant vitamin A, C and E are best at reducing progression. – note contraindicated if smoking due to beta carotenes increasing risk of lung cancer.

Question 10

What is chronic glaucoma?

Answer 10

Optic neuropathy with characteristic visual field defects and death of retinal ganglion cells. IOP may be raised but is not actually part of the definition. If raised IOP is found, then lifelong follow up is required. In open angle glaucoma the iris is clear of the trabecular meshwork.

Question 11

How is intraocular pressure controlled by the body?

Answer 11

Autonomic control of IOP
This is via adrenergic receptors. Cholinergic mechanisms have little direct effect on aqueous production.
• Alpha 2 receptors – stimulation reduces IOP by reducing aqueous production and may increase uveoscleral outflow
• Beta 2 receptors – stimulation increases IOP by increasing aqueous production

Question 12

What are the risk factors for open angle glaucoma?

Answer 12

Increasing age 
Black race
Family history – those with 1st degree family history should be screened yearly from age 40 
Raised IOP 
Hypertension 
Diabetes 
Myopia 
Steroid use

Question 13

How does chronic glaucoma present?

Answer 13

Asymptomatic until visual field defects (hence screening) – usually a sausage shaped (arcuate) nasal scotoma around the blind spot which progress to tunnel vision.
Decreased visual acuity and Optic disc cupping

Question 14

What investigations should be done in suspected chronic glaucoma?

Answer 14

IOP measurement with tonometry
Central corneal thickness measurement (as a thick cornea can cause a false positive raised IOP)
Peripheral anterior chamber configuration and depth assessment using gonioscopy (measures the angle between the iris and the cornea)
Visual field measurement – automated perimetry
Optic nerve assessment (fundoscopy) with dilated pupil signs include
1. Cupping
2. Atrophy
3. Vessels bayonetting (disappearing and reappearing)
4. Cup notching

Question 15

When is a diagnosis of glaucoma made?

Answer 15

Diagnosis can be made when there are 3 or more locations of optic field testing that are outside normal limits and the cup to disc ratio on fundoscopy is greater than is considered normal.

Question 16

Who is offered screening for glaucoma and what does it involve?

Answer 16

Screening is free and is offered to those with risk factors over the age of 35. It involves tonometry, visual fields and optic disc assessment.

Question 17

After a diagnosis of glaucoma how often are patients followed up?

Answer 17

Once diagnosed regular follow up is required. 4-6monthly visits if IOP not conforming otherwise 1-2 years is fine.

Question 18

What is the 1st line management of glaucoma?

Answer 18

Reduce IOP but it is unclear how affective this is at stopping glaucoma. Surgery is also an option if drugs fail.

1st line
Prostaglandin analogues – latanoprost, bimataprost or travoprost these increase uveoscleral outflow. SE = red eye, iris colour change, periocular skin pigmentation and eyelash growth

Question 19

What’s the second line management for glaucoma?

Answer 19

2nd line
Beta blockers – timolol, carteolol or betaxolol these reduce production of aqueous. SE = dry eyes, cornea anaesthesia and reduced exercise tolerance
Alpha 2-adrenergic agonists – brimonidine or apraclonidine these reduce production of aqueous and increase drainage. SE = lethargy and dry mouth.
Carbonic anhydrase inhibitors – dorzolamide and brinzolamide or acetazolamide (TABLETS) these reduce production of aqueous. SE = lassitude, dyspepsia, low K+ and paraesthesia. Avoid if pregnant.
Miotics – pilocarpine these reduce resistance to aqueous flow. SE – miosis, brow ache and reduced acuity
Sympathomimetic – dipivefrine which reduces aqueous production and increases outflow. SE = sore, smarting, red eyes and reduced vision

Question 20

What is 3rd line management for glaucoma?

Answer 20

3rd line
Laser therapy = trabeculoplasty – to increase aqueous flow. Similar to medical management for efficacy but may be more cost effective.
Surgery – trabeculectomy and establishment of a pressure valve in the limbus.

Question 21

What are cataracts?

Answer 21

Any opacity found in the lens and is the leading cause of blindness worldwide. They are extremely common and found in 75% of >65s.

Question 22

What are the risk factors for cataracts?

Answer 22

Increasing age and female
Genetic in children 
Diabetes (should always measure BM when a cataract is found) 
Steroid use 
High myopia 
Smoking 
Alcohol excess
Sunlight exposure 
Trauma 
Radiotherapy 
HIV

Question 23

Describe the clinical features of cataracts?

Answer 23

Blurred vision and faded colours
May be asymptomatic if unilateral but may have difficulty with distance judgements
Gradual painless loss of vision in bilateral cataracts (frequent eye prescription changes)
Monocular diplopia
Especially problems at night with haloes around street lamps
Defect in the red reflex

Question 24

How is the diagnosis of cataracts made?

Answer 24

Ophthalmoscopic and slit lamp examination – lens appearance with loss of red reflex and difficulty seeing fundus.

Question 25

Describe the 3 main types of cataracts?

Answer 25

Nuclear cataracts – involves the lens nucleus, change in refractive index causing myopia and dulling colours
Cortical cataracts – involves cortex, causes astigmatism with worst symptoms in the dark
Subcapsular cataracts – directly under the lens capsule, faster progression and cause bright glare from sunlight affecting near vision more.

Question 26

How are cataracts managed?

Answer 26

Can use mydriatic drops, sunshades, higher prescription and sunglasses but if symptoms are severe or need to see for work surgery is the best treatment.

Question 27

Describe the surgery involved in cataracts?

Answer 27

Ideally day case local anaesthetic with small incision, phacoemulsion and intraocular lens implant. GA is an option if required. Ocular biometry must be done prior to the surgery to measure corneal thickness and globe length to decide on lens implant choice.

Usually return home same day with a small dressing and can begin normal activities next day. Go home with antibiotics and anti-inflammatory drops for 3-6 weeks

Question 28

What are the common complications following cataracts surgery?

Answer 28

2% get serious complications and glasses may still be needed.
Retinal detachment, posterior capsule rupture and endophthalmitis (inflammation of the aqueous or vitreous humour)
Most common post op complication is posterior capsule thickening – appears like a cataract is returning but can easily be resolved.

Question 29

How are congenital cataracts managed?

Answer 29

If seen at birth or in the early years, then patients must be seen by an ophthalmologist within 4 weeks. This is because surgery must be done in the first 6 weeks of life during the latent period of visual development.