Ophthalmology - Gradual Loss of Vision Flashcards
What are cataracts?
Cataracts = Common eye condition where the lens of the eye progressively opacifies
Epidemiology:
- Women > men
- Incidence ↑ with age
Features:
- ↓ visual acuity
faded colour vision (difficult to distinguish colours)
- glare - lights appear brighter than normal
- halos around lights
- defect in red-reflex - cataract prevents light getting to retina thus preventing the red reflection of light off the retina
Investigations:
- Ophthalmoscopy w/ pupil dilation - normal fundus + optic nerve
- Slit lamp exam - visibile cataracts
What is the most common cause of cataracts?
What other causes of cataracts are there?
Normal ageing process (commonest cause)
Other causes:
- Smoking
- High alcohol consumption
- Diabetes
- Long-term corticosteroids
- Myotonic dystrophy
- genetic muscular disorder, muscles contract and unable to relax - thus progressive atrophy + weakness - Radiation exposure
- Trauma
How are cataracts managed?
Non-surgical - stronger glasses / lenses, use brighter lighting (nothing can slow down the progression of cataracts)
Surgery:
- commonest operation in the UK
- decision depends on; impact on QoL, degree of visual impairment
- remove cloudy lens + replace with artificial lens
- high success rate = 85-90% of pts achieve 6/12 post op
What are the complications of cataract surgery?
Complications are rare!
Bleeding - choroidal haemorrhage
Posterior capsule:
- opacification (thickening of posterior lens capsule)
- rupture
Endophthalmitis - inflammation of aqueous and/or vitreous humour
- Retinal detachment
- Glaucoma
What is the difference between open-angle and closed-angle glaucoma?
Open-angle:
- Iris IS NOT occluding trabecular network i.e. angle between cornea and iris is ‘open’
- ↑ IOP is due to ↓ functional clearance of aqueous humour by the trabecular network –> build up of aqueous humour in the anterior chamber
- Chronic, progressive condition
Closed-angle:
- Iris IS occluding the trabecular network i.e. angle between cornea and iris is ‘closed’
- ↑ IOP is due to blockage of trabecular network –> causing build up of aqueous humour in the anterior chamber
- Acute, eye emergency!
What are the risk factors for primary open-angle glaucoma (POAG)?
Risk factors:
- Genetics - 1st degree relatives of POAG pt have ~16% of POAG
- Old age
- Black pts
- Myopia (short-sighted)
- HTN
- Diabetes
- Corticosteroids
- Thin cornea
- Wearing tight collar and tie
What are the features of POAG?
Symptomless for a long period
Features of POAG:
- progressive peripheral field loss - often nasal scotomas –> then ‘tunnel vision’ (see image for visual field loss)
- ↓ visual acuity
- Painless
Fundoscopy:
- optic disc cupping (cup:disc ratio ↑ e.g. > 0.7)
- pale optic disc
- ‘bayonetting of vessels’ - vessels have kinks as they cross into the cup
How is POAG investigated?
Applanation tonometry e.g. Goldmann tonometer - to measure IOP ( 10-20 mmHg = normal)
- involves flat-tipped cone coming into contact with cornea to measure pressure required to flatten
Central corneal thickness measurement
Gonioscopy
- to assess anterior chamber depth and iridocorneal angle (between iris and cornea)
Slit lamp exam - may see optic nerve head damage e.g. cup:disc ratio > 0.7
Automated perimetry - assess visual fields
How is POAG managed?
Mainly with eye-drops!
1st line = Prostaglandin analogue (PGA) eyedrop e.g. Latanoprost once daily
- ↑ uveoscleral outflow
- Adverse effects: brown pigmentation of iris, ↑ eyelash length
2nd line:
Beta-blocker
- e.g. timolol, betaxolol
- ↓ aqueous production
- avoid in asthma + heart-block
Carbonic anhydrase inhibitor
e. g. dorzolamide
- ↓ aqueous production
- can cause Stevens–Johnson syndrome, toxic epidermal necrolysis
sympathomimetic eyedrop
e. g. brimonidine (alpha-2 adrenoreceptor agonist)
- ↓ aqueous production + ↑ outflow
- avoid if on MAO-inhibitors or TCAs
- Adverse effects: hyperaemia
3rd line = surgery / laser treatment
How is aqueous humour drained?
Drained via 2 mechanisms:
Trabecular meshwork - located between iris and cornea - drains aqueous humour into Schlemm's canal drains ~90% of aqueous humour - is IOP dependent
Uveoscleral drainage
drains ~10% of aqueous humour
- is IOP independent
What are the risk factors for Acute close-angle glaucoma (AACG)?
Risk factors for AACG:
- women
- hypermetropia (long-sightedness)
- pupillary dilatation
- age - lens growth association with age
What are the features of AACG?
Features of AACG:
- Unilateral Pain (can be severe) - may be ocular or progressive headache
- ↓ visual acuity
- symptoms worse with mydriasis (e.g. pupil dilation when watching TV in a dark room)
- Red-eye + hard
- Haloes around lights
- ↑ IOP - typically > 40 mmHG
- Semi-dilated, non-reacting pupil - iris ischaemia due to ↑ IOP can cause this
- Dull / hazy cornea - due to corneal oedema
- systemic upset may be seen: nausea & vomiting / abdominal pain
How is AACG managed?
Urgent referral to opthalmologist
1st line:
carbonic anhydrase inhibitors e.g. dorzolamide (eyedrop) or acetazolamide (oral)
- ↓ aqueous secretions
- topical > oral
beta-blockers e.g. timolol or betaxolol (eyedrops)
Alpha2 adrenergic agonist e.g. bromonidine (eyedrops)
Adjunct:
Pilocarpine - if AACG is secondary to pupillary block
- muscarinic ACh receptor agonist
- pupillary contraction –> increases space for flow of aqueous humour
Mannitol - osmotic agent, draws fluid into vasculare compartment
- ↓ IOP + ↓ intracranial pressure
- ↓ blood viscosity –> ↑ cerebral blood flow –> autoregulatory vasocontriction which may ↓ ICP
2nd line:
Laser peripheral iridotomy - laser hole in iris to equalise pressure between posterior + anterior chamber (relieves pupillary block)
- This is also done prophylactically in the other eye if it has signs of ↑ IOP
Anterior chamber paracentesis
What is the commonest cause of blindness in the UK?
Age-related macular degeneration
What is age-related macular degeneration (ARMD)?
Degeneration of the central retina (macula), usually bilaterally
Characterised by degeneration of retinal photoreceptors that results in the formation of drusen (seen on fundoscopy)
Drusen = yellow lipid deposits under the retina (see image)
- Avg age on onset > 70yrs
- Women > men
What are the risk factors for ARMD?
Risk factors:
- AGE!! (biggest factor)
- Smoking
- 1st degree relatives with ARMD
- cataract surgery
Risk factors for ischaemic heart disease:
- HTN
- Dyslipidaemia
- Diabetes
What are the features of macular degeneration?
Features:
- Progressive loss of vision in 1 or both eyes
- Subacute blurring or distortion of vision (indicates ‘wet’ form)
- ↓ visual acuity (particularly for close objects)
- ↓ night vision and ability to adapt to dark
- fluctuations in visual disturbance (varies day-to-day)
- may experience photopsia (perception of flickering or flashing lights) + glare around objects
Signs:
- Distortion of lines on Amsler grid testing (see image)
- Drusen on fundoscopy
- Demarcated red patches (intra-retinal or sub-retinal haemorrhage or fluid leak - seen in ‘wet’ ARMD)
How do you investigate macular degeneration?
Slit lamp exam + colour fundus photography
- Identify exudative or haemorrhagic changes (‘wet’ ARMD)
Fluorescein angiography
- Identify neovascular ARMD (used to be called ‘wet’) - neovascularisation can indicate anti-VEGF therapy
Ocular coherence tomography
- Provides 3D image of retina to identify pathology not seen with microscopy alone
What are the types of ARMD?
Early age-related macular degeneration (dry / non-exudative):
- Drusen present
- Alterations to retinal pigment epithelium
- 90% of cases
Late age-related macular degeneration (wet / exudative):
- Choroidal neovascularisation
- Leakage of serous fluid / haemorrhages
- 10% of cases
- Worse prognosis
How is ARMD managed?
Refer to retinal specialist opthalmologist
Risk factor modification:
- smoking cessation
- low glycaemic index diet (avoid diabetes)
- ↓ cholesterol
- managed HTN
Zinc, anti-oxidant vitamins A, C + E, copper:
- For moderate ‘dry’ ARMD - shows some benefit in reducing progression
anti-VEGF:
- can limit progression in ‘wet’ AMRD
- administer in < 2 months of diagnosis
- given as 4-weekly injection
- e.g. ranibizumab, bevacizumab and pegaptanib
Who must pts diagnosed with POAG inform of their diagnosis?
Family - there is a genetic risk component for glaucoma
DVLA
What are the most common causes of sudden, painless loss of vision?
ISCHAEMIC / VASCULAR: e.g. occlusion of central retinal artery / vein
large artery disease e.g.
- atherothrombosis
- embolus
- dissection
small artery occlusive disease e.g.
- anterior ischemic optic neuropathy - occlusion of short posterior ciliary arteries –> causing dmg to optic nerve
- vasculitis (e.g.) temporal arteritis
venous disease
hypoperfusion
OTHER CAUSES:
- vitreous haemorrhage
- retinal detachment
- retinal migraine - aura of only one eye (can include temporary blindness)
What is the medical term for sudden, painless, loss of vision?
Amaurosis fugax
Define: painless, temporary loss of vision in one or both eyes
N.B. a minority of pts describe this as the classic “black curtain descending”
