Ophthalmology Flashcards
aetiology of acute angle-closure glaucoma
optic neuropathy due to raised IOP
RFs (impairment to aqueous outflow)
- hypermetropia (long sightedness)
- pupillary dilatation
- lens growth associated w age
px of acute angle-closure glaucoma
- haloes around lights
- semi-dilated non-reacting pupils
- severe pain
- worse with mydriasis
- hard, red eye
- corneal oedema -> dull or hazy cornea
- decreased visual acuity
acute angle-closure glaucoma ix & mx
ix
- tonometry to check for elevated IOP
- gonioscopy - slit lamp lens which allows for visualisation of the angle
Mx
- urgent opthal referral
initial:
- combination eye drops (direct parasympathomimetic- pilocarpine, beta blocker- timolol, alpha-2 agonist- apraclonidine)
- IV acetazolamide
definitive mx
- laser peripheral iridotomy
(tiny holes in peripheral iris)
Age-related macular degeneration aetiology
Degeneration of the central retina (macula)
degeneration of retinal photoreceptors that results in the formation of drusen
Drusen may become confluent in late disease to form a macular scar
most common cause of blindness in the UK
ARMD RFs
advancing age (!!)
smoking
family hx
cvd rfs
dry macular degeneration features (ARMD)
a.k.a atrophic / early ARMD
90% of cases
drusen -> yellow round spots in Bruch’s membrane
Gradual reduction in visual acuity
alteration to retinal pigment epithelium (RPE)
wet macular degeneration features (ARMD)
a.k.a exudative / neovascular/ late ARMD
Choroidal neovascularisation
Leakage of serum fluid & blood
10 % of cases
worst prognosis
subacute reduction in visual acuity
ARMD px
Reduction in visual acuity, esp near field objects
Difficulties in dark adaption
Poor night vision
Daily visual fluctuations
Photopsia (flickering/ flashing) lights
Glare around objects
Charles-Bonnet syndrome - visual hallucinations
ARMD ix
Amsler grid testing -> distortion of line perception
Fundoscopy/ Slit lamp microscopy -> drusen (yellow pigment deposition in macula), pigmentary, exudative or haemorrhagic changes of retina
if neovascular ARMD: Fluorescein angiography -> to guide anti-VEGF therapy. Add indocyanine green angiography to visualise choroidal circulation changes.
Optical coherence tomography -> 3D retinal visualisations to reveal areas of disease which aren’t visible using microscopy alone
ARMD tx
Dry
- combination of zinc with anti-oxidant vitamins A,C and E
Wet
- vascular endothelial growth factor (VEGF)
— e.g. ranibizumab, bevacizumab and pegaptanib
— 4 weekly injection, start w/in first 2 months
- laser photocoagulation (complication: acute visual loss)
Allergic conjunctivitis tx
(usually seen in context of hay fever)
first-line: topical or systemic antihistamines
second-line: topical mast-cell stabilisers, e.g. Sodium cromoglicate and nedocromil
Anterior uveitis associations
HLA-B27
Ankylosing spondylitis
reactive arthritis
Ulcerative colitis
Crohn’s disease
Behcet’s disease
Sarcoidosis: bilateral disease may be seen
Anterior uveitis mx
urgent review by ophthalmology
cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate
steroid eye drops
Argyll-Robertson pupil px & aetiology
small, irregular pupils
no response to light but there is a response to accommodate
Causes
- diabetes mellitus
- syphilis
mnemonics
- Argyll-Robertson Pupil (ARP) is Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)
- prostitutes accommodate, but don’t react
Blepharitis aetiology
Inflammation of the eyelid margins -> dry eyes -> grittiness, esp at eyelid margins (usually bilateral)
meibomian gland dysfunction (common, posterior blepharitis)
OR seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis)
associated w rosacea
Blepheritis tx
hot compresses BD - softening of the lid margin
‘lid hygiene’, mechanical removal of the debris
- cotton wool buds in cooled boiled water, baby shampoo, sodium bicarbonate
artificial tears for dry eyes
assessment & mx of blurred vision
visual acuity with a Snellen chart
- pinhole occluders to check if refractive error is cause
visual fields
fundoscopy
Mx
- refractive error -> optician review
- other -> opthalmology (urgent if pain or visual loss)
cataracts RFs
Ageing (!!)
Smoking
Increased alcohol
Trauma
Diabetes mellitus
Long-term corticosteroids
Radiation exposure
Myotonic dystrophy
Hypocalcaemia
Defect in the red reflex & Faded colour vision in which condition??
Cataracts
Cataracts Ix
Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
Slit-lamp examination. Findings: visible cataract
cataract classification
Nuclear: change lens refractive index, common in old age
Polar: localized, commonly inherited, lie in the visual axis
Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy
Cataract mx
Non-surgical conservative mx initially - stronger glasses/contact lens, or use brighter lighting
Surgical - removing the cloudy lens and replacing this with an artificial one
referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice !!
cataract surgery complications
Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
Endophthalmitis: inflammation of aqueous and/or vitreous humour
Central retinal artery occlusion causes
thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)
features of Central retinal artery occlusion
sudden, painless unilateral visual loss
relative afferent pupillary defect
‘cherry red’ spot on a pale retina
Central retinal vein occlusion (CRVO) px
sudden, painless reduction or loss of visual acuity, usually unilaterally
fundoscopy
- widespread hyperaemia
- severe retinal haemorrhages:’stormy sunset’
Central retinal vein occlusion (CRVO) mx
conservatively
indications for treatment in patients with CRVO include:
- macular oedema - intravitreal anti-vascular endothelial growth factor (VEGF) agents
- retinal neovascularization - laser photocoagulation
corneal foreign body indications for referral to ophthalmology
Suspected penetrating eye injury due to high-velocity injuries (e.g. drilling, lawn moving or hammering) or sharp objects (e.g. as glass, knives, pencils or thorns)
Significant orbital or peri-ocular trauma has occurred.
A chemical injury has occurred (irrigate for 20-30 mins before referring)
Foreign bodies composed of organic material (such as seeds, soil) -higher risk of infection and complications
Foreign bodies in or near the centre of the cornea
Any red flags e.g. severe pain; irregular, dilated or non-reactive pupils; significant reduction in visual acuity.
Corneal ulcer aetiology
RFs
- contact lens use
- vitamin A deficiency: a particular problem in the developing world
causes
- bacterial keratitis
- fungal keratitis
- viral keratitis: herpes simplex, herpes zoster - may lead to a dendritic ulcer
- Acanthamoeba keratitis: associated with contact lens use
non-proliferative diabetic retinopathy diabetic retinopathy features depending on classification
Mild NPDR
- 1 or more microaneurysm
Moderate NPDR
- microaneurysms
- blot haemorrhages
- hard exudates
- cotton wool spots (‘soft exudates’ - represent areas of retinal infarction)
- venous beading/looping
- intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR
Severe NPDR
- blot haemorrhages and microaneurysms in 4 quadrants
- venous beading in at least 2 quadrants
- IRMA in at least 1 quadrant
proliferative diabetic retinopathy features
Retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc
more common in Type I DM, 50% blind in 5 years
Maculopathy (diabetic retinopathy) features
based on location rather than severity, anything is potentially serious
hard exudates and other ‘background’ changes on macula
check visual acuity
more common in Type II DM