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
diabetic retinopathy mx
All patients
- optimise glycaemic control, blood pressure and hyperlipidemia
- regular review by ophthalmology
Maculopathy
- if visual acuity affected -> intravitreal vascular endothelial growth factor (VEGF) inhibitors
Non-proliferative retinopathy
- regular observation
- if severe/very severe consider panretinal laser photocoagulation
Proliferative retinopathy
- panretinal laser photocoagulation
- intravitreal VEGF inhibitors. e.g. ranibizumab
- if severe or vitreous haemorrhage: vitreoretinal surgery
complications of pan retinal laser photocoagulation
- following treatment around 50% of patients develop a noticeable reduction in their visual fields due to the scarring of peripheral retinal tissue
- decrease in night vision (rods are predominantly responsible for vision in low light conditions, the majority of rod cells are located in the peripheral retina)
- a generalised decrease in visual acuity
- macular oedema
what medication can differentiate between episcleritis and scleritis?
phenylephrine drops
phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels
if the eye redness improves after phenylephrine a diagnosis of episcleritis can be made
Episcleritis causes & mx
idiopathic
inflammatory bowel disease
rheumatoid arthritis
Management
- conservative
- artificial tears may sometimes be used
types of stye (infection of the glands of the eyelids) & mx
- external (hordeolum externum): infection (usually staphylococcal) of the glands of Zeis (sebum producing) or glands of Moll (sweat glands).
- internal (hordeolum internum): infection of the Meibomian glands. May leave a residual chalazion (Meibomian cyst)
-management includes hot compresses and analgesia. CKS only recommend topical antibiotics if there is an associated conjunctivitis
Herpes simplex keratitis mx
(most commonly presents with a dendritic corneal ulcer)
immediate referral to an ophthalmologist
topical aciclovir
Herpes zoster ophthalmicus mx
oral antiviral treatment for 7-10 days
- start w/in 72hrs
- iv for very severe infection or if immunocompromised
topical corticosteroids may be used to treat any secondary inflammation of the eye
ocular involvement requires urgent ophthalmology review
Holmes-Adie pupil px
- unilateral in 80% of cases
- dilated pupil
- once the pupil has constricted it remains small for an abnormally long time
- slowly reactive to accommodation but very poorly (if at all) to light
Holmes-Adie syndrome
- Holmes-Adie pupil with absent ankle/knee reflexes
Horner syndrome px
- miosis (small pupil)
- ptosis
- enophthalmos (sunken eye)
anhidrosis (loss of sweating one side - depends on location of lesion) - pupillary dilation with apraclonidine drops*
(*an alpha-adrenergic agonist causes mild pupillary constriction in the normal pupil by down-regulating the norepinephrine release at the synaptic cleft)
Horner syndrome
- central lesion px & causes
Anhidrosis of the face, arm and trunk
Stroke
Syringomyelia
Multiple sclerosis
Tumour
Encephalitis
Horner syndrome
- pre-ganglionic lesion px & causes
Anhidrosis of the face
Pancoast’s tumour
Thyroidectomy
Trauma
Cervical rib
Horner syndrome
- post-ganglionic lesion px & causes
No anhidrosis
Carotid artery dissection
Carotid aneurysm
Cavernous sinus thrombosis
Cluster headache
hypertensive retinopathy classification (Keith-Wagener classification)
- Arteriolar narrowing and tortuosity
Increased light reflex - silver wiring - Arteriovenous nipping
- Cotton-wool exudates
Flame and blot haemorrhages
These may collect around the fovea resulting in a ‘macular star’ - Papilloedema
Infective conjunctivitis mx
- normally self limiting in 1-2 wks
- topical antibiotic therapy (Chloramphenicol: drops are given 2-3 hourly or ointment qds)
- topical fusidic acid BD is alternative (in pregnancy)
- advice should be given not to share towels
- school exclusion is not necessary
contact lens users
- topical fluoresceins to identify any corneal staining
- do not wear until it resolves
- tx as above
causes of keratitis
(red eye w pain, photophobia, gritty sensation, maybe hypopyon)
bacterial
- Staphylococcus aureus
- Pseudomonas aeruginosa is seen in contact lens wearers
fungal
amoebic
- acanthamoebic keratitis
- increased incidence if eye exposure to soil or contaminated water
- pain is classically out of proportion to the findings
parasitic:
- onchocercal keratitis (‘river blindness’)
viral
- herpes simplex keratitis
environmental
keratitis mx
contact lens wearers w painful red eye
- same-day referral to an eye specialist for slit lamp to rule out microbial keratitis
stop using contact lens until the symptoms have fully resolved
topical antibiotics
- typically quinolones are used first-line
cycloplegic for pain relief
e.g. cyclopentolate
Causes of mydriasis (large pupil)
Third nerve palsy
Holmes-Adie pupil
Traumatic iridoplegia
Phaeochromocytoma
Congenital
Drugs which cause mydriasis
topical mydriatics: tropicamide, atropine
sympathomimetic drugs: amphetamines, cocaine
anticholinergic drugs: tricyclic antidepressants
nasolacrimal duct obstruction mx
- teach parents to massage the lacrimal duct
- usually resolves in 1 yr
- if not, opthal referral for probing
why is hyphema dangerous?
Hyphema = blood in the anterior chamber of the eye
main risk to sight comes from raised intraocular pressure due to the blockage of the angle and trabecular meshwork with erythrocytes
ocular trauma & hyphema mx
Strict bed rest - excessive movement can redisperse blood that had previously settled
high-risk cases are often admitted otherwise daily ophthalmic review and pressure checks initially as an outpatient.
assess for orbital compartment syndrome (e.g. secondary to retrobulbar haemorrhage) -> true ophthalmic emergency
optic neuritis causes
multiple sclerosis: the commonest associated disease
diabetes
syphilis
optic neuritis features & mx
- acute unilateral decreased visual acuity - hrs or days
- poor discrimination of colours (red desaturation)
- pain worse on eye movement
- RAPD
- central scotoma
ix
MRI of the brain and orbits with gadolinium contrast
mx
high-dose steroids
recovery usually in 4-6 weeks
Preorbital vs orbital cellulitis
Periorbital (preseptal) cellulitis - infection anterior to the orbital septum
Orbital cellulitis - infection of fat and muscles posterior to the orbital septum, within the orbit but not involving the globe
reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements, restricted movements, chemosis, RAPD = orbital
causes of papiloedema
increased intracranial pressure
- space-occupying lesion: neoplastic, vascular
- malignant hypertension
- idiopathic intracranial hypertension
- hydrocephalus
- hypercapnia
rare other causes
- hypoparathyroidism and hypocalcaemia
- vitamin A toxicity
vitreous detachment ix & mx
RF
- age
- highly myopic (near-sighted)
ix
- Weiss ring on ophthalmoscopy (the detachment of the vitreous membrane around the optic nerve to form a ring-shaped floater).
- examined by an ophthalmologist within 24hrs to rule out retinal tears or detachment.
mx
- nothing - gradually improve over a period of around 6 months
- if retinal tear/ detachment -> surgery
orbital cellulitis ix & mx
CT contrast of orbit & blood culture
medical emergency -> hospital admission for IV antibiotics, urgent senior review
orbital cellulitis causes & RFs
- Most common bacterial causes – Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.
Risk factors
- Childhood
- Mean age of hospitalisation 7-12 years
- Previous sinus infection
- Lack of Hib vaccination
- Recent eyelid infection/ insect bite on eyelid (periorbital cellulitis)
- Ear or facial infection
preseptal cellulitis mx
All cases should be referred to secondary care for assessment
Oral antibiotics are frequently sufficient - usually co-amoxiclav
contrast CT of orbit if suspecting orbital cellulitis
night blindness and tunnel vision?
Retinitis pigmentosa
fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
Ocular manifestations of rheumatoid arthritis?
25% of patients having eye problems
Ocular manifestations
keratoconjunctivitis sicca (most common)
episcleritis (erythema)
scleritis (erythema and pain)
corneal ulceration
keratitis
Iatrogenic
steroid-induced cataracts
chloroquine retinopathy
primary open-angle glaucoma mx
- offer 360° selective laser trabeculoplasty (SLT) first-line to people with an IOP of ≥ 24 mmHg
2.prostaglandin analogue (PGA) eyedrops
- beta-blocker eye drops
/ carbonic anhydrase inhibitor eye drops
/ sympathomimetic eye drops - surgery in the form of a trabeculectomy may be considered in refractory cases
Prostaglandin analogues
example
MoA in eye
Advese effects
latanoprost
Increases uveoscleral outflow
OD eye drops
Adverse effects include brown pigmentation of the iris, increased eyelash length
Beta-blocker eye drops
example
MoA in eye
CI
(e.g. timolol, betaxolol)
Reduces aqueous production
Should be avoided in asthmatics and patients with heart block
Sympathomimetics eye drops
example
MoA in eye
CI
(e.g. brimonidine, an alpha2-adrenoceptor agonist)
Reduces aqueous production and increases outflow
Avoid if taking MAOI or tricyclic antidepressants
Adverse effects include hyperaemia
Carbonic anhydrase inhibitors
(e.g. Dorzolamide)
Reduces aqueous production
Systemic absorption may cause sulphonamide-like reactions
Miotics (e.g. pilocarpine, a muscarinic receptor agonist)
Increases uveoscleral outflow
Adverse effects included a constricted pupil, headache and blurred vision
peripheral visual field loss- nasal scotoma -> tunnel vision
decreased visual acuity
optic disc cupping
what is this?
primary open-angle glaucoma (POAG)
Fundoscopy signs of primary open-angle glaucoma
- Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen
- Optic disc pallor - indicating optic atrophy
- Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
- Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages
Marcus-Gunn pupil?
a.k.a relative afferent pupillary defect
- found by swinging light test
- caused by a lesion anterior to the optic chiasm-> retina: detachment or optic nerve: optic neuritis e.g. multiple sclerosis
finding: the affected and normal eye appears to dilate when light is shone on the affected
Pathway of pupillary light reflex
afferent: retina → optic nerve → lateral geniculate body → midbrain
efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve
Retinal detachment aetiology & RFs?
neurosensory tissue that lines the back of the eye comes away from its underlying pigment epithelium
reversible cause of visual loss, provided it is recognised and treated before the macula is affected, otherwise permanent visual loss
RFs
- diabetes mellitus
- myopia
- age
- previous cataract surgery
- eye trauma
pt seeing flashes & floaters. what now?
most likely just posterior vitreous detachment
But refer urgently (<24 hours) to an ophthalmologist for assessment with a slit lamp and indirect ophthalmoscopy for pigment cells and vitreous haemorrhage
retinal detachment - also have dense shadow that starts peripherally progresses towards the central vision, central visual loss, straight lines -> curved
Scleritis RFs
rheumatoid arthritis: the most commonly associated condition
systemic lupus erythematosus
sarcoidosis
granulomatosis with polyangiitis
scleritis mx
same-day assessment by an ophthalmologist
oral NSAIDs first-line
oral glucocorticoids for more severe presentations
immunosuppressive drugs for resistant cases (and also to treat any underlying associated diseases)
Squints types
concomitant (common)
- Due to imbalance in extraocular muscles
Convergent is more common than divergent
paralytic (rare)
- Due to paralysis of extraocular muscles
squint ix & mx
important to detect as uncorrected -> amblyopia (the brain fails to fully process inputs from one eye and over time favours the other eye)
ix
- corneal light reflection test - holding a light source 30cm from face to see if the light reflects symmetrically on the pupils
- cover test - focus on object, cover one eye, observe movement of other eye
mx
- referral to secondary care
- eye patches may help prevent amblyopia
most common causes of a sudden painless loss of vision
- ischaemic/vascular a.k.a amaurosis fugax e.g. thrombosis (CRVO, CRAO), embolism, temporal arteritis, TIA, ischaemic optic neuropathy
- vitreous haemorrhage
- retinal detachment
- retinal migraine
Causes of tunnel vision
papilloedema
glaucoma
retinitis pigmentosa
choroidoretinitis
optic atrophy secondary to tabes dorsalis
hysteria
Common causes of vitreous haemorrhage
proliferative diabetic retinopathy (over 50%)
posterior vitreous detachment
ocular trauma: the most common cause in children and young adults
