Ophthalmology Flashcards
Glaucoma
a group of eye disease associated with acute or chronic damage to the optic nerve head with progressive loss of retinal ganglion feels & their axons leading to progressive visual field loss
one of the most common eye conditions
Types of glaucoma
open angle (90%)
angle-closure
Open angle glaucoma
generally bilateral progressive loss of optic nerve fibres with open chambre angles (ie the trabecular meshwork not obstructed) but obstructed & slowed drainage system outflow leads to ↑IOP (intraoccqular pressure)
most common form of glaucoma
prevalence ↑ with age
Risk factors for open angle glaucoma
↑ age Family history ↑ IOP (ocular hypertension) afro-carribbean race myopia (short-sightedness) HTN diabetes corticosteroids
Presentation of open angle glaucoma
vast majority of pts are asymptomatic
very insidious onset
may be detected at routine optometry appointment
↓visual acuity
bilateral peripheral visual field loss (nasal scotoma progressing to tunnel vision)
mild headaches
impaired adaption to darkness
NB pts often only notice visual loss once severe & permanent damage has occurred
Investigating open angle glaucoma
ophthalmoscopy (↑ cup-to-disc ratio, >0.7, disc cupping optic disc pallor, bayoneting of vessels, cup notching, disc haemorrhages)
slit lamp (normal appearing anterior chamber angle)
tonometry (↑IOP)
nerve fibre layer analysis (loss/thinning of nerve fibre layer)
Optical coherence tomography (OCT) & automated perimetry
Management of open angle glaucoma
Eye drops/pharmacological:
1st line: prostaglandin analogues e.g. latanoprost
Beta blockers e.g. timolol
Sympathomimetics e.g. brimodine
carbonic anhydrase inhibitors e.g. donzolamide
meiotic e.g. pilocarpine
laser treatment/surgery (considered in refractory cases)
Driving with open angle glaucoma
the pt must inform the DVLA who will asses pt to see if they are fit to continue driving
if pt does not inform DVLA despite clear advice you can break confidentiality & inform the DVLA in public interest but you are advised to inform the pt of your intentions to do so
Angle-closure glaucoma
a group of disease where there is a reversible (appositional) or adhesion (synechial) closure of the anterior chamber angle resulting in ↑ IOP
more common in females
Types of angle-closure glaucoma
Acute: rapid rise in IOP due to relatively sudden blockage of the trabecular meshwork by the iris via the pupillary block mechanism
chronic: may develop after acute form where synechial closure of the angle persists for it may develop over time as angle closes from prolonged/repetitive contact between peripheral iris & the trabecular meshwork
Risk factors for angle-closure glaucoma
female sex hyperopia (far-sightedness) southeast asian/inuit/asian heritage ↑ age family history mydriasis (e.g. drug induced via anticholinergics)
Presentation of angle closure glaucoma
chronic: similar to open-angle glaucoma
acute:
sudden onset unilateral reddened & severely painful eye
↓ visual acuity, blurred vision
coloured haloes around lights, symptoms worse in dark (due to mydriasis)
hard-red eye
corneal oedema (dull/hazy cornea)
non reactive mid dilated pupil
Investigating angle closure glaucoma
vision threatening emergency requiring emergency treatment as soon as clinically suspected
gonioscopy (trabecular meshwork not visible) slit lamp (shallow anterior chamber, signs of glaucoma e.g. large cup, nerve fibre loss) automatic static perimetry (visual field defect) tonometry (↑IOP, typically >40mmHg)
Treatment of angle closure glaucoma
Pharmacological :
1st line: IV acetazolamide + supine position + topicals (e.g. beta blockers (timolol), steroids (prednisolone), pilocarpine, phenylephrine)
definitive management:
surgery/laser treatment e.g. laser peripheral iridotomy or surgical iridotomy
Cataracts
an opacification of the crystalline lens due to protein aggregation, leading cause of visual impairment & blindness world wide
very common (>50% aged >65) more common in women
Aetiology of cataracts
congenital (<1%):
hereditary congenital cataracts associated with Trisomy 13/18/21, Marfan’s, Neurofibromatosis 2
acquired (>99%): age related (>90%), Diabetes, glucocorticoid use, eye infections
Presentation of cataracts
depend on size & location of opacity
gradual painless visual loss (blurred, cloudy, dim vision)
glare (associated with halos around lights)
washed out colour vision
grey/yellow/brownish clouding visible in lens
↓ red reflex
Investigations for cataracts
fundoscopy (normal fungus & optic nerve) slit lamp (visible cataract)
Management of cataracts
Early stages: conservative (not frequently used)
Cataract surgery (lens removal & replacement, most pts >60y/o)
Retinal detachement
typically a progressive condition in which the neuroretina separates (detaches) from the retinal pigment epithelium (RPE)
most retinal detachments are preceded by posterior virtuous detachment causing traction on the retina
incidence ↑ with age, average age of presentation ~40yrs
Risk factors for retinal detachment
myopia (↑ risk of posterior virtuous detachment)
Family history of retinal break/detachment
personal history or retinal break
Classification of retinal detachment
Rhegmatogenous RD:
most common, due to retinal break e.g. posterior vitreous detachment allowing retinal fluid formed y vitreous degeneration to seep in between RPE & neuroretina
Non-rhegmatogenous RD:
exudative: sub retinal fluid accumulation without retinal tears
tractional: uncommon, fibres in vitreous contract pulling retina away
Presentation of retinal detachment
Posterior vitrous detachment (PVD) as prodrome: floaters, flashes of light in vision, blurred vision, cobwebs across vision, dark curtain descending down vision
Weiss ring on ophthalmology
floaters, flashes of light (photopsia), scotoma, veil/curtain over vision
sudden painless visual loss
Investigations of retinal detachment
visual acuity (↓)
slit lamp (shows retinal detachment/defect)
indirect opthalmoscopy
USS or OCT
Management of retinal detachment
cryotherapy/laser photocoagulation (permanent adhesion of RPE & retina)
vitrectomy (removes traction)
pneumatic retinopexy
Central retinal artery occlusion
an ophthalmic emergency characterised by occlusion of the retinal artery essentially an ischaemic stroke of the eye
one of the more common causes of severe visual impairment in elderly pts
pts usually >60y/o, more common in men
Aetiology of Central retinal artery occlusion
thrombotic emboli from carotid artery atherosclerosis = most common
embolism
thrombosis
vasculitis
arteritis
Presentation of central retinal artery occlusion
sudden unilateral painless visual loss (mostly reduced to finger counting, often described as ascending curtain)
+
relative afferent pupil defect
history of amaurosis fugax (transient loss of vision i.e. angina of the eye)
if branches affected = scoots
Investigations of central retinal artery occlusion
ophthalmoscopy (greyish white retinal discolouration - pale), cherry red spot on macula, retinal plaques/emboli, segmentation of blood column in arteries)
Bruits over carotids (on carotid doppler)
ESR/CRP (to rule out temporal arteritis)
Management of central retinal artery occlusion
ophthalmologic emergency, must reperfuse tissue asap
firm ocular massage
artery dilation (sublingual nitrites, carbon therapy)
hyperbaric oxygen
Central retinal vein occlusion
an interruption of the normal venous drainage from the retinal tissue affecting either the central retinal vein or its branches
one of the most common causes of painless unilateral vision loss
usually seen in pts >65 yrs
more common than central retinal artery occlusion
Risk factors for central retinal vein occlusion
atherosclerosis HTN diabetes smoking cardiovascular disease glaucoma COCP use sickle cell disease ↑ age
presentation of central retinal vein occlusion
sudden reduction/loss of visual acuity (unilateral)
blurred vision
afferent pupillary defect
Investigations for central retinal vein occlusion
ophthalmoscopy (dot-and-blot and/or flame haemorrhages in all 4 quadrants, cotton wool spots, macular oedema, papilloedema, venous dilation & tortiosity)
fluorescin angiography (to differentiate ischaemic & non ischaemic)
OCT (macular oedema)
Management of central retinal vein occlusion
emergency opthalmic presentation
pan retinal photocoagulation (prevents neovascularisation) ± intravitreal anti-VEGF agents
Diabetic retinopathy
the retinal consequence of chronic progressive diabetic microvascular leakage & occlusion, a potentially sight threatening disease, almost all diabetic pts well develop some degree of retinopathy
most common cause of blindness in those aged 35-65
Presentation of diabetic retinopathy
generally asymptomatic until late stages
progressive blindness & visual impairment (gradual)
Ophthalmological finding for non proliferative diabetic retinopathy
most common form of diabetic retinopathy
intraretinal microvascular abnormalities, micro aneurysms, intraretinal haemorrhage, hard exudates, cotton wool spots, retinal oedema, dot-and-blot haemorrhages
Ophthalmological finding for proliferative diabetic retinopathy
pre retinal neovascularisation, vitreous haemorrhages, plus finding of non proliferative retinopathy
Ophthalmological finding for diabetic maculopathy
macula oedema, dot haemorrhages, macular ischaemia, hard exudates on macula
more common in T2DM
Investigating diabetic retinopathy
OCT (for macula oedema)
generally fundoscopy sufficient
Management of diabetic retinopathy
improved diabetic control
intravitreal anti-VEGF injections
pan retinal photocoagulation / focal photocoagulation
Vitreous haemorrhage
extravasation of blood in & around the vitreous body, one of the most common causes of painless visual loss
caused include proliferative diabetic retinopathy (accents for ~50% of cases), posterior vitreous detachment, ocular trauma, retinal vein occlusion
Risk factors for vitreous haemorrhage
neovascularisation
trauma
anticoagulants/antiplatelets
high myopia
Presentation of vitreous haemorrhage
sudden onset of unilateral painless visual loss
red-hue to vision (haze may turn green as Hb breaks down)
floaters & cobwebs
symptoms generally worse in mornings
Investigations of vitreous haemorrhage
slit lamp (RBCs in anterior vitreous) dilated fundoscopy (haemorrhage in vitreous cavity)
fluorescein angiography (to identify neovascularisation)
USS (to rule out retinal tear/detachement)
OCT
Management of vitreous haemorrhage
observation (haemorrhage may resolve spontaneous)
treat underlying cause
photocoagulation (for vitreous tears & neovascularisation)
Macular degeneration/age related macular degeneration
potentially progressive maculopathy i.e. progressive degenerative changes of the macula,
most common cause of blindness in the UK
Types of age related macular degeneration (AMD)
Dry AMD: (~90%)
also referred to as non-exudative
characterised by drusens (yellow round spots), on retinal pigment epithelium (RPE) + hyper/hypopigmentation of RPE
gradual progression of visual loss
Wet AMD (~10%) also referred as exudative/neovascular characterised by choroidal neovascularisation with leakage of serous fluid & blood between RPE & Bruch's membrane leads to sudden or rapid visual loss worse prognosis
Risk factors of age related macular degeneration (AMD)
↑ age smoking family history of AMD obesity caucasian ethnicity cardiovascular disease risk factors (HTN, Diabetes, dyslipidaemia)
Presentation of age related macular degeneration (AMD)
painless central/pericentral visual impairement (dry: usually over years/decades, wet: acute/weeks to months)
scotomas
loss/↓ contrast sensitivity
photopsia
Investigations/examinations age related macular degeneration (AMD)
Ampler grid (focal area of distortion) OCT (intra/subretinal fluid, RPE detachement/loss) fluorescein angiography ( to identify neovascularisation) fundoscopy (dry: drusens, RPE atrophy/hypertrophy) (wet: sub/intraretinal haemorrhage/exudate, scarring, retinal discolouration)
Management of dry age related macular degeneration (AMD)
lifestyle modifications pt education & advice dietary supplements smoking cessation must inform DVLA
Management of wet age related macular degeneration (AMD)
1st line: anti-VEGF injections e.g. ranibizumab
2nd line: laser photocoagulation
Giant cell arteritis
type of autoimmune vasculitis causing chronic inflammation of large & medium sized arteries particularly the carotids and its major branches (common carotid, ICA, ECA)
most common form of systemic vasculitis in adults
2-3x more common in females, usually aged >50 yrs
Presentation of giant cell arteritis
recent onset temporal headaches, myalgia, malaise, fever jaw claudication scalp tenderness on palpation double vision/blurred vision visual loss (scotoma, amaurosis fungal)
Investigations for giant cell arteritis
CRP/ESR (↑) FBC (normochromic normocytic anaemia) LFTs (mildly ↑ ALP & AST/ALT) temporal artery biopsy (gold standard) temporal artery USS
Management of giant cell arteritis
high dose corticosteroids (can be given even if negative’ biopsy if high suspicion due to skip lesions)
low dose aspirin
NB visual loss often irreversible
Conjunctivitis (pink eye)
inflammation of the conjunctiva (the lining of the eyelids & eyeball) caused by bacteria/viruses/allergies/immunological reactions/mechanical irritation
if corneal involvement: keratoconjunctivitis
Presentation of conjunctivitis
conjunctival injections (conjunctival hyperaemia with blood vessel dilation = ocular hyperaemia & reddening)
discharge & crust formation
chemises (oedema of eyelids and/or conjunctiva)
photophobia
itching (mainly in allergic types)
Viral conjunctivitis
most common type of conjunctivitis usually caused by adenovirus
presents with unilateral symptoms but quickly spreads bilaterally
clear watery discharge, ↑ lacrimation
normal vision
often recent history of URTI
mangement:
supportive (cold compresses, lubricants) topical steroids if adenospots, topical antiviral e.g. ganciclovir if HSV
Bacterial conjunctivitis
most commonly due to staph aureus, usually unilateral
presents with thick purulent discharge (yellow/white/green), eyes feel stuck together in morning, reduced vision
management:
topical Abx e.g. chloramphenicol (give topical fusidic acid if pregnant)
Neisseria gonorrhoea conjucnitivits
ocular emergency that can lead to keratitis, perforation & blindness without treatment
give IM/IV ceftriaxone + PO azithromycin
Allergic conjunctivitis
inflammation of the ocular surface in response ti a transient allergen e.g. pollen, which may be seasonal in nature
presents with bilateral symptoms of conjunctivitis, excessive itching, ↑ lacrimation, sneezing
managed by avoiding irritants, topical or systemic antihistamines
Episcleritis
inflammation of the episclera, lasting 7-10 days and then generally self resolved
characterised by vascular congestion of the episcleral surfaces
if there is a discrete elevated area of episclera = nodular episcleritis
usually idiopathic, but also associated with Rheumatoid arthritis
Presentation of episcleritis
unilateral red eye
generally not painful (unlike scleritis which is painful)
vessels are mobile when gentle pressure applied
vision not affected
acute onset
Investigations of episcleritis
use phenylephrine drops to differentiate from scleritis, normally blanches episcleral & conjunctival vessel but not scleral vessels
i.e. if there is improved redness post phenylephrine then episcelritis
Management of episcleritis
lubricants
cold compresses
oral/topical NSAIDs
Scleritis
transmural inflammation of the sclera, generally more severe than episcleritis & requiring systemic treatment
often associated with underlying systemic disorder, most commonly rheumatoid arthritis
Presentation of scleritis
subacute/gradual onset
deep boring eye pain, exacerbated by movements redness watering loss of vision photophobia
up to 50% of cases are bilateral
Investigating scleritis
test for underlying conditions e.g. RF, ANA, ANCA, HLA typing
USS to check for posterior scleritis
Management of scleritis
oral NSAIDs (1st line) oral steroids (2nd line) rheumatological inputs
Keratitis
inflammation of the cornea, the transparent & clear covering of the iris & pupil, generally has an infective cause
commonly seen in contact lens wearers (especially if wearing for prolonged period)
General features of keratitis
painful red eye ↓ vision photophobia foreign body/gritty sensation discharge hypopyon (sediment of leukocytes at bottom of anterior chamber) corneal ulcer
Characteristic ulcer for herpes simplex keratitis
dendritic/geographical corneal ulcer
Herpes simplex keratitis
most common viral keratitis
characterised by dendritic/geographical corneal ulcers
treated with ganciclovir
Bacterial keratitis
most common keratitis, usually due to staph aureus or pseudomonas aeruginosa (if contact lens wearer)
↑ risk in contact lens wearers
frequently has hypopyon & purulent discharge
usually seen with round corneal ulcer
treatment with topical broad spectre Abx
acanthamoebic keratitis
Primarily occurs in immunocompetent contact lens wearers
increased incidence if eye exposure to soil or contaminated water
Topical amoebicides are used in association with topical steroids
Photokeratitis
welders arc eye
Uveitis (anterior uveitis or iritis)
inflammation of the uvea (middle layer of eye consisting of iris, ciliary body & choroid)
anterior uveitis: affects iris & ciliary body (most common)
posterior uveitis: affects vitreous body, choirs, reitna
Aetiology of uveitis
anterior uveitis is usually idiopathic but may be associated with HLA-B27 (ankylosing spondylitis) & IBD
Rheumatological condition associated with anterior uveitis
HLA-B27 e.g. in ankylosing spondylitis
also IBD (e.g. Crohns)
Presentation of uveitis
dull progressive periocular pain intense photophobia red eye (ocular hyperaemia) blurry vision ↓ vision acuity ↑ lacrimation
Investigations for uveitis
slit lamp (leukocytes in anterior chambre vitreous haze, signs of inflammation of iris)
Management of uveitis
topical steroids e.g. dexamethasone 0.1%
topical dilating drops e.g. cyclopentolate 1%
NB if posterior uveitis = intraocular steroid injections
Endopthalmitis
inflammation of the vitreous humour usually due to infection (e.g. staph aureus & strep after ocular surgery)
rare sight threatening ophthalmic emergency
Aetiology of endopthalmitis
most commonly post ocular surgery especially cataract surgery (most common cause of bacterial endopthalmitis)
causes usually staph aureus & strep
NB candida most common fungal cause
Presentation of endopthalmitis
severe deep seated ocular pain (usually dull & intense) acute loss/reduction of vision photophobia redness floated systemic features of infection
Investigations for endopthalmitis
vitreous & aqueous samples for microbiology
USS (may confirm vitreous involvement)
slit lamp (conjunctival hyperaemia, chemises , hazy cornea, hypopyon)
Management of endopthalmitis
intravitreal Abx (for all cases) ± intravitreal antifungals (if fungal infection suspected e.g. candida)
Peri-orbital cellulitis (pre-septal cellulitis)
infection/inflammation of the eyelid & periorbital soft tissue without involvement of the orbital contents/globe
i.e. it is anterior to orbital septum
usually seen in children (80% of pts <10y/o)
Aetiology of peri-orbital cellulitis
usually due to spread of focal infection e.g. sinusitis (so ↑ incidence in winter), systemic infection or trauma
causative organisms include staph aureus, staph epidermis, strep
presentation peri-orbital cellulitis
acute onset swelling/erythema/tenderness of eyelids
partial/complete ptosis
fever, malaise, irritability
NO orbital signs (e.g. pain on eye movements, proptosis or visual disturbance)
Investigations peri-orbital cellulitis
generally clinical diagnosis
FBC (↑ WCC), CRP (↑)
CT orbit/sinuses (to differentiate pre & post septal)
Management of peri-orbital cellulitis
close follow up (due to risk of progressing to orbital cellulitis)
oral Abx e.g. co-amoxiclav
children may need admission for observation (NB if discharging must safety net)
Orbital cellulitis
infection/inflammation of the orbital soft tissue occurring posterior to the orbital septum, the globe is however not involved
most commonly due to spreading URTI e.g. bacterial rhino sinusitis
usually seen in children aged 7-12 yrs
Causative organisms of orbital cellulitis
strep pneumonia
staph aureus
H. Influenzae (especially in unvaccinated children)
Presentation of orbital cellulitis
acute onset unilateral swelling of conjunctiva & eyelid oedema/erythema/painful eyelids & chemosis ophthalmoplegia proptosis ↓ visual acuity blurred vision/diplopia pain on eye movement relative afferent pupillary defect
headache, fever, malaise
Investigating orbital cellulitis
FBC (↑WCC), CRP (↑)
blood cultures/microbiological swab (to detect underlying organism)
CT orbit/sinuses + contrast (add contrast CT brain if abscess suspected)
LP (if cerebral or menial signs)
Management of orbital cellulitis
hospital admission (under ENT & opthal) systemic Abx (IV/PO co-amoxiclav, if severe/intracranial give cefotaxime/ceftriaxone + metronidazole)
neonatal conjunctivitis
conjunctivitis within 30 days of birth
causes include:
-chemical exposure e.g. silver nitrate, treat with saline washout
- Neisseria gonorrhoea infection, treat with cefotaxime/ceftriaxone for mother & child
- Chlamydial conjunctivitis, treat with erythromycin/azithromycin
- viral conjuncitivits, treated with acyclovir
Hypertensive retinopathy
arteriosclerotic & hypertensive related changes of the retinal vessels, which is generally asymptomatic till late in the disease when it presents with ↓ vision
Fundoscopy for hypertensive retinopathy
cotton wool spots
retinal haemorrhages (i.e. flame shaped)
microaneurysms
macular star (due to exudation of macular)
arteriovenous nicking/nipping (tapering of retinal venue where it is crossed by arteriole)
marked swelling & prominence of optic disc (due to optic atrophy/papilloedema)
Keith-Wagener scale
used for hypertensive retinopathy
I: arteriolar narrowing & tortuosity, silver wiring (↑ light reflex)
II: arteriovenous nipping (Gunn sign)
III: cotton wool exudates, flame & blot haemorrhages, macular star formation
IV: papilloedema, optic atrophy
Blepharitis
inflammation of the eyelid margin, which can present as chronic and/or recurrent scaly inflammation of the eyelid margins
can be infectious (staph aureus), seborrheic
Presentation of blepharitis
generally bilateral
chronic/recurrent swollen & erythematous eyelids margins
grittiness & discomfort around eyelid margins
dry eyes
itchiness
crusting of eyelids
lash loss (madarosis)
Management of blepharitis
hot compresses
lid hygiene
lubricants/artificial tears
Hordeolum (Stye)
common acute inflammation of the tear gland or eye lash follicles (meibomian glands) mainly caused by staph aureus
Presentation of Hordeolum (Stye)
painful erythematous nodule (may be puss filled)
may perforate & discharge spontaneously
no eyelid/occular pain
Management of Hordeolum (Stye)
generally self limiting, resolving in 1-2 weeks
hot compresses & eyelid hygiene
topical Abx if severe
Chalazion
meibomian cyst, may be seen secondary to stye
presents as chronic slow growing firm rubbery nodule of eyelid & heavy feeling o the lid
generally self-resolves
Thyroid eye disease
most common extra-thyroidal manifestation of graves disease (affects 25-50% of pts with graves)
due to an antibody mediated autoimmune reaction leading to retro-orbital inflammation which leads to collagen/glycosaminoglycan deposition in the msucles
Presentation of thyroid eye disease
exophthalmos (often asymmetric ) retropulsion ocular motility problems (diplopia, poor convergence) lid retraction conjunctival inactions sore dry eyes ophthalmoplegia
Investigations for thyroid eye disease
TFTs (↓ TSH, ↑T3/T4)
TSH receptor antibodies (+ve)
CT/MRI orbits
Management of thyroid eye disease
topical lubricants
smoking cessation
controlling thyroid disease
Strabismus (squint)
a misalignment of the visual axis of the eyes
Types of Strabismus (squint)
concomitant:
common, due to imbalance in extraocular muscles
paralytic:
less common, due to paralysis of extra ocular muscles
latent squint terminology
Heterophoria
manifest squint terminology
tropia
Squint in deviation terminology
esotropia
Squint out deviation terminology
exo
Squint up deviation terminology
hyper
Squint down deviation terminology
hypo
convergent squint terminology
esotropia
divergent squint terminology
exotropia
concomitant squint
usually congenital
children have full movement in both eyes if tested separately
no diplopia, pts may intermittently close one eye
Paralytic squint
acquired due to damage to extra ocular muscles or nerves
diplopia common
Investigating strabismus
cover test (cover/uncover test or alternate cover test)
Hirschberg test (to determine eye alignment)
Management of strabismus
correction of refractory errors
strabismus surgery
occlusion therapy (eye patches, more effective if used early)
Ambylopia (functional visual impairment)
↓ best corrected corrected visual acuity in one or both eyes that is not attributable to a structural abnormality of the eye/visual pathways
usually due to developmental vision disorder during early childhood e.g strabismus, congenital cataracts
treat early in childhood, correct refractive error, occlusion (patching) correct underlying cause e.g. strabismus
Myopia (near sighted)
eyes have excessive optical power for the axial length of the eyeball and/or the eyeball is too long leading to focus pf the image in front of the retina
objects at distance are blurred
corrected by concave (minus) lens
Hypermyetropia / Hyperopia (far sighted)
eyes have insufficient optical power for tis reactive length so the focus of the image is behind the retina or eyeball may be too short
objects up close are blurred
corrected with convex (plus) lens
Astigmatism
normally light from a point in the visual field has to focus on a single point on the retina, in astigmatism the cornea & lens curvatures result in the light failing to focus on a single point
corrected with bifocal lens
Presbyopia
↓ power of accommodation usually becoming significant at age of 40-50 when focusing on near objects e.g. reading becomes difficult
corrected using reading glasses
Emmertropia
eye with no visual defects or refractive errors
i.e. light is perfectly focused on the retina
Left eye anopsia
caused by optic nerve lesion e.g. optic neuritis or central retinal artery occlusion
left nasal hemianopia
ipsilateral left temporal fibres of optic nerve damaged e.g. from ICA aneurysm expanding medially
bitemporal hemianopia
optic chasm compression
if upper quadrants worse = inferior compression e.g. from pituitary adenoma
if lower quadrants worse = superior compression e.g. from craniopharyngioma
Right homonymous hemianopia
damage to contralateral optic tract or lateral geniculate body e.g. from MCA infarction
Right homonymous superior quadrantanopia
contralateral temporal radiation/meyers loop damage e.g. in MCA occlusions or temporal lobe tumour
Left homonymous inferior quadrantanopia
contralateral parietal radiation/non-meters loop
right homonymous hemianopia with macula sparing
contralateral damage to primary visual cortex e.g. from PCA occlusion
NB macular is spared due to contralateral blood supply
nasolacrimal duct obstruction
nasolacrimal duct commonly canalises at ~8moths of fatal life but there is commonly a delay in this developmental process which can result in residual membrane tissue or stenosis at any level in the duct
most common cause of persistent watery eye in infants
investigated with fluroscein disappearance test
treated with massaging lacrimal ducts, 95% will resolve by age 1, if persistent >1y/o = surgery
Retinopathy of prematurity
disease of the retina with abnormal vessel proliferation that affects preterm infants, due to ↑/fluctuating levels of PaO2 leading to extra retinal neovascularisation as it causes ↑ VEGGF
risk factors:
prematurity, ventialtion, O2 administration, birth weight <1500g
management:
laser photocoagulation (1st line)
anti-VEGF injections (2nd line)
Screening for retinopathy of prematurity
screen all infants born <32 weeks or weighing <1501g
those born at 32-36 weeks with O2 administration
weekly/fortnightly screening
discontinued after completed retinal vascularisation
Retinoblastoma
most common primary intraocular malignancy in children, usually diagnosed around age 18months
due to mutation of retinoblastoma gene (Rb)
if hereditary (autosomal dominant) = bilateral sporadic = unilateral
Presentation of retinoblastoma
leukocoria (white pupillary reflex, i.e. absent red reflex) strabismus loss of vision painful red eye retinal detachment
Investigations for retinoblastoma
fundoscopy (chalky white-grey retinal mass)
ocular USS
MRI head
Management of retinoblastoma
localised:
eye conceiving therapy (photocoagulation, cryotherapy, radio & chemotherapy)
enucleation:
removal of eye & adult size implant to replace
Holmes-Adie pupil
affects women in 3rd/4th decade of life
80% are bilateral
dilated pupil
once pupil is constricted it remains small for abnormally long period of time
slowly reactive to accommodation but very poor if any accommodation to light
Argyll-Robertson pupil
highly specific for neurosyphilis
usually bilateral
tonically small pupil that treats poorly to light but briskly to accommodation (light-near dissociation)
difficult to pharmacological dilate pupil
Marcus-Gunn pupil (relative afferent pupillary defect)
found on the swinging light test
the affected and normal eye appears to dilate when light is shone in the affected eye
caused by a lesion anterior to the optic chiasm e.g. optic neuritis or retinal detachment
Retinitis pigmentosa
inherited condition (i.e. usually family history), primarily affects the peripheral retina resulting in tunnel vision, usually bilateral
Features
night blindness (initial sign)
tunnel vision due to loss of the peripheral retina
fundoscopy: arteriolar attenuation, black/bone–spicule peripheral retinal pigmentation and waxy optic disc pallor, mottling of the retinal pigment epithelium
