Opthalmology Flashcards
features of acute angle closure glaucoma
severe pain: may be ocular or headache
decreased visual acuity
symptoms worse with mydriasis
hard, red-eye
haloes around lights
semi-dilated non-reacting pupil
corneal oedema results in dull or hazy cornea
causes of acute angle closure glaucoma
raised intraocular pressure (IOP) secondary to an impairment of aqueous outflow:
hypermetropia (long-sightedness)
pupillary dilatation
lens growth associated with age
management of acute angle closure glaucoma
emergency - urgent ophthalmologist referral
must lower IOP
eye drops
direct parasympathomimetic (pilocarpine) to contract ciliary muscle
beta blocker - timolol to reduce aq humor production
alpha2 agonist -
IV acetazolamide - reduce aq secretions
laser peripheral iridotomy - creates hole in peripheral iris
risk factors for age-related macular degeneration
advancing age
smoking
family history
increased risk of ischaemic cardiovascular disease, such as hypertension, dyslipidaemia and diabetes mellitus.
pathophysiology of age related macular degeneration
most common cause of blindness in the UK
bilateral degeneration of the central retina (macula)
ARMD is characterised by degeneration of retinal photoreceptors - results in the formation of drusen which can be seen on fundoscopy and retinal photography
features of dry macular degeneration
90% of cases
also known as atrophic
characterised by drusen - yellow round spots in Bruch’s membrane
features of wet macular degeneration
10% of cases
also known as exudative or neovascular macular degeneration
characterised by choroidal neovascularisation
leakage of serous fluid and blood can subsequently result in a rapid loss of vision
carries the worst prognosis
presentation of age related macular degeneration
subacute visual loss with reduced visual acuity - gradual (dry) and subacute (wet)
poor dark adaptation, poor night vision
fluctuant visual disturbance
photopsia
visual hallucinations - charles bonnet syndrome
investigation findings in age related macular degeneration
distorted line perception on amsler grid testing
fundoscopy - drusen, yellow areas of pigment deposition in the macular
wet ARMD - well demarcated red patches - intra retinal / sub retinal fluid leakage or haemorrhage
slit-lamp microscopy - identify any pigmentary, exudative or haemorrhagic changes affecting the retina
fluorescin angiography - can guide anti VEGF
treatment of age related macular degeneration
zinc + vitamins ACE
anti-VEGF vascular endothelial growth factor
4 weekly injection
laser photocoagulation if new vessel formation present
features of allergic conjunctivitis
Bilateral symptoms conjunctival erythema, conjunctival swelling (chemosis)
Itch is prominent
the eyelids may also be swollen
May be a history of atopy
May be seasonal (due to pollen) or perennial (due to dust mite, washing powder or other allergens)
management of allergic conjunctivitis
first-line: topical or systemic antihistamines
second-line: topical mast-cell stabilisers, e.g. Sodium cromoglicate and nedocromil
features of anterior uveitis
inflammation of the anterior portion of the uvea - iris and ciliary body
acute onset painful red eye
pupil may be small +/- irregular due to sphincter muscle contraction
photophobia (often intense)
lacrimation
ciliary flush: a ring of red spreading outwards
hypopyon; describes pus and inflammatory cells in the anterior chamber
impaired visual acuity and blurriness
associated conditions with anterior uveitis
ankylosing spondylitis
reactive arthritis
ulcerative colitis, Crohn’s disease
Behcet’s disease
sarcoidosis: bilateral disease may be seen
management of anterior uveitis
urgent review by ophthalmology
cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate
steroid eye drops
features of argyll robertson pupil
Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)
small, irregular pupils
no response to light but there is a response to accommodate
due to diabetes and syphilis
causes of blepharitis
meibomian gland dysfunction (common, posterior blepharitis)
seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis)
common in pt with rosacea
features of blepharitis
symptoms are usually bilateral
grittiness and discomfort, particularly around the eyelid margins
eyes may be sticky in the morning
eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis
styes and chalazions are more common in patients with blepharitis
secondary conjunctivitis may occur
management of blepharitis
hot compresses twice a day
‘lid hygiene’
artificial tears
causes of blurred vision
refractive error: most common
cataracts
retinal detachment
age-related macular degeneration
acute angle closure glaucoma
optic neuritis
amaurosis fugax
testing for blurred vision
visual acuity with a Snellen chart
if the blurring improves with a pinhole occluder then likely cause is a refractive error
visual fields
fundoscopy
causes of cataract
lens of the eye gradually opacifies
Normal ageing process: most common cause
Smoking, alcohol
Trauma
Diabetes mellitus
Long-term corticosteroids
Radiation exposure
Myotonic dystrophy
Metabolic disorders: hypocalcaemia
more common in women
presentation of cataracts
a gradual onset of:
Reduced vision
Faded colour vision: making it more difficult to distinguish different colours
Glare: lights appear brighter than usual
Halos around lights
defective red reflex - due to cataracts preventing light from getting to the retina
classification of cataracts
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
management of cataracts
surgery - to remove cloudy lens and replace with artificial one
consider side effects
Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
Endophthalmitis: inflammation of aqueous and/or vitreous humour
features of central retinal artery occlusion
rare cause of sudden unilateral visual loss - due to thromboembolism or arteritis
sudden, painless unilateral visual loss
relative afferent pupillary defect
‘cherry red’ spot on a pale retina
features of central retinal vein occlusion
sudden, painless reduction or loss of visual acuity, usually unilaterally
fundoscopy
widespread hyperaemia
severe retinal haemorrhages - ‘stormy sunset’
features of branch retinal vein occlusion
when a vein in the distal retinal venous system is occluded and is thought to occur due to blockage of retinal veins at arteriovenous crossings - more limited area of fundus is affected
management of central retinal vein occlusion
conservative
indications for treatment - macular oedema - antiVEGF
retinal neovascularisation - laser photocoagulation
indications for referral to ophthalmology in corneal foreign body
suspected penetrating eye injury due to high velocity injury
significant orbital/periocular trauma
chemical injury (irrigate 20-30min before referring)
organic material
neare centre of cornea
red flags e.g. severe pain; irregular, dilated or non-reactive pupils; significant reduction in visual acuity.
risk factors and causes of corneal ulcers
defect in cornea 2* to infective cause (usually)
RF - contact lenses, vitamin A deficiency
abacterial keratitis
fungal keratitis
viral keratitis: herpes simplex, herpes zoster - may lead to a dendritic ulcer
Acanthamoeba keratitis: associated with contact lens use
features of corneal ulcers
eye pain
photophobia
watering of the eye
focal fluorescein staining of the cornea
pathophysiology of diabetic retinopathy
damage to cells due to increased blood flow and abnormal metabolism in retinal vessel walls –> increased vascular permeability - exudates on fundoscopy
can be non-proliferative or proliferative
features of non-proliferative diabetic retinopathy
microaneurysms
blot haemorrhages
hard exudates
cotton wool spots ‘soft exudates’ - retinal infarction
severe NPDR
blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant
features of proliferative diabetic retinopathy
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
management of diabetic retinopathy
optimise glycaemic control, blood pressure and hyperlipidemia
regular review by ophthalmology
Non-proliferative retinopathy
regular observation
if severe/very severe consider panretinal laser photocoagulation
Proliferative retinopathy
panretinal laser photocoagulation
intravitreal VEGF inhibitors - if change in visual acuity
severe or vitreous haemorrhage: vitreoretinal surgery
pathophysiology of episcleritis
acute onset of inflammation in the episclera of one or both eyes
usually idiopathic
inflammatory bowel disease
rheumatoid arthritis
features of episcleritis
red eye
50% bilateral
mild pain/irritation
watering and mild photophobia may be present
episcleritis - injected vessels are mobile when gentle pressure - blanched by phenylephrine
scleritis - vessels are deeper, dont move
common eyelid problems
blepharitis: inflammation of the eyelid margins typically leading to a red eye
stye: infection of the glands of the eyelids
chalazion (Meibomian cyst)
entropion: in-turning of the eyelids
ectropion: out-turning of the eyelids
types of stye
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)
common presentations of herpes simplex keratitis
dendritic corneal ulcer
Features
red, painful eye
photophobia
epiphora
visual acuity may be decreased
fluorescein staining may show an epithelial ulcer
management of herpes simplex keratitis
immediate referral to an ophthalmologist
topical aciclovir
features of herpes zoster ophthalmicus
Herpes zoster ophthalmicus (HZO) - reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve
vesicular rash around the eye - may involve the actual eye itself
Hutchinson’s sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement
management of herpes zoster ophthalmicus
oral antiviral treatment for 7-10 days
start <within 72 hours
IV antivirals if severe or immunocompromised
topical corticosteroids - to treat any secondary inflammation of the eye
ocular involvement requires urgent ophthalmology reviewV
features of holmes-adie pupil
benign condition in females - unilateral dilated pupil
slowly reactive to accomodation
features of horner’s sydrome
miosis (small pupil)
ptosis
enophthalmos* (sunken eye)
anhidrosis (loss of sweating one side)
sites of lesions causing horners and subsequent effects
central lesions - anhidrosis of face, arm, trunk
stroke, syringomyelia, MS
tumour, encephalitis
pre-ganglionic - anhidrosis of face
pancoast tumour, thyroidectomy, trauma, cervical rib
post-ganglionic lesions - no anhidrosis
carotid artery/aneurysm, cavernous sinus thrombosis, cluster headache
classification of hypertensive retinopathy
I Arteriolar narrowing and tortuosity
Increased light reflex - silver wiring
II Arteriovenous nipping
III Cotton-wool exudates
Flame and blot haemorrhages
These may collect around the fovea resulting in a ‘macular star’
IV Papilloedema
bacterial vs viral conjunctivitis
common eye problem- sore, red eyes with sticky discharge
Bacterial conjunctivitis Purulent discharge
Eyes may be ‘stuck together’ in the morning)
Viral conjunctivitis Serous discharge
Recent URTI
Preauricular lymph nodes
management of infective conjunctivitis
normal self-limiting condition
topical antibiotic therapy e.g., chloramphenicol
topical fusidic acid for women
causes of keratitis
inflammation of the cornea
bacterial - Staphylococcus aureus, Pseudomonas aeruginosa in contact lens wearers
fungal
amoebic - acanthamoebic keratitis
parasitic: onchocercal keratitis (‘river blindness’)
viral - herpes simplex keratitis
environmental - photokeratitis, exposure keratitis, contact lens acute red eye
clinical features of keratitis
red eye: pain and erythema
photophobia
foreign body, gritty sensation
hypopyon may be seen
management of keratitis
stop using contact lenses
topical antibiotics - quinolones
cycloplegic - for pain relief
causes of mydriasis
third nerve palsy
Holmes-Adie pupil
traumatic iridoplegia
phaeochromocytoma
congenital
topical mydriatics: tropicamide, atropine
sympathomimetic drugs: amphetamines, cocaine
anticholinergic drugs: tricyclic antidepressants
features of nasolacrimal duct obstruction
most common cause of a persistent watery eye in an infant.
It is caused by an imperforate membrane, usually at the lower end of the lacrimal duct.
Around 1 in 10 infants have symptoms at around one month of age
causes of optic neuritis
multiple sclerosis: the commonest associated disease
diabetes
syphilis
features of optic neuritis
unilateral decrease in visual acuity over hours or days
poor discrimination of colours, ‘red desaturation’
pain worse on eye movement
relative afferent pupillary defect
central scotoma
management of optic neuritis
high-dose steroids
recovery usually takes 4-6 weeks
pathophysiology of orbital cellulitis
infection affecting the fat and muscles posterior to the orbital septum, within the orbit but not involving the globe
caused by a spreading URTI from the sinuses and carries a high mortality rate
a medical emergency requiring hospital admission and urgent senior review
risk factors for orbital cellulitis
Childhood - mean age of hospitalisation 7-12 years
Previous sinus infection
Lack of Haemophilus influenzae type b (Hib) vaccination
Recent eyelid infection/ insect bite on eyelid (periorbital cellulitis)
Ear or facial infection
presentation of orbital cellulitis
Redness and swelling around the eye
Severe ocular pain
Visual disturbance
Proptosis
Ophthalmoplegia/pain with eye movements
Eyelid oedema and ptosis
Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)
differentiating orbital from preseptal cellulitis - reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements are NOT consistent with preseptal cellulitis
fundoscopy findings in papilloedema
venous engorgement: usually the first sign
loss of venous pulsation: although many normal patients do not have normal pulsation
blurring of the optic disc margin
elevation of optic disc
loss of the optic cup
Paton’s lines: concentric/radial retinal lines cascading from the optic disc
causes of papilloedema
space-occupying lesion: neoplastic, vascular
malignant hypertension
idiopathic intracranial hypertension
hydrocephalus
hypercapnia
describe posterior vitreous detachment
separation of the vitreous membrane from the retina due to natural changes to the vitreous fluid of the eye with ageing
common condition, does not cause any pain or loss of vision.
may sometimes lead to tears and detachment of the retina.
must rule out retinal tears or retinal detachment in anyone with suspected posterior vitreous detachment, as they may result in permanent loss of vision.
risk factors of posterior vitreous detachment
As people age, the vitreous fluid in the eye becomes less viscous, and thus, does not hold its shape as well. Therefore, it pulls the vitreous membrane away from the retina towards the centre of the eye.
Highly myopic (near-sighted) patients are also at increased risk of developing posterior vitreous detachment earlier in life. This is because the myopic eye has a longer axial length than an emmetropic eye.
features of posterior vitreous detachment
The sudden appearance of floaters (occasionally a ring of floaters temporal to central vision)
Flashes of light in vision
Blurred vision
Cobweb across vision
The appearance of a dark curtain descending down vision (means that there is also retinal detachment)
management of posterior vitreous detachment
examination by an ophthalmologist within 24hours to rule out retinal tears or detachment.
Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.
If there is an associated retinal tear or detachment the patient will require surgery to fix this.
management of primary open angle glaucoma
prostaglandin analogues - latanoprost - increase uveoscleral outflow
beta blockers - timolol - reduce aq production
sympathomimetics - brimoniodine - reduce aq production, increases outflow
carbonic anhydrase inhibitors - dorzolamide - reduce aq production
miotics - pilocarpine - increase uveoscleral outflow
fundoscopy of primary open angle glaucome
- 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
investigation findings in primary open angle glaucoma
automated perimetry to assess visual field
slit lamp examination
applanation tonometry to measure IOP
central corneal thickness measurement
gonioscopy
describe a relative afferent pupillary defect
Marcus-Gunn pupil, caused by a lesion anterior to the optic chiasm
the affected and normal eye appears to dilate when light is shone on the affected eye
causes
retina: detachment
optic nerve: optic neuritis e.g. multiple sclerosis
causes of red eye
Acute angle closure glaucoma
Anterior uveitis
Scleritis
Conjunctivitis
Subconjunctival haemorrhage
Endophthalmitis
pathway of pupillary light reflex
afferent: retina → optic nerve → lateral geniculate body → midbrain
efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve
describe retinal detachment
occurs when the neurosensory tissue that lines the back of the eye comes away from its underlying pigment epithelium
reversible cause of visual loss if recognised and treated before the macula is affected
f left untreated and symptomatic, retinal detachment will inevitably lead to permanent visual loss.
risk factors for retinal detachment
diabetes mellitus
myopia
age
previous surgery for cataracts (accelerates posterior vitreous detachment)
eye trauma e.g. boxing
features of retinal detachment
new onset floaters or flashes
sudden onset, painless and progressive visual field loss - a curtain, or shadow progressing to the centre of the visual field from the periphery
if macula is involved = central visual acuity, visual outcomes become much worse
reduced peripheral visual fields
fundoscopy findings in retinal detachment
the red reflex is lost and retinal folds may appear as pale, opaque or wrinkled forms
if the break is small, however, it may appear normal.
features of retinitis pigmentosa
primarily affects the peripheral retina resulting in tunnel vision
night blindness is often the initial sign
tunnel vision due to loss of the peripheral retina (occasionally referred to as funnel vision)
fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
ocular manifestations of rheumatoid arthritis
keratoconjunctivitis sicca (most common)
episcleritis (erythema)
scleritis (erythema and pain)
corneal ulceration
keratitis
risk factors of scleritis
rheumatoid arthritis: the most commonly associated condition
systemic lupus erythematosus
sarcoidosis
granulomatosis with polyangiitis
causes and types of strabismus
Squint (strabismus) = misalignment of the visual axes.
concomitant (common) - due to imbalanced extraocular muscles, convergent>divergent
paralytic (rare) - due to paralysis of extra-ocular muscles
uncorrected may lead to amblyopia (the brain fails to fully process inputs from one eye and over time favours the other eye).
features of scleritis
scleritis = full thickness inflammation of sclera, causes red, painful eye
red eye
classically painful (in comparison to episcleritis), but sometimes only mild pain/discomfort is present
watering and photophobia are common
gradual decrease in vision
investigation of squint
corneal light reflection test - holding a light source 30cm from the child’s face to see if the light reflects symmetrically on the pupils
The cover test is used to identify the nature of the squint
ask the child to focus on an object
cover one eye
observe movement of uncovered eye
cover other eye and repeat test
causes of sudden vision loss
ischaemic/vascular (e.g. thrombosis, embolism, temporal arteritis etc). This includes recognised syndromes e.g. occlusion of central retinal vein and occlusion of central retinal artery
vitreous haemorrhage
retinal detachment
retinal migraine
causes of tunnel vision
due to concentric diminution of the visual fields
papilloedema
glaucoma
retinitis pigmentosa
choroidoretinitis
optic atrophy secondary to tabes dorsalis
hysteria
features of vitreous haemorrhage
painless visual loss or haze (commonest)
red hue in the vision
floaters or shadows/dark spots in the vision
decreased visual acuity: variable depending on the location, size and degree of vitreous haemorrhage
visual field defect if severe haemorrhage
causes of vitreous haemorrhage
proliferative diabetic retinopathy (over 50%)
posterior vitreous detachment
ocular trauma
investigation findings in vitreous haemorrhage
dilated fundoscopy: may show haemorrhage in the vitreous cavity
slit-lamp examination: red blood cells in the anterior vitreous
ultrasound: useful to rule out retinal tear/detachment and if haemorrhage obscures the retina
fluorescein angiography: to identify neovascularization
orbital CT: used if open globe injury
management of corneal foreign body
suspected penetrating eye injury due to high-velocity injuries
Significant orbital or peri-ocular trauma
chemical injury - irrigate 20-30mins
organic foreign bodies
red flag sx
