Opthal - 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:
- Opthalmoscopy 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 cloudly 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 detatchment
- 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
-
Beta-blocker
- 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)
- carbonic anhydrase inhibitors e.g. dorzolamide (eyedrop) or acetazolamide (oral)
-
Adjunct:
-
Pilocarpine - if AACG is 2ndary to pupillary block
- muscarinic ACh receptor agonist
- pupillary contriction –> 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
-
Pilocarpine - if AACG is 2ndary to pupillary block
-
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
-
Laser peripheral iridotomy - laser hole in iris to equalise pressure between posterior + anterior chamber (relieves pupillary block)
What is the commonest cause of blindness in the UK?
Age-realted 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 sign does this image show?
Cherry Red spot
(sign of central retinal artery occlusion)
What are the most common causes of sudden, painless loss of vision?
-
Ichaemic / 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
- large artery disease e.g.
- 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”
What are the causes and features of central retinal artery occlusion?
Cause:
- thromboembolism (due to atherosclerosis)
- arteritis (e.g. temporal arteritis / giant cell)
Features:
- sudden, painless loss of vision
- RAPD
- fundoscopy - ‘cherry red’ spot on pale retina
What are the causes and features of vitreous haemorrhage?
Causes:
- diabetes
- bleeding disorders
- anticoagulants
Features:
- sudden, painless loss of vision
- dark spots or floaters
What are the causes and features of retinal detachment?
N.B. retinal detachment has different forms which can present acutely or chronically
Causes:
- posterior vitreous detachment
- choroidal tumours
- trauma
- myopia (risk factor)
Features:
- dense shadow
- starts peripherally and progresses toward central vision
- feels like ‘veil or curtain’ over field of vision
- straight lines appear curved
- central vision loss
- photopsia - i.e. flashes of light (often seen in temporal visual field)
- floaters
What are the causes and features of central retinal vein occlusion?
N.B. central retinal vein occlusion is more common than central retinal artery occlusion
Causes:
- glaucoma
- polycythaemia
- HTN
Features:
- sudden, painless loss of vision
- fundoscopy - severe retinal haemorrhages
What does the central retinal artery supply?
What do the posterior ciliary arteries supply?
- Central retinal artery = retina
-
Posterior ciliary arteries:
- short posterior ciliary artieries (6-12 per eye) = choroid up to equator + ciliary processes
- long posterior ciliary artieries (2 per eye) = iris, ciliary body and choroid
What is orbital cellulitis?
Infection affecting the fat + muscles posterior to the orbital septum, within the orbit but not the globe
- Cause - often caused by spreading URTI from sinuses
- HIGH mortality = EMERGENCY!!
- Periorbital cellulitis = superficial infection anterior to orbital septum (less serious but can progress to orbital cellulitis)
- Avg age of hospitalisation = 7-12yrs
What are the risk factors for orbital cellulitis?
Risk factors:
- Childhood
- Previous sinus infection
- Lack of Haemophilus influenzae type b vaccination
- Recent infections:
- eyelid infection / insect bite on eyelid (peri-orbital cellulitis)
- ear infection
- facial infection
What are the features of orbital cellulitis?
*
Features:
- Red eye + swelling around the eye
- Eyelid oedema and ptosis
- Proptosis (i.e. protrusion of eyeball)
- Severe ocular pain
- Visual disturbance (↓ visual acuity + RAPD)
- Ophthalmoplegia / pain with eye movements
- Drowsiness
- Nausea / vomiting in meningeal involvement (Rare)
What symptoms differentiate orbital cellulitis from periorbital / preseptal cellulits?
The following are NOT consistent with periorbital / preseptal cellulits:
- ↓ visual acuity
- proptosis
- ophthalmoplegia / pain with eye movements
What do you see in this image?
Endophthalmitis (rare)
(i.e. infection of intraocular fluids i.e. vitreous and/or aqueous)
- Injected conjunctiva (red + bloodshot)
- Pus in anterior chamber
- Hypopyon = inflammatory accumulation of WBC (leukocytic exudate) seen as white ‘fluid level’ in anterior chamber + redness of conjunctiva
- Corneal sutures (top left)
Risk factors associated with endophthalmitis:
- Poorly controlled diabetes (↑ infection risk)
- Painful sudden visual loss (is their eye at risk?)
- Hx of recent ocular surgery (surgery caused infection)
- ITU / HDU admission
- IV lines / catheters
What are the features of anterior uveitis?
Features:
- acute onset
- red-eye
- eye pain
- blurred vision
- photophobia (often intense)
- hypopyon
- small, fixed, oval pupil
- ciliary flush - ring of red or violet spread out from around cornea
What conditions is anterior uveitis associated with?
(5 listed)
- ankylosing spondylitis
- reactive arthritis
- IBD i.e. ulcerative colitis & Crohn’s disease
- Behcet’s disease (autoimmune vasculitis, triad: oral ulcers, genital ulcers and anterior uveitis)
- sarcoidosis: bilateral disease may be seen
What structures does uveitis affect?
Anterior:
- Iris
- Ciliary body
Posterior:
- Choroid
What are the features of conjunctivitis?
Features:
- Red-eye
- Recent exposure to others with infected eye
- Recent URTI (more likely viral)
- Allergen exposure (allergic conjunctivitis)
-
Discharge
- watery = viral
- mucoid = allergic
- purulent = bacterial
- Itchy (allergic)
- Eyes stuck together in morning
- Pre-auricular lymphadenopathy (viral)
- Normal; visual acuity, reactive pupils
What are the risk factors for conjunctivitis?
Risk factors:
- Exposure to infected person
- Infection in one eye (can spread to other)
- Atopy
- Contact lens use
- Topical eye medication
- Hx of rheumatological disease
What investigations might you do for conjunctivitis?
-
Chlamydial swabs - chlamydia can cause a reactive arthritis which has a triad of:
- urethritis
- conjunctivitis
- arthritis
- Bacterial swabs
- Viral swabs
What test can be used to investigate the condition of the cornea?
Fluorescein
- Is an orange-water soluable dye, used IV (angiogram) and topically for cornea examination
- Fluorescein - can be used to identify regions of corneal epithelium loss:
- Intact corneal epithelium = not stained
- Deeper corneal stroma = stained
- Image shows dendritic ulcer in corneal stroma highlighted by fluorescein
For a dendritic ulcer - what is the likely pathogen?
Herpes simplex virus (HSV)
- HSV is enveloped with a cuboidal capsule and has a linear double-stranded DNA genome
- HSV resides in almost all neuronal ganglia
- Sub-types:
- HSV 1 - causes infection above the waist (principally the face, lips and eyes)
- HSV 2 - causes venereally-acquired infection (genital herpes)
What medication can be used in the management of HSV?
Aciclovir - (antiviral)
Which organisms commonly cause bacterial conjunctivitis?
- Streptococcus. pneumoniae
- S. aureus,
- Haemophilus. influenzae
- Moraxella catarrhalis
What might be involved in the management of conjunctivitis?
Most (~60%) cases resolve without treatment in 1-2 weeks
-
Chloramphenicol (topical Abx):
- Eye drops - 1 drop 3-4 times per day and for 48hrs after healing
- Ointment - apply QDS
- Topical lubricants
- Cool compress
- DON’T wear contact lenses until 48hrs after complete resolution
- Avoid sharing towels
What does this image show?
Bacterial keratitis causing a corneal ulcer (white circle)
- Keratitis = red eye, pain, ↓ eye-sight, photophobia, ‘gritty’ sensation
- Avoid contact lens wear
- Treatment = frequent topical broad-spectrum Abx
- Contraindicated: steroid eye drops, oral abx
What is not included in the management of severe contact lens related keratitis?
- Oral antibiotics
- Daily review
- Corneal Scrape
- Frequent topical broad-spectrum antibiotics
- requent Chloramphenicol drops
Frequent Chloramphenicol drops
- Pseudomonas Aeruginosa is the most frequent bacteria associated with contact lens wear and it’s not sensitive to Chloramphenicol
What can cause a 6th CN palsy?
-
Microvascular:
- Diabetes
- Atherosclerosis
- Smoking
- Trauma
- Idiopathic
- ↑ ICP
- GCA
- Cavernous sinus mass
- MS
- Sarcoidosis
- LP
- Hydrocephalus
- Idiopathic intracranial hypertension
What are the features of a 6th CN palsy?
-
Sudden onset, Horizontal Diplopia - worse when looking toward the affected side
- Pts often turn hear to affected side to compensate by maintaing binocular vision
- Esotropia (i.e. convergent squint) - during distance fixation the affected eye om directed medially
- Lateral rectus palsy on affected side
Is a 6th CN palsy an indication for urgent neuro-imaging?
NO!!
Commonly caused by microvascular pathologies e.g. diabetes, atherosclerosis etc.
Is a 3rd CN palsy an indication for urgent neuro-imaging?
Yes!!
Especially if w/ sudden pain as it can be a sinister cause e.g.
aneurysm
What are the features of a 3rd CN palsy?
- Affected eye = deviated laterally + inferiorly i.e. ‘down and out’
- Ptosis (CN III innervates levator palpebrae superioris)
- Dilated pupil (CN III caries parasympathetic fibres for pupil constriction)
What can cause a 3rd CN palsy?
- Diabetes
- Vasculitis e.g. temporal arteritis
- Posterior communicating artery aneurysm
- Pupil dilated
- Often painful
- Cavernous sinus thrombosis
- Weber’s syndrome = ipsilateral 3rd nerve palsy + contralateral hemiplegia (midbrain stroke)
- MS
- Amyloidosis
What are the features of a 4th CN palsy?
- Vertical diplopia
- Torsional diplopia - subjective tilting of objects
- Eye - deviates superiorly + rotated laterally
- May have head tilt (might not be aware)
- classically noticed when reading a book or going downstairs
Can pts with double vision drive?
No!!
-
Group 1 licence (cars):
- Pts can return to driving after a period of adaptation or if double revision resolves
- Pt can drive is double vision is controlled with prisms or occlude (patch) one eye (assuming vision is remaining eye is 6/12 and good fields)
- Group 2 licence (HGV /buses) = never!
What does Leukocoria mean?
Leukocoria = ‘White Pupil’
- Is a concerning sign (especially in children)
- It indicates absence of the red-reflex = opacity of optical media (anterior chamber, humour, lens, vitrous chamber)
- It can be a sign of Retinoblastoma - needs to be exluded URGENTLY!
What is a Retinablastoma + what are it’s features?
Retinablastoma = most common ocular malignancy in children (still rare)
- Avg age of diagnosis = 18 months
- ~ 40% are hereditary - autosomal dominant - LoF of retinoblastoma tumour supressor gene on chromosome 13
Features:
- Leukocoria (white pupil) - absence of red-reflex (commonest symptom)
- Strabismus - eyes don’t align with each other
- Visual problems
What is retinopathy of prematurity (ROP)?
ROP - is a proliferative retinopathy affecting premature infants of low birth weight, who have often been exposed to high ambient O2 concs.
Risk factors:
- Either of the following = screen at 4-7 weeks posnatally for ROP:
- born at or before 31 weeks
- born 1500g or less
- ~8% of babies screened require treatment (laser photocoagulation - successful in ~ 80% of cases)
Mechanism:
- Retina doesn’t start being vascularised until 4/12 gestation
- Retinal nasal periphery is vascularised at 8/12 gestation
- Retinal temporal periphery is vascularised at ~ 1 mo after delivery
- Incompletely vascularized retina = susceptible to O2 dmg in premature infant
- Normally - avascular retina produces VEGF –> stims vessel migration/growth
- But if born premature + O2 therapy –> the VEGF is down-regulated as retina experiences hyperoxia –> then as the infant grows at home the metabolic demand of the eye ↑ –> causing excessive VEGF production –> neovascular proliferative retinopathy
Congenital cateracts are rare (3 in 10,000 birth) + take many forms
e.g. dense large areas to fine blue dots.
Name 5 syndromes / microorganisms associated with congenital cataract formation.
- Rubella
- Varicella
- Cytomegalovirus
- Edward syndrome
- Down syndrome
