Opthal - Gradual loss of vision Flashcards
1
Q
What are cataracts?
A
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
2
Q
What is the most common cause of cataracts?
What other causes of cataracts are there?
A
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
3
Q
How are cataracts managed?
A
- 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
4
Q
What are the complications of cataract surgery?
A
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
5
Q
What is the difference between open-angle and closed-angle glaucoma?
A
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!
6
Q
What are the risk factors for primary open-angle glaucoma (POAG)?
A
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
7
Q
What are the features of POAG?
A
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
8
Q
How is POAG investigated?
A
-
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
9
Q
How is POAG managed?
A
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
10
Q
How is aqueous humour drained?
A
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
11
Q
What are the risk factors for Acute close-angle glaucoma (AACG)?
A
Risk factors for AACG:
- women
- hypermetropia (long-sightedness)
- pupillary dilatation
- age - lens growth association with age
12
Q
What are the features of AACG?
A
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
13
Q
How is AACG managed?
A
- 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)
14
Q
What is the commonest cause of blindness in the UK?
A
Age-realted macular degeneration
15
Q
What is age-related macular degeneration (ARMD)?
A
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
16
Q
What are the risk factors for ARMD?
A
Risk factors:
- AGE!! (biggest factor)
- Smoking
- 1st degree relatives with ARMD
- cataract surgery
- Risk factors for ischaemic heart disease:
- HTN
- Dyslipidaemia
- Diabetes
17
Q
What are the features of macular degeneration?
A
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)
18
Q
How do you investigate macular degeneration?
A
-
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
19
Q
What are the types of ARMD?
A
-
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
20
Q
How is ARMD managed?
A
- 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
21
Q
Who must pts diagnosed with POAG inform of their diagnosis?
A
- Family - there is a genetic risk component for glaucoma
- DVLA
22
Q
What sign does this image show?
A
Cherry Red spot
(sign of central retinal artery occlusion)
23
Q
What are the most common causes of sudden, painless loss of vision?
A
-
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)
24
Q
What is the medical term for sudden, painless, loss of vision?
A
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”
25
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**
26
What are the causes and features of **vitreous haemorrhage**?
**Causes:**
* diabetes
* bleeding disorders
* anticoagulants
**Features:**
* sudden, painless loss of vision
* dark spots or floaters
27
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**
28
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**
29
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
30
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
31
What are the risk factors for orbital cellulitis?
**Risk factors**:
* **Child**hood
* **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
32
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)
33
What symptoms differentiate orbital cellulitis from periorbital / preseptal cellulits?
The following are NOT consistent with periorbital / preseptal cellulits:
1. ↓ visual acuity
2. proptosis
3. ophthalmoplegia / pain with eye movements
34
What do you see in this image?
**Endophthalmitis** (rare)
(i.e. infection of intraocular fluids i.e. vitreous and/or aqueous)
1. Injected conjunctiva (red + bloodshot)
2. Pus in anterior chamber
1. **Hypopyon** = inflammatory accumulation of WBC (leukocytic exudate) seen as white 'fluid level' in anterior chamber + redness of conjunctiva
3. 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
35
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
36
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
37
What structures does uveitis affect?
Anterior:
* Iris
* Ciliary body
Posterior:
* Choroid
38
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
* P**re-auricular lymphadenopathy** (viral)
* Normal; visual acuity, reactive pupils
39
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
40
What investigations might you do for conjunctivitis?
1. **Chlamydial** swabs - chlamydia can cause a reactive arthritis which has a triad of:
* urethritis
* **conjunctivitis**
* arthritis
2. **Bacterial** swabs
3. **Viral** swabs
41
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
42
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)
43
What medication can be used in the management of HSV?
**Aciclovir** - (antiviral)
44
Which organisms commonly cause bacterial conjunctivitis?
* Streptococcus. pneumoniae
* S. aureus,
* Haemophilus. influenzae
* Moraxella catarrhalis
45
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
46
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
47
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**
48
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
49
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
50
Is a 6th CN palsy an indication for urgent neuro-imaging?
NO!!
Commonly caused by microvascular pathologies e.g. diabetes, atherosclerosis etc.
51
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
52
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)
53
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
54
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
55
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**!
56
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!
57
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**
58
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
59
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.
1. Rubella
2. Varicella
3. Cytomegalovirus
4. Edward syndrome
5. Down syndrome
