Acute Painful Eye Flashcards
1
Q
Causes of a painful red eye
A
◦ Corneal abrasions
◦ Corneal ulcers
◦ Corneal foreign bodies
◦ Chemical injuries
◦ Acute anterior uveitis
◦ Anterior scleritis
◦ Acute angle-closure glaucoma
◦ Endophthalmitis
◦ Trauma
◦ Ectropion and entropion
◦ Trichiasis
- conjunctivitis
2
Q
Causes of a painless red eye
A
Subconjunctival haemorrhage
Blepharitis
Episclertisi
Conjunctivitis
Dry eyes
Allergic conjunctivitis
3
Q
What are the 2 parts of the conjunctiva?
A
the thin, transparent mucous membrane lining the anterior part of sclera = bulbar conjunctiva
and the under-surface of the eyelids = palpebral conjunctiva
4
Q
What can cause conjunctivitis?
A
• allergies
• Infections
• Mechanical irritation
• Neoplasia
• Contact with toxic substances
Up to 80% of all cases of acute conjunctivitis are caused by viral infections.
But 50-75% of cases of infective conjunctivitis in children are thought to be bacterial
Most common viral - adenovirus. Others include herpes simplex, VZV, molluscum contagiosum, EBV, coxsackie, enteroviruses
Bacterial - step pneumoniae, staph aureus, H.influenza or moraxella catarrhalis in children
5
Q
Whats the most common viral cause of conjunctivitis?
A
Adenovirus
6
Q
What is acute. And chronic conjunctivitis?
A
Acute <4 weeks
Chronic >4 weeks
7
Q
What is hyper acute conjunctivitis and what typically causes it?
A
rapidly developing severe conjunctivitis - typically neisseria gonorrhoeae
8
Q
What is ophthalmia neonatorum?
A
Conjunctivitis occurring within the first 4 weeks of life
Can be infectious - neisseria gonorrhoeae or chlamydia
Or can be non infectious
9
Q
What are the clinical features of conjunctivitis?
A
• acute onset conjunctival erythema
• Grittiness or burning or foreign body sensation
• Watering and discharge which may cause transient blurring of vision
• Purulent or Mucopurulent discharge with crusting of lids which may be stuck together on waking - bacterial
• Pre-auricular lymphadenopathy - often seen with hyperacute bacterial conjunctivitis
• Petechial Subconjunctival haemorrhages - viral
• URTI symptoms - viral
• Bilateral itching with associated swelling of eyelids and conjunctiva (chemosis) - allergic conjunctivitis!
10
Q
How does herpes conjunctivitis typically present?
A
unilateral red eye with vesicular lesions visible on the eyelid and watery discharge
11
Q
What is Hutchinson’s sign?
A
Herpes zoster lesions on tip of nose = ocular involvement
indicates involving of the nasociliary nerve
12
Q
How does neisseria gonorrhoeae conjunctivitis typically present?
A
12-24 hours rapid onset with copious mucopurulent discharge, eyelid swelling and tender preauricular lymphadenaopthy
13
Q
What investigation for ?ophthalmia neonatorum?
A
Swabs of the discharge urgently
14
Q
How do we treat acute non-herpetic viral conjunctivitis?
A
self-limiting resolves in 1-2 weeks, self care e.g. clean eyelids with boiled and cooled water, cool compresses and avoid spreading it
15
Q
Tx acute bacterial conjunctivitis?
A
self-limiting in 5-7 days.
If severe or circumstances required rapid relation then chloramphenicol drops 2-3 hrly, chloramphenicol ointment QDS or fusidic acid eye drops (mainly latter if pregnant)
Advice not to share towels
16
Q
Moa chloramphenicol?
A
antimicrobial that inhibits proteins synthesis by binding 50s
17
Q
How is management of conjunctivitis different in contact lens wearers?
A
You must advise them to Stop lens use until infection symptoms are completely gone
Same management but use topical fluorescein to identify any corneal staining
18
Q
Tx allergic conjunctivitis?
A
Topical or systemic antihistamines
Reduce causative allergic
Topical mast cell stabilisers e.g. sodium cromoglicate can also be used
19
Q
Prognosis of viral conjunctivitis, bacterial conjunctivitis and ophthalmia neonatorum?
A
Viral - resolves within 7 days
Bacterial - 5-10 days
Ophthalmia - Most cases are mild but untreated infections can lead to serious complications such as sight loss and mortality
20
Q
What are some of the differentiating features of viral and bacterial conjunctivitis?
A
Bacterial - purulent discharge and eyes may be stuck together in the morning
Viral - serous discharge, recent URTI, preauricular lymphadenopathy
21
Q
How should you manage bacterial conjunctivitis in women who are pregnant?
A
Topical fusidic acid twice daily
22
Q
What is the episclera?
A
A thin vascular layer sandwiched between the superficial conjunctiva and deeper sclera; its the outermost layer of the sclera
23
Q
What causes episcleritis?
A
Idiopathic in 70% of cases
related to IBD and RA
24
Q
How often is episcleritis bilateral?
A
In 50%
25
Presentation of episcleritis?
• acute onset unilateral localised/diffuse redness
• No or very mild pain
- watering and mild photophobia may be present
• Dilated episcleral vessels (moveable with a swab as its superficial + it will blanch with topical phenylephrine)
26
How can we differentiate between scleritis and episcleritis?
Scleritis is painful and epi is not
Applying phenylephrine eye drops will call blanching of episcleral vessels but not sclera vessels
27
How do we manage episcleritis?
Conservative as self limiting in 1-2 weeks
Artificial tears may sometimes be used
28
What is scleritis?
Full thickness inflammation of the sclera (the outer layer of connective tissue surrounding most of the eye and forming the visible white part of the eye - continuous with the cornea)
29
What causes scleritis?
Most commonly idiopathic
Related to RA mostly. Other relations include SLE, sarcoidosis and granulomatosis with polyangiitis. 50% cases linked to systemic conditions
Less commonly can be infective cause
30
What is the most severe type of scleritis?
Necrositing scleritis which can lead to perforation of the sclera
31
How does scleritis present?
• red eye
• A boring pain with painful eye movements and tender to touch (in comparison to episcleritis)
• Watering and photophobia are common
• Gradual decrease in vision
• If recurrent there may be sclera thinning
32
How do we manage scleritis?
same-day assessment by an ophthalmologist
oral NSAIDs are typically used first-line
oral glucocorticoids may be used for more severe presentations
immunosuppressive drugs for resistant cases (and also to treat any underlying associated diseases)
33
What is a subconjuntcival haemorrhage?
When small blood vessels within the conjunctiva rupture releasing blood into the space between the sclera and conjunctiva
34
What causes a subconjunctival haemorrhage?
Episodes of strenuous activity - heavy coughing, weight lifting, vomiting, straining in constipation
Trauma to the eye
Or idiopathic with risk factors such as hypertension, bleeding disorders, whooping cough, meds such as antiplatelets or NAI
35
How does a subconjuntival haemorrhage present?
A painless bright red blood patch covering the white of the eye
The haemorrhage will stop at the limbus! Will not affect vision!
36
what is the limbus?
Junction between cornea and conjunctiva
37
What investigations could we do when someone presents with a subconjuntival haemorrhage?
Check bp if idiopathic
Check INR if pt on warfarin
38
how do we manage a subconjuntival haemorrhage?
Harmless and will resolve spontaneously without treatment within 2 weeks
39
What is blepharitis?
Inflammation of the lid margins
40
How does blepharitis present?
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
41
What causes blepharitis?
It may due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis).
Blepharitis is also more common in patients with rosacea
42
Whats the function of Meibomian glands?
Responsible for secreting meibum (oil) onto the surface of the eyes to prevent the rapid evaporation of the tear film
43
How do we manage blepharitis?
softening of the lid margin using hot compresses twice a day
'lid hygiene' - mechanical removal of the debris from lid margins
cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used
an alternative is sodium bicarbonate, a teaspoonful in a cup of cooled water that has recently been boiled
artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film
44
What is a stye?
An infection of the glands of the eyelids
45
What are the types of stye?
Hordeolum externum: infection (usually staphylococcal) of the glands of Zeis or glands of Moll
Hordeolum internum: infection of the Meibomian glands. May leave a residual chalazion (Meibomian cyst)
46
what are the glands of Zeis?
Sebaceous glands at the base of eyelashes
47
What are the glands of Moll?
Sweat glands at the base of eyelashes
48
What does a Hordeolum externum look like?
A red tender lump along the eyelid that will likely have a yellow head as it contains pus
49
What does a Hordeolum internum look like?
Deep painful lumps that may point inwards towards the eyeball underneath the eyelid
50
What is a Chalazion?
Aka a Meibomian cyst
It is a retention cyst of the Meibomian gland. It presents as a firm painless lump in the eyelid. The majority of cases resolve spontaneously but some require surgical drainage
51
How do we manage a stye?
Hot compress and analgesia
Only use topical antibiotics if associated with conjunctivitis
52
What is an entropion?
In turning of the eyelid with lashes pressed against the eye
This causes pain and can result in corneal damage/ulceration
53
How do we manage an entropion?
Tape the eyelids down and eye drops
Definitive management is surgical
54
what is an ectropion?
When the eyelid is turned outward exposing the inner aspect of the eye
It usually affects the bottom lid
55
What can an ectropion lead to?
Exposure keratopathy as the eyelid is exposed and not adequately lubricated and protected
56
How do we manage ectropion?
Mild cases may not require treatment other than regular lubricator eye drops to protect the eye surface
More significant cases may require surgery to correct the defect
57
What causes entropions and ectropions?
Ectropion is usually associated with ageing. It can happen as the tissues and muscles of the eyelids become weaker as you get older.
Less common causes of ectropion include:
- Bell’s palsy
- a lump, cyst or tumour on the eyelid
- damage to the skin around the eyelid as a result of an injury, a burn, a skin condition such as contact dermatitis, or previous surgery
Rarely, ectropion can be present from birth if the muscles under the eyelid do not develop properly.
58
What is trichiasis?
The inward growth of eyelashes which causes pain and can sometimes cause corneal damage
59
How do we manage trichiasis?
Remove the affected eyelashes
Recurrent cases may require electrolysis, cryotherapy or laser treatment to prevent re growth
60
What is herpes zoster ophthalmicus? what are the features?
The reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve
Features: vesicular rash around the eye which may or may not involve the eye, Hutchinson’s sigh
61
How do we manage herpes zoster ophthalmicus?
oral antiviral treatment for 7-10 days ideally started within 72 hours
IV antivirals may be given for very severe infection or if the patient is immunocompromised
topical corticosteroids may be used to treat any secondary inflammation of the eye
!!ocular involvement requires urgent ophthalmology review!!
62
What are complications of herpes zoster ophthalmicus?
Ocular - conjunctivitis, keratitis, episcleritis, anterior uveitis
Ptosis
Post-hermetic neuralgia
63
Why are annual eye exams recommended for rheumatoid arthritis patients?
Retinopathy can occur due to hydroxychloroquine use in rheumatoid arthritis
64
What can we use to determine if blurred vision is due to a refractive error?
pinhole occluders
if the blurring improves with a pinhole occluder then likely cause is a refractive error
It is a simple way to focus light, temporarily removing the effects of refractive errors such as myopia.
65
What is preseptal cellulitis?
Aka periorbital cellulitis
An infection of the soft tissues anterior to the orbital septum - eyelids, skin and subcutaneous tissue of the face (not contents of orbit!!)
66
What causes periorbital cellulitis?
Infection usually spreads to the structures surrounding the orbit from other nearby sites, most commonly from breaks in the skin or local infections such as sinusitis or other respiratory tract infections.
The most frequently causative organisms are Staph aureus, Staph epidermidis, streptococci and anaerobic bacteria.
67
What age does preseptal cellulitis typicall affect?
Children - 80% of Pt are <10 and median age of presentation is 21 months
68
Why is orbital cellulitis more common in winter?
Due to increased prevalence of RTIs
69
How does preseptal cellulitis present?
Red, swollen, painful eye of acute onset
Parital or complete ptosis of the eye due to swelling
70
Investigations s for preseptal cellulitis?
Bloods - raised inflammatory markers
Swab of any discharge present
Contrast CT of the orbit may help to differentiate between preseptal and orbital cellulitis. It should be performed in all patients suspected to have orbital cellulitis
71
how do we manage preseptal cellulitis?
All cases should be referred to secondary care for assessment
Oral antibiotics are frequently sufficient - usually co-amoxiclav
Children may require admission for observation
72
Complication of preseptal cellulitis?
Bacterial infection. May spread into the orbit and evolve into orbital cellulitis
73
What is orbital cellulitis?
An infection affecting the fat and muscles posterior to the orbital septum
A medical emergency requiring hopsital admission and urgent senior review
74
What causes orbital cellulitis?
Spreading URTI from the sinuses usually
75
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
76
How does orbital cellulitis present?
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)
77
How do we differentiate orbital from preseptal cellulitis?
reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements are NOT consistent with preseptal cellulitis
78
How do we investigate orbital cellulitis?
Full blood count – WBC elevated, raised inflammatory markers.
Clinical examination involving complete ophthalmological assessment – Decreased vision, afferent pupillary defect, proptosis, dysmotility, oedema, erythema.
CT with contrast – Inflammation of the orbital tissues deep to the septum, sinusitis.
Blood culture and microbiological swab to determine the organism.
79
Most common bacterial causes of orbital cellulitis?
Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.
80
How do we manage orbital cellulitis?
Admission to hospital for IV antibiotics
81
What are corneal abrasions?
Scratches or damage to the cornea
82
What causes corneal abrasions?
Damaged contacts
Finger nails
Foreign bodies
Makeup brushes
Entropion etc
83
How does corneal abrasion present?
a history of trauma followed by a painful red eye, photophobia, foreign body sensation, Epiphora, blurred vision.
The pain will typically be surface sympotms e.g. grittiness
84
How do we diagnose a corneal abrasion
Fluorescein stain - yellow-orange colour collects in abrasions of ulcers highlighting them under cobalt blue light
85
How do we manage a corneal abrasion?
Usually heals over in 2-3 days
86
What is a corneal ulcer?
A defect on the cornea, typically secondary to an infective cause
87
What are risk factors for a corneal ulcer?
Contact lens use
Vitamin A deficiency in the developing world
88
Causes of corneal ulcer?
bacterial keratitis
fungal keratitis
viral keratitis: herpes simplex, herpes zoster - may lead to a dendritic ulcer
Acanthamoeba keratitis: associated with tap water and contact lens use
89
Features of corneal ulcer?
eye pain
photophobia
watering of the eye
focal fluorescein staining of the cornea
90
What is a corneal ulcer also known as?
Microbial keratitis
91
How do we manage a corneal ulcer?
Topical antibiotics, antiviral sor antifungal
Corneal transplant for permenatn scarring and vision loss
Without treatment they can cause rapid, permenantsight loss!
92
What is an alkali chemical injury of the eye worse than an acid injury?
Acids have a lower pH than the eye so they precipitate tissue protein which creates a barrier preventing further ocular penetration
Alkalis are more severe as they penetrate deeper into ocular tissue
93
How do we manage a chemical injury to the eye?
Immediate irrigation of the eye until pH neutralises before conducting any further investigation
Control pain and nausea
Specialist referral!!
94
Typical clinical findings in a chemical injury to the eye?
• conjunctival hyperaemia
• Corneal haze with an impaired view of the underlying iris and pupil if severe
• Blanched blood vessels
• After instilling fluorescein 2% under blue light areas of corneal/conjunctival epithelial defect will glow green
95
What is the most common cause of abnormal tearing in infants and children in the first year of life?
Nasolacrimal duct obstruction
96
How does nasolacrimal duct obstruction present?
History of chronic or intermittent tearing and occasionally redness of the conjunctiva
97
Why do pt with orbital cellulitis require admission and IV antibiotics?
Due to the risk of cavernous sinus thrombosis and intracranial spread
98
What is anterior uveitis also known as?
Irititis
99
What is anterior uveitis?
Inflammation of the anterior portion of the urea - iris and ciliary body
100
What is the uvea?
Middle portion of the eye between the sclera and retina
It contains the iris, ciliary body (part of eye that helps lens focus) and and choroid (part of eye connecting retina to sclera)
101
What conditions are associated with anterior uveitis?
HLA-B27 related conditions:
ankylosing spondylitis
reactive arthritis
IBD
Behcet's disease
sarcoidosis: bilateral disease may be seen
102
What are symptoms of anterior uveitis?
acute onset ocular discomfort & pain (may increase with use)
pupil may be small +/- irregular due to sphincter muscle contraction
photophobia (often intense)
blurred vision
red eye
lacrimation
ciliary flush: a ring of red spreading outwards
hypopyon
visual acuity initially normal → impaired
103
How do we manage anterior uveitis?
urgent review by ophthalmology
cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate
steroid eye drops
104
Examples of cycloplegics?
Atropine
Cyclopentolate
105
What is endophthalmitis?
An infection of the intraocular fluids (vitreous and aqueous) and internal eye tissues
106
What can cause endophthalmitis?
May be secondary to an exogenous source - recent cataract surgery or intravitreal injection
May be secondary to an endogenous source e.g. seeded from endocarditis or candida sepsis
107
Features of endophthalmitis?
Red eye - diffuse conjunctival injection
Severe Pain
Rapidly progressive visual loss
Photophobia
Floaters
Corneal haze
Hypopyon
RAPD
108
What is glaucoma?
A group of disorders characterised by optic neuropathy. In the majority of pt this is caused by a raised intraocular pressure
109
What is acute angle-closure glaucoma?
There is a rise in intraocular pressure secondary to an impairment of aqueous outflow
The iris bulges forward and seals off the trabecular meshwork from the anterior chamber, preventing aqueous humour from draining and leading to an increase in IOP. The pressure builds in the posterior chamber, pushing the iris foeward and exacerbating the angle closure
110
Risk factors for acute angle-closure glaucoma?
Hypermetropia
Pupillary dilatation
Lens growth associated with age
Certain meds - adrenergic meds, Anticholinergics, TCAs etc
111
Features of acute angle-closure glaucoma?
severe pain: may be ocular or headache
decreased visual acuity
symptoms worse with mydriasis (e.g. watching TV in a dark room)
hard, red-eye
haloes around lights
semi-dilated non-reacting pupil
corneal oedema results in dull or hazy cornea
systemic upset may be seen, such as nausea and vomiting and even abdominal pain
112
Investigations for acute angle-closure glaucoma?
Tonometry to assess for elevated IOP
Genioscopy - special lens for the slit lamp that allows visualisation of the angle
113
How do we manage acute angle-closure glaucoma?
Should prompt urgent referral to ophthalmology
Emergency medical treatment to lower IOP:
- eye drops - direct parasympathomimetics, beta blockers, alpha-2 agonists
- IV acetazolamide
Definitive surgical treatment:
- laser periperal iridotomy
114
what is laser peripheral iridotomy?
Creating a tiny hole in the peripheral iris so aqueous humour can flow to the angle
115
Give examples of a direct parasympathomimetic eye drop you can use for acute angle-closure glaucoma? How does it work?
Pilocarpine
Causes contraction of ciliary muscles which opens the trabecular meshwork and increases the outflow of the aqueous humour
116
Give examples of a beta blocker eye drop you can use for acute angle-closure glaucoma? How does it work? Side effects?
Timelol
Decreases aqueous humour production
117
Give examples of a alpha-2 agonist eye drop you can use for acute angle-closure glaucoma? How does it work? Side effects?
Apraclonidine
Decreases aqueous humour production and increases uveoscleral outflow
118
How does acetazolamide work for acute angle-closure glaucoma?
Blocks carbonic anhydrase which reduces the amount of aqueous secretions
119
What is hyphema?
Blood in the anterior chamber of the eye most commonly caused by trauma
120
Why does hyphema warrant urgent referral to ophthalmology?
As There’s a risk to sight from raised IOP which can develop due to blockage of the angle and trabecular meshwork with erythrocytes
121
Management of hyphema?
Strict bed rest - excessive movement can re disperse blood that had settled
High-risk cases admitted
Daily ophthalmic review and pressure checks
Assessment for orbital compartment syndrome
122
What are features of orbital compartment syndrome?
eye pain/swelling
proptosis
'rock hard' eyelids
relevant afferent pupillary defect
123
Management of orbital compartment syndrome?
urgent lateral canthotomy (before diagnostic imaging) to decompress the orbit
124
What most commonly causes orbital compartment syndrome
A retrobulbar haematoma after blunt trauma or surgery
125
What is optic neuritis?
Inflammation of the optic nerves
126
What causes optic neuritis?
MS - most common
Diabetes - due to ischaemia
Syphilis
Can also be antibody-mediated, associated with sarcoidosis, Lyme disease or ethambutol
127
How does MS cause optic neuritis?
T cells directed against CNS antigens which destroys the myelin sheath = inflammation of optic nerves
128
What % of MS patients will have at least 1 episode of optic neuritis?
70%
129
Features of optic neuritis?
unilateral decrease in visual acuity over hours or days
poor discrimination of colours, 'red desaturation' - as optic nerve carries these colour symptoms
pain worse on eye movement (when eye moves, inflamed optic nerve is pulled triggering discomfort)
relative afferent pupillary defect
central scotoma (as central area of optic nerve is more susceptible to damage in optic neuritis)
130
Investigation of optic neuritis?
MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases
131
How do we manage optic neuritis?
high-dose steroids
recovery usually takes 4-6 weeks
132
How can MRI in optic neuritis help tel us the risk of the pt developing MS?
MRI: if > 3 white-matter lesions, 5-year risk of developing multiple sclerosis is c. 50%
133
What is a relative afferent pupillary defect?
Aka a Marcus Gunn pupil
The pupil will remain dilated despite exposure to bright lights and the individuals pupils may become different sizes
When a light is shone into the affected eye, it will not constrict as much as the unaffected eye
134
What causes a relative afferent pupillary defect?
Optic neuritis
Retinal detachment
Severe glaucoma
135
What is the most common cause of blindness in adults aged 35-65 years?
Diabetic retinopathy
136
Pathophysiology of diabetic retinopathy
Hyperglycaemia causes increased retinal blood flow and abnormal metabolism in the retinal vessel walls -> damage to endothelial cells and pericytes
This endothelial dysfunction leads to increased vascular permeability = exudates
Pericytes dysfunction = predisposition to formation of microaneurysms
Retinal ischaemia leads to production of growth factors = Neovasculization
137
What are blot haemorrhages seen in diabetic retinopathy caused by?
Increased vascular permeability
138
What are hard exudates seen in diabetic retinopathy caused by?
Endothelial dysfunction causing increased vascular permeability = Deposits of lipids and proteins in the retina
139
What are microaneurysms and venous beading seen in diabetic retinopathy caused by?
Damaged blood vessel walls
140
What are cotton wool spots seen in diabetic retinopathy caused by?
Represents nerve fibre layer infarction and ischaemia
Also known as soft exudates
141
How do we classify diabetic retinopathy?
Non-proliferative - microaneryssm, blot haemorrhages, hard exudates, cotton wool spots, venous beading, intraretinal micro vascular abnormalities. But NO neovascularisation
Proliferative diabetic retinopathy - retinal neovasculiration which may need to vitroeous haemorrhage - more common in type 1 diabetes
142
What % of proliferative diabetic retinopathy will be blind in 5 years?
50%
143
What is maculopathy?
When diabetic retinopathy affects the macula - poor central vision
Known as diabetic macular oedema
Hard exudates and other ‘background’ changes on macula
More common in typ2 diabetes
144
How do we manage all pt with diabetic retinopathy?
optimise glycaemic control, blood pressure and hyperlipidemia
regular review by ophthalmology
145
How do we manage maculopathy?
If there is a change in visual acuity then intravitreal VEGF inhibitors
146
How do we manage non-proliferative diabetic retinopathy?
regular observation
if severe/very severe consider panretinal laser photocoagulation
147
How do we manage proliferative diabetic retinopathy?
panretinal laser photocoagulation
intravitreal VEGF inhibitors - often now used in combination with panretinal laser photocoagulation. E.g. ranibizumab
if severe or vitreous haemorrhage: vitreoretinal surgery
148
What are the complications of panretinal laser photocoagulation?
50% of pt will develop a noticeable reduction in their visual fields due to scarring of peripheral retinal tissue
Decrease in night vision - most rods are in peripheral retina and these are responsible for vision
General decrease in visual acuity
Macular oedema
149
What is the important of detection and management of diabetic eye disease?
Can result in severe vision impairment and even blindness
Early detection saves vision as we can catch it in early stages to allow for timely intervention
With proper management we can prevent progression
Vision loss can significantly impact on an indiviual’s quality of life
Diabetic eye disease can serve as an indicator of other complications related to diabetes e.g. heart disease
150
Outline screening in the UK for diabetic eye disease?
Every over 12 with diabetes is entitles to NHS diabetic eye screening at least once every 2 years (at first it will be annually and this will change dependant on results)
151
What is a vitreous haemorrhage?
Bleeding into vitreous humour
One of the most common causes of sudden painless loss of visual
152
What causes a vitreous haemorrhage?
50% is proliferative diabetic retinopathy
Posterior vitreous detachment
Ocular trauma - most common cause in children
153
How does a vitreous haemorrhage present?
painless visual loss or haze (commonest)
red hue in the vision
floaters or shadows/dark spots in the vision
Visual field defects if severe haemorrhage
154
What will you see on slit lamp examination in a vitreous haemorrhage?
RBCs in anterior vitreous
155
Why do we use USS on vitreous haemorrhage?
To rule out retinal tear or detachment and if haemorrhage obscures the retina
156
What investigations for 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
157
What is hypertensive retinopathy?
Damage to small blood vessels in the retina relating to hypertension
These changes can happen slowly with chronic hypertension or quickly in response to malignant hypertension
158
What are the features of hypertensive retinopathy?
• silver or copped wiring - walls of arteries become thickened and sclerosed and reflect more light on examination
• Arteriovenous nipping - atterioles causing compression of the veins where they cross due to sclerosis and hardening of the arterioles
• Cotton wool spots - ischaemia and infarction in the retina causing damage to nerve fibres
• Hard exudates - damaged vessels leaking lipids onto the retina
• Retinal haemorrhages - damaged vessels rupturing and releasing blood in the retina - dot, blot and flame
• Papilloedema - ischaemia to optic nerve causing oedema
159
What classification system for hypertensive retinopathy?
Keith-Waganer classification
Stage 1 : mild narrowing of atterioles and silver wiring
Stage 2 : AV nipping
Stage 3 : cotton wool patches, exudates and haemorrhages - haemorrhages may collect around fovea resulting in a ‘macula star’
Stage 4 : papilloedema
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How do we manage hypertensive retinopathy/
Control bp and risk fatcors
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What is papilloedema?
Optic disc swelling caused by increased ICP
Almost always bilateral
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Fundoscopy signs of 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
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What are the causes of papilloedema?
space-occupying lesion: neoplastic, vascular
malignant hypertension
idiopathic intracranial hypertension
hydrocephalus
hypercapnia
Rare causes include:
hypoparathyroidism and hypocalcaemia
vitamin A toxicity
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What is the Hirschberg test?
Corneal light reflection test - shining a light into pt eyes and observing the reflection on their corneas. If reflections are symmetrical it suggests normal alignament of eyes. If asymmetrical it may indicate a squint.
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What are cataracts?
Common eye condition where the lens of the eye gradually opacifies making it more difficult for light to reach the retina and thus causing reduced or blurred vision
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What is the leading cause of curable blindness worldwide?
Cataracts
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What causes cataracts?
Normal ageing process is the most common cause - 30% of pt over 65 have one
Other possible causes: smoking, alcohol, trauma, DM, long term steroids, radiation exposure, myotonic dystrophy, hypocalcaemia
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How do cataracts present?
Reduced vision
Faded colour vision: making it more difficult to distinguish different colours
Glare: lights appear brighter than usual
Halos around lights
Defect in red reflex
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Investigations for cataracts?
Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
Slit-lamp examination. Findings: visible cataract
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Management of Cataracts?
Non-surgical: In the early stages, age-related cataracts can be managed conservatively by prescribing stronger glasses/contact lens, or by encouraging the use of brighter lighting. These options help optimise vision but do not actually slow down the progression of cataracts, therefore surgery will eventually be needed.
Surgery is the only effective treatment for cataracts. This involves removing the cloudy lens and replacing this with an artificial one.
NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice. Also whether both eyes are affected and the possible risks and benefits of surgery should be taken into account.
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Complications following surgery of cataracts?
Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
Endophthalmitis: inflammation of aqueous and/or vitreous humour
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Pathophysiology of primary open-angle glaucoma?
A gradual increase in resistance to flow through trabecular meshwork causing increased IOP
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Risk factors for primary open-angle glaucoma?
increasing age
genetics (first degree relatives of an open-angle glaucoma patient have a 16% chance of developing the disease)
Afro Caribbean ethnicity
myopia
hypertension
diabetes mellitus
corticosteroids
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How does primary open-angle glaucoma present?
May present insidiously so is often detected during routine optometry appointments!
Peripheral visual field loss - nasal scotomas progressing to tunnel vision
Decreased visual acuity
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Fundoscopy findings in primary open-angle glaucoma?
Optic disc cupping - cup-to-disc ratio >0.7
Optic disc pallor indicating optic atrophy
Bayoneting of vessels
Cup notching and disc haemorrhages
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Investigations for primary open-angle glaucoma?
automated perimetry to assess visual field
slit lamp examination with pupil dilatation to assess optic nerve and fundus for a baseline
applanation tonometry to measure IOP
central corneal thickness measurement
gonioscopy to assess peripheral anterior chamber configuration and depth
Assess risk of future visual impairment, using risk factors such as IOP, central corneal thickness (CCT), family history, life expectancy
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Management primary open-angle glaucoma?
First line - 360 degree selective laser trabeculoplasty for pt with IOP >=24
Second line - prostaglandin analogue eye drops
Third line - beta blocker, carbonic anhydrase inhibitor or sympathomimetic eye drops
In refractory cases - trabeculectomy surgery
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Give example, MOA and SE of prostaglandin analogues for treatment of primary open-angle glaucoma
Latanoprost
Increases uveoscleral outflow
Brown pigmentation of iris and increased eyelash length
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Give example, MOA of beta blocker eye drops for treatment of primary open-angle glaucoma
Timolol or betaxolol
Reduces aqueous production
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Give example, MOA and SE of sympathomimetic eye drops for treatment of primary open-angle glaucoma
Brimonidine - alpha 2 adrenoreceptor agonist
Reduces aqueous production and increased outflow
Hyperaemia
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Give example, MOA and SE of carbonic anhydrase inhibitors for treatment of primary open-angle glaucoma
Dorzolamide
Reduces aqueous production
Sulphonamide-like reactions if systemic absorption
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Give example, MOA and SE of miotics for treatment of primary open-angle glaucoma
Pilocarpine - muscarinic receptor agonist
Increases uveoscleral outflow
Constricted pupil, headache, blurred vision
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What is retinal detachment?
When neurosensory layer of the retina comes away from its underlying pigment epithelium attaching to the choroid
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What causes retinal detachment?
Usually due to a retinal tear allowing vitreous fluid to get under the neurosensory layer of the retina and fill this space
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What % of those pt with untreated symptmatic retinal breaks will progress to retinal detachment?
50%
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Risk factors for retinal detachment?
Diabetes - retinal breajs due to traction by vitreous humour
Myopia - increases risk of posterior vitreous detachment and peripheral retina may be thinned and more likely to tear
Age
Previous cataract surgery accelerates posterior vitreous detachment
Eye trauma e.g. boxing
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What is rhegmatogenous retinal detachment?
Most common type of retinal detachment
A retinal tear causing fluid to enter the subretinal space causing retinal detachment
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What is exudative retinal detachment?
When fluid builds up in the subretinal space but there aren’t any tears in the retina
This can be caused by inflammation in the eye
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What is tractional retinal detachment?
When scar tissue on the retina pulls your retina away from the back of your eye
Most commonly seen in pt with proliferative diabetic retinopathy - damaged blood vessels scar retina
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Features of retinal detachment?
new onset floaters or flashes, as these indicate pigment cells entering the vitreous space or traction on the retina respectively
sudden onset, painless and progressive visual field loss, described as a curtain or shadow progressing to the centre of the visual field from the periphery should also raise suspicion of detachment
if the macula is involved, central visual acuity and visual outcomes become much worse
peripheral visual fields may be reduced, and central acuity may be reduced to hand movements if the macula is detached
the swinging light test may highlight a relative afferent pupillary defect if the optic nerve is involved
fundoscopy
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.
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Who should you refer to ophthalmology for ?retinal detachment?
Any pt with new onset flashes or floaters - within 24 hours
Visual field loss, changes in visual acuity or fundoscopic sigs of retinal detachment - immediate
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How do we manage retinal tears?
Laser therapy or cryotherapy to create a scar adhesions between retina and retinal pigment epithelium to seal the hole and prevent more fluid accessing the subretinal space
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How do we manage retinal detachment?
Virectomy
Sclera buckling
Pneumatic retinopexy
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What is virectomy?
keyhole surgery on the eye. relieves traction by removing the vitreous attached to the retinal breaks. A gas or oil bubble is then used to span and close the retinal break until a scar develops
Used in retinal detachment
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What is sclera buckling?
a silicone buckle is places on the sclera surface over retinal breaks; this puts pressure on the sclera from outside the eye, squashing the eye inwards to reconnect the layers of the retina
Used In retinal detachment
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What is pneumatic retinopexy?
injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble presses the separated
Used in retinal detachment
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What is the most common cause of blindness in the UK?
Age-related macular degeneration
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What is age-related macular degeneration
Degeneration of the macula (central retina) - degeneration of retinal photoreceptors that results in formation of drusen
Usually bilateral
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Risk factors for age-related macular degeneration?
Advancing age is the greatest ris factors
Smokers are twice as likely
FHx - first degree relatives are 4x more likely
RF for ischaemic CVD
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2 forms of macular degeneration?
Dry macular degeneration - 90% of causes
Wet macular degeneration - 10%
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What is dry macular degeneration also known as and what is it characterised by?
Atrophic
Drusen - yellow round spots in Bruch’s membrane
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What is wet macular degeneration also known as and what is it characterised by?
Exudative or neovascular macular degeneration
Characterised by choroidal neovasculiarisation
Carries worst prognosis as can cause rapid loss of vision
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Clinical features of macular degeneration?
Reduction in visual acuity, particuarly for near field objects - over years in dry or more rapid in wet ARMD
Deterioration in night vision
Photopsia (flickering or flashing lights)
Glare around objects
Visual hallucinations may occur = Charles-bonnet syndrome
Distortion of line perception on Amsler grid testing
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What is Amsler grid testing?
It’s a grid of straight lines
Hold it at ~12-14 inches away from face, cover 1 eye and focus on black dot in the middle of grid
Cover the other eye and repeate
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What would you see on fundoscopy in macular degeneration?
Drusen - yellow areas of pigment deposition in macular area
In wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage
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Investigations for age-related macular degeneration?
Slit-lamp microscopy - initial investigation of choice to identify any pigmentary, exudative or haemorrhage changes
Fluorescein angiography is neovascular ARMD is suspected as this can guide intervention with anti-VEGF therapy
Optical coherence tomography to visualise retina in 3D to reveal areas of disease which aren’t visible on microscopy alone
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Management of dry age-related macular degeneration?
Zinc with anti-oxidant vitamin A, C and E - reduces progression
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Management of wet age-related macular degeneration?
Anti-VEGF intravitreal injections every 4 weeks
Laser photocoagulation can slow progression where there is new vessels but risk of acute visual loss
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Examples of anti-VEGF agents?
Ranibizumab
Bevacizumab
Pegaptanib
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What is squint also known as?
Strabismus
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What is strabismus?
Misalignment of the visual axes
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What is concomitant squint?
Due to an imbalance in extraocular muscles
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What is paralytic squint?
Due to paralysis of extraocular muscles
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What are the different names for the types of squint?
Esotropia - eye towards nose
Exotropia - eye towards ear
Hypertropia - eye up
Hypotropia - eye down
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Why is it important to detect and correct a squint?
As untreated they can lead to amblyopia - Bain fails to fully process inputs from the eye with the squint so favours the other eye causing visual acuity issues
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How can we detect a squint?
Using a corneal light reflection test
Cover test is used to identify the nature of the squint
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What can help prevent amblyopia in a child with a squint?
An eye patch
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Whats the leading cause of visual loss globally?
Cataracts
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What is a congruous visual field defect?
When there is a complete or symmetrical visual field loss
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What is an incongruous visual field defect?
When there is an incomplete or asymmetric visual field loss
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Where is the lesion in an incongruous defect of Homonymous haemianopia?
Optic tract
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Where is the lesion in an congruous defect of Homonymous haemianopia?
Optic radiation or occipital cortex
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Where is the lesion in a superior Homonymous quadrantanopia?
And in the inferior?
Superior -> lesion is in the Inferior optic radiation’s in temporal lobe
Inferior -> lesions of the superior optic radiations in parietal lobe
PITS parietal inferior temporal superior
(Note this is very much an exam answer as most research suggests the majority of quadrantanopias are caused by occipital love lesions)
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Where is the lesion in bitemporal haemianopia?
In the optic chiasm
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What causes a central scotoma?
Macula degeneration
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What causes a constricted visual field?
Glaucoma
Retinitis pigmentosa
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What should you do with contact lens wearers who present with a red painful eye as only symptoms?
Always refer to the eye clinic to exclude microbial keratitis
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What is central retinal vein occlusion?
A relatively rare cause of sudden painless, unilateral visual loss
Obstruction to blood flow through central retinal artery
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What causes central retinal arterial occlusion?
Thromboembolism from atherosclerosis or arteritis e.g. temporal arteritis
Both cause obstruction to blood flow through central retinal artery
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Risk factors for central arterial occlusion
• CVD risk factors which increase the risk of atherosclerosis causing central retinal aretry occlusion
• White ethnicity, older age, female, poly myalgia rheumatica - risk factors for temporal arteritis
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Features of central retinal arterial occlusion?
Sudden unilateral painless visual loss “a curtain coming down”
Relative afferent pupillary defect - this is because the input is not sensed by the ischaemic retina when testing the direct light reflex but is sensed during the consensual light reflex
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Fundoscopy findings central retinal artery occlusion?
Cherry red spot on a pale retina
(Retina is pale due to lack of perfusion and the cherry red spot is the fovea which has a thin surface so shows the red-coloured choriod)
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Management of central retinal arterial occlusion?
Identify and treat underlying conditions e.g. ESR and temporal artery biopsy for temporal arteritis
If pt attained acutely then intraarterial thrombolysis can be artrempted but trials show mixed results
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What % of patients with Graves’ disease have thyroid eye disease?
25-50%
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Risk factors for thyroid eye disease?
Smoking
Radioiodine treatment
236
Features of thyroid eye disease?q
• exophthalmos
• Conjunctival oedema
• Optic disc swelling
• Opthalmoplegia
• Inability to close the eyelids which may lead to sore, dry eyes. If severe and left untreated, pt can be at risk of exposure keratopathy
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Circular muscles in iris:
Function?
Which nervous system stimulates?
Neurotransmitter?
Pupil constriction
PNS
Acetylcholine
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Radial muscles in iris:
Function?
Which nervous system stimulates?
Neurotransmitter?
Pupil dilatation
SNS
Adrenalin
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What can cause abnormal pupil shapes?
• trauma to sphincter muscles e.g. During cataract surgery
• Anterior uveitis - can cause adhesions in iris
• Acute angle-closure glaucoma - can cause ischaemic damage to iris muscles and abnormal pupil shape, usually a vertical oval
• Rubeosis iridis (neovascularisation of the iris) - associated with poorly controlled diabetes and diabetic retinopathy
• Coloboma - a congenital malformation that causes a hole in the iris and an irregular shaped pupil
• Tadpole pupils - muscle spasms in part of the dilation muscle. Temporary and associated with migraines and Horner syndrome.
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What is a Coloboma?
A congenital malformation that causes a hole in the iris
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What causes a tadpole pupil?
Migraines or Horner syndrome
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What causes miosis?
• Horner syndrome
• Cluster headahces
• Opiates
• Nicotine
• Pilocarpine
• Argyll-Robertson pupil
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Features of occulomotor nerve palsy?
Ptosis
Dilated non-reactive pupil
Divergent strabismus - down and out in affected eye
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Why does occulomotor nerve palsy cause a divergent strabismus?
As palsy of all eye muscles except lateral rectus and superior oblique = eye pulled down and out
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Why does 3rd nerve palsy cause ptosis?
As occulomotor nerve usually supplies the levator palpebrae superioris which is responsible for lifting the upper eye lid so palsy = droop
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Why does 3rd nerve palsy cause dilated non-reactive pupil?
As the occulomotor nerve carries the parasympathetic fibres that innervate the circular muscles of the iris so palsy = dilated non-reactive
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Causes of 3rd nerve palsy
Idiopathic
Compression of nerve - tumour, trauma, cavernous sinus thrombosis, posterior communicating artery aneurysm, raised ICP
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What are the features of Horner syndrome?
Ptosis
Miosis
Anhidrosis
Enopthalmos
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What generally causes Horner syndrome?
Damage to the symaoethtic nervous system. These nerves arse from the spinal cord in the chest and the post-ganglion is nerves travel to the head alongside the internal carotid artery
250
Outline the specific causes of Horner syndrome?
4S, 4Ts, 4Cs for sentral, torso (pre-ganglionic) and cervical (post-ganglionic)
Central lesions:
Stroke
MS
Swelling - tumour
Syringomyelia (cyst in spinal cord)
Pre-ganglionic:
Tumour pancoast
Trauma
Thyroidectomy
Top rib/cervical rib
Post-ganglionic:
Carotid aneurysm
Cartotid artery dissection
Cavernous sinus thrombosis
Cluster headache
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How can you tell where a lesion is in horners syndrome from the symptoms?
Central lesions - causes anhidrosis of arm, trunk and face
Pre-ganglion lesiosn cause anhidrosis only on face
Post-ganglion lesions dont cause anhidrosis
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What is a distinguishing features of congenital Horner syndrome?
Heterochromia (difference in iris colour on affected side)
253
What is a Holmes-Adie pupil?
A benign condition mostly seen in women
A dilated pupil that is sluggish to react to light
normal accommodation but slow to dilate following constriction “tonic pupil”
254
What is Holmes-Adie syndrome?
A Holmes-Adie pupil with absent ankle and knee reflexes
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What is a Argyll-Robertson pupil?
A specific findings in neurosyphilis
A constricted pupil that accommodates but doesnt react to light
Often irregularly shaped
Accommodation Reflex Present but Pupillary Reflex Absent
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What is posterior vitreous detachment?
Separation of the vitreous membrane from the retina
This occurs due to natural changes to the vitreous fluid of the eye with ageing
257
Epidemiology of posterior vitreous detachment?
>75% of people over 65
258
What must you rule out in posterior vitreous detachment?
Retinal tears or retinal detachment as these can result in permenant loss of vision
259
Risk factors posterior vitreous detachment?
Age - vitreous fluid becomes les svsicous as we age and doesnt hold its shape as well so it pulls it away from the retina
Highly myopic people - myopic eye has a longer axial length
260
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)
261
Ophthalmoscopy findings in posterior vitreous detachment?
Weiss ring - detachment of vitreous membrane around the optic nerve to form a. Ring-shaped floater
262
Referral for posterior vitreous detachment?
All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or detachment.
263
Tx of posterior vitreous 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.
264
What is central retinal vein occlusion?
When a thrombus forms in the retinal vein, blocking drainage of blood from the retina
265
2 types of retinal vein occlusion?
Central retinal vein occlusion - causes problems with entire retina
Branch retinal vein occlusion - affects smaller area which was drained by that branch
266
Risk factors central retinal vein occlusion?
increasing age
hypertension
cardiovascular disease
glaucoma
Diabetes
polycythaemia
267
Features of central retinal vein occlusion?
sudden, painless reduction or loss of visual acuity, usually unilaterally
268
Fundoscopy findings in central retinal vein occlusion?
widespread hyperaemia
severe retinal haemorrhages - 'stormy sunset'
269
Management of central retinal vein occlusion?
Majority managed conservatively
Indications for treatment:
- macular oedema
- retinal neovascularisation
Treat macular oedema with intravitreal VEGF agents
Treat retinal neovascularisation with laser photocoagulation
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What is retinitis pigmentosa?
A genetic condition that causes degeneration of photoreceptors in the retina, particuarly the rods, causing loss of vision
271
Features of retinitis pigmentosa?
Night blindness is often the initial sign
Tunnel vision due to loss of peripheral retina
(These symptoms occur first as rods degenerate more than the cones and these are responsible for light and peripheral vision)
272
Fundoscopy findings in retinitis pigmentosa?
black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
273
Retinitis pigmentosa associated conditions?
Refsum disease: cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis
Usher syndrome
abetalipoproteinemia
Lawrence-Moon-Biedl syndrome
Kearns-Sayre syndrome
Alport's syndrome
274
What systemic diseases are related to scleritis?
RA
SLE
Sarcoidosis
Granulomatoss with polyangiitis
275
What systemic diseases are related to episcleritis?
IBD
RA
276
What systemic diseases are related to uveitis?
Ankylysing spondylsos
Reactive arthritis
IBD
Behçet’s disease
Sarcoidosis
277
What is anisocoria?
Difference in size of pupils
278
Causes of a pale optic disc?
Glaucoma
Retinitis pigmentosa
Choroiditis
Centralretinal artery occlusion
MS
Leber’s optic atrophy
Syphilis
279
What does sixth nerve palsy look like?
Double vision as convergent strabismus due to lack of function from lateral rectus muscle
280
What is Leber optic neuropathy?
A rare mitochondrial disorder that typically presents in young males with progressive visual loss due to optic neuropathy
281
Causes of sudden loss of vision?
Occlusion of central retinal vein or artery
Vitreous haemorrhage
Retinal detachment
Amaurosis fugax
282
What is transient monocular visual loss?
Sudden, transient loss of vision that lasts less than 24 hours
283
Screening for open angle glaucoma?
First relative with glaucoma then screen them from age of 40 annually
284
Who do we refer to ophthalmology for suspected strabismus?
Any child under age of 4
