Module 3C Ophthalmology - Conditions Flashcards
(134 cards)
1
Q
What 3 parts is the uvea made up of?
A
Uvea = middle layer of the eye, located between the retina and the sclera, it consists of the:
- iris
- ciliary body
- choroid (layer between retina and sclera)
2
Q
What usually causes anterior uveitis + what genotype is anterior uveitis usually associated with?
A
- usually caused by an autoimmune process
- particularly HLA-B27 - associated with ankylosing spondylitis and reactive arthritis
3
Q
Anterior uveitis - symptoms and signs O/E
A
Symptoms:
- Painful red eye
- Reduced visual acuity
- photophobia - due to ciliary muscle spasm
- excessive lacrimation
Signs O/E:
- ciliary flush - ring of red spreading from cornea outwards
- abnormally shaped pupil (posterior synechiae)
- hypopyon - pus and inflammatory cells in the anterior chamber
4
Q
Anterior uveitis - investigations
A
- Slit-lamp biomicroscopy - key for diagnosis
- IOP measurement + dilated fundus examination - to assess posterior segment involvement and for complications
(3. Serology for underlying cause can be done in addition)
5
Q
Anterior uveitis - management
A
- Topical corticosteroids (eg. prednisolone acetate, dexamethasone) - to relieve inflammation/pain
- Cytoplegics (eg. cyclopentolate or atropine eye drops) - helps relieve ciliary spasm and pain
(3. recurrent cases may require biologics - DMARDs or anti-TNFs)
6
Q
what are the 2 types of glaucoma?
A
- open-angle glaucoma (chronic glaucoma)
- acute angle-closure glaucoma
7
Q
What is (primary) open-angle glaucoma?
A
- chronic, progressive optic nerve damage caused by a rise in intraocular pressure - characterised by the degeneration of retinal ganglion cells and their axons, leading to irreversible visual field loss
- raised IOP is caused by a blockage in aqueous humour trying to escape the eye
8
Q
What is the function of aqueous humour, where is it produced, and how is it drained?
A
- function - supplies nutrients to the cornea + lens
- produced by the ciliary body
- drains through the trabecular meshwork to the canal of Schlemm at the angle between the cornea and iris
9
Q
Open VS Acute angle-closure glaucoma - anatomy
A
- Open glaucoma - there is a gradual increase in resistance to flow through the trabecular meshwork
- Acute angle-closure glaucoma - iris bulges forward and seals off trabecular meshwork from anterior chamber - preventing aq humour from draining –> continual build-up of pressure and acute onset of symptoms
10
Q
What effect does a raised intraocular pressure have on the optic disc?
A
- Raised IOP causes cupping of the optic disc
- optic cup is usually < 50% of the size of the optic disc - raised IOP causes this indent to become wider and deeper (“cupping”)
11
Q
(primary) Open-angle glaucoma - symptoms and signs O/E
A
Symptoms:
- Peripheral visual field loss - nasal scotomas progressing to ‘tunnel vision’
- decreased visual acuity - blurred vision +/- halos around lights (particularly at night)
Fundoscopy signs:
- optic disc cupping - cup-to-disc ratio > 0.5 (due to increased IOP)
- optic disc pallor (indicating optic atrophy)
12
Q
How is intraocular pressure (IOP) measured?
A
Goldmann applanation tonometry
- gold-standard test to measure IOP
13
Q
Open-angle glaucoma - investigations
A
Diagnosis is based on:
- Goldmann applanation tonometry - measures IOP
- Slit lamp with pupil dilation - assess cup-disc ratio and optic nerve/fundus health
- Visual fields (automated perimetry)
- Gonioscopy - to assess angle between iris and cornea
- Central corneal thickness measurement
14
Q
Open-angle glaucoma - management
A
Aim of treatment is to lower IOP and prevent progressive visual field loss:
1. IOP lowering:
- 360° selective laser trabeculoplasty - 1st-line to pts with an IOP ≥ 24 mmHg
- Prostaglandin analogue eye drops (eg. latanoprost) - increases uveoscleral outflow
- Reduction of aq humour:
- beta-blockers (timolol)
- carbonic anhydrase inhibitors
- sympathomimetics (eg. Brimonidine) - Trabeculoectomy (new channel created for aq humour to drain)
15
Q
Adverse effects of prostaglandin analogues (eg. latanoprost)
A
- eyelash growth
- eyelid pigmentation
- iris pigmentation
16
Q
Acute angle closure glaucoma - pathophysiology
A
- iris bulges forward and blocks off trabecular meshwok from the anterior chamber –> preventing aq humour from draining and leading to a continual increase in intraocular pressure
- as pressure builds in posterior chamber, iris is further pushed forward and exacerbates the angle closure
17
Q
Open-angle glaucoma VS Acute angle closure glaucoma - difference in at risk ethnic groups?
A
- Open-angle glaucoma - black ethnic origin
- Acute angle closure glaucoma - female + Asian
18
Q
Acute angle closure glaucoma - Symptoms + Signs O/E
A
Symptoms:
- severely painful red eye +/- headache
- decreased visual acuity - blurred vision +/- halos around lights
Signs O/E:
- Red eye
- Hazy cornea
- fixed + dilated pupil
19
Q
Acute angle closure glaucoma - investigations
A
- Gonioscopy - to assess iridocorneal angle –> a closed angle is diagnostic of AACG
- Tonometry - elevated IOP is a hallmark of AACG
20
Q
Acute angle closure glaucoma - management
A
Immediate admission required, initial management:
1. Lie pt supine
2. Pilocarpine eye drops (2% for blue eyes, 4% for brown eyes) - causes pupil constriction + ciliary muscle contraction –> opens up trabecular meshwork for drainage of aq humour
3. IV acetazolamide - reduces aq humour production
(+/- IV mannitol +/- timolol +/- dorzolamide +/- brimonidine)
Definitive management:
1. Laser peripheral iridotomy - creates tiny hole in peripheral iris
21
Q
What is the most common cause of blindness in the UK?
A
Age-related macular degeneration
22
Q
Wet VS Dry age-related macular degeneration
A
Dry (non-neovascular) - 90% cases:
- characterised by Drusen deposits in Bruch’s membrane
Wet (neovascular/exudative) - 10% cases:
- characterised by choroidal neovascularization - VEGF stimulates the development of new vessels
- these vessels can leak fluid - causing oedema and vision loss (worse prognosis)
23
Q
What stimulates development of new vessels in wet AMD (age-related macular degeneration)?
A
Vascular endothelial growth factor (VEGF)
24
Q
Age-related macular degeneration (AMD) - Presentation/findings on examination
A
- Reduced visual acuity (gradual in dry AMD, subacute in wet AMD)
- CENTRAL SCOTOMA - gradual loss of central vision
- Struggle with vision at night/dark adaptation
- Metamorphopsia (wavy appearance to straight lines)
O/E:
- Fundoscopy - Drusen deposits in dry AMD
- Fluorescein angiography to view retina - shows oedema and neovascularization in wet AMD
- Ocular coherence tomography - gives cross-sectional view of layers of retina
25
What test is used to assess for metamorphosis in AMD?
Amsler grid test
26
Age-related macular degeneration (AMD) - Management
Dry AMD - no specific treatment, management involves reducing risk of progression by:
1. Avoiding smoking
2. Controlling BP
3. Vitamin supplementation (A, C, and E) + Zinc
Wet AMD:
1. intravitreal anti-VEGF injections (eg. ranibizumab, aflibercept) - block VEGF and slow development of new vessels
27
What does the term cataracts mean?
- Cataracts describe a progressively opaque eye lens, which reduces the light entering the eye and visual acuity
28
What is the role of the lens and how does it receive its nourishment?
- role of the lens is to focus light on the retina - ciliary body contracts and relaxes to change the shape of the lens
- the lens has no blood supply and is nourished by the aqueous humour
29
Presentation of cataracts and signs O/E
Symptoms are usually asymmetrical:
- slow reduction in visual acuity
- progressive blurring of vision
- colours becoming more faded, brown, or yellow
- 'starbursts' can appear around lights (particularly at night)
O/E:
- loss of red reflex
- lens can appear grey or white using an ophthalmoscope
30
Cataracts - management
1. if symptoms manageable - no intervention needed
2. Cataract surgery - lens replaced with an artificial lens
31
Endophthalmitis describes inflammation of the inner contents of the eye, usually caused by infections, and is a rare but serious complication of cataract surgery (it can lead to vision loss) - how is this treated?
intravitreal antibiotics injected directly into the eye
32
Central retinal artery occlusion - aetiology
1. Carotid artery stenosis/atherosclerosis - most common cause
- the central retinal artery is a branch of the ophthalmic artery, which is a branch of the internal carotid artery
2. GCA can also be a cause (where vasculitis affecting the ophthalmic or central retinal artery reduces blood flow)
3. Cardiac emboli - most common cause under 40 yrs
33
Central retinal artery occlusion - risk factors
CVD risk factors (atherosclerosis):
- smoking
- hypertension
- diabetes
- raised cholesterol
34
Central retinal artery occlusion - presentation + signs O/E
Symptoms:
- sudden painless loss of vision - like a "curtain coming down"
O/E:
- Swinging right test - RAPD
- Fundoscopy - 'cherry red spot' + pale retina
35
Differentials for a sudden painless vision loss
- retinal detachment
- central retinal artery occlusion
- central retinal vein occlusion
- vitreous haemorrhage (due to diabetic retinopathy)
36
Fundoscopy findings in central retinal artery occlusion
- 'cherry red spot'
- pale retina - due to ischaemia
37
Central retinal artery occlusion - management (acute and long-term)
Immediate referral (vision-threatening emergency) - management aims to remove/dislodge the blockage:
1. Ocular massage (to improve blood flow and potentially dislodge a clot)
2. Intra-arterial thrombolysis: urokinase administered via ophthalmic artery (risk VS benefit)
3. Reduction of IOP: IV acetazolamide OR IV mannitol +/- topical timolol
4. Vasodilator therapy: sublingual isosorbide dinitrate OR inhaled carbogen (95% oxygen + 5% carbon dioxide) --> aimed to reperfuse retina
(5. GCA is a reversible cause - ESR + temporal artery biopsy --> high dose steroids)
(6. Long-term management - treat reversible risk factors + secondary prevention of CVD)
38
What rheumatological condition is GCA associated with?
Polymyalgia rheumatica (PMR)
39
Giant cell arteritis - clinical features + signs O/E
Symptoms:
- unilateral headache - typically severe and around temple and forehead
- scalp tenderness, jaw claudication, blurred/double vision
O/E:
- temporal artery may be tender and thickened to palpation (with reduced or absent pulsation)
(50% have associated PMR symptoms too - eg. shoulder and pelvic girdle pain and stiffness)
40
Giant cell arteritis - investigations
- Raised inflammatory markers - ESR > 50 mm/hr
- Temporal artery biopsy - multinucleated giant cells
- Duplex USS - "halo" sign and stenosis of temporal artery
41
Giant cell arteritis - Management
1. Immediate high-dose steroids (to prevent vision loss) - prednisolone OR methylprednisolone
2. Adjunctive therapy - Aspirin 75mg OD (decreases stroke risk) +/- PPI (for GI protection while on steroids) + Bisphosphonates and Adcal D3 (for bone protection while on steroids)
(3. MDT approach - rheumatology, vascular surgeons, ophthalmology)
42
In GCA, vision loss is the most feared and serious complication - what is this due to?
Anterior ischaemic optic neuropathy
43
Central VS Branch retinal vein occlusion
- occurs when a blood clot (thrombus) forms in the retinal veins, blocking drainage of blood form the retina
- the branch retinal veins drain into the central retinal vein which runs through the optic nerve to drain into either the superior ophthalmic vein or cavernous sinus
- blockage of one of the branch veins affects the area drained by that branch
- blockage in the central vein causes problems with the whole retina
- there are 4 branch retinal veins that drain about 1/4 of the retina each
44
Retinal vein occlusions - which sites are at a higher risk of occlusion?
sites where the retinal arteries cross over the top of the veins can cause narrowing of the vein - these sites ar more vulnerable to occlusion
45
Retinal vein occlusion - pathology of vision loss
- Blockage (thrombus) of a retinal vein causes increased pressure in the vessels draining the eye
- this results in fluid and blood leaking into the retina, causing macular oedema and retinal hemorrhages --> this results in retinal damage and vision loss
46
Retinal vein occlusions - what are the 2 types and which is worse (what can it lead to?)
- Ischaemic or non-ischaemic
- Retinal ischaemia leads to release of vascular endothelial growth factor (VEGF) - resulting in new blood vessel development (neovascularisation)
47
Retinal vein occlusion - clinical features + signs O/E
Symptoms:
- painless reduciton of vision or vision loss
- branch occlusion - vision loss corresponds to affected area of retina
- if involves branch draining macula - central vision is lost
O/E:
- Fundoscopy (more so in ischaemic CRVO) - cotton wool spots, venous tortuosity, retinal oedema, flame-shaped hemorrhages)
- Snellen chart - < 6/60
- RAPD
48
Branch retinal vein occlusion - fundoscopy
49
Retinal vein occlusion - management
Refer immediately to ophthalmologist, management aims to treat macular oedema and prevent neovascularization:
1. Anti-VEGF therapies (eg. ranibizumab and aflibercept)
2. Intravitreal dexamethasone
3. Laser photocoagulation (to get rid of new vessels)
50
Corneal abrasions - Clinical features + O/E
- painful, red eye
- photophobia
- decreased visual acuity in affected eye - blurred vision
- foreign body sensation
O/E - usually visible to naked eye, but a fluorescein stain can be applied to the eye to aid diagnosis
51
Corneal abrasions - management
Usually heal over 2-3 days, more serious may need treatment:
1. Antibiotic eye drops
(2. remove foreign body if there is one)
3. Simple analgesia - paracetamol
4. lubricating eye drops
52
Give 3 examples of lubricating eye drops in order of their viscosity (least viscous to most viscous)
- Hypromellose drops (least viscous) - effects last around 10 mins
- Polyvinyl alcohol drops (middle viscous choice)
- Carbomer drops (most viscous) - effects last 30-60 mins
53
Corneal foreign body - management (include post-removal care)
1. Anaesthesia
2. Foreign body removals - irrigation OR needle technique OR Jeweller's forceps OR Alger brush (if residual rust rings or iron deposits)
3. Post-removal care - antibx prophylaxis +/- cycloplegics +/- analgesia +/- tetanus prophylaxis
4. Follow-up - 24-48hrs post-procedure
54
Retinal detachment - pathophysiology + why this can be sight-threatening
- neurosensory layer (photoreceptor - rods/cones) separates from the retinal pigment epithelium (base layer attached to the choroid)
- usually due to a retinal tear - allowing vitreous fluid to get under the neurosensory retina and fill the space between the layers
- the neurosensory retina relies on the blood vessels of the choroid for its blood supply - therefore, retinal detachment can disrupt the blood supply and cause permanent damage to the photoreceptors
55
Retinal detachment - clinical features + O/E
Symptoms:
- new-onset floaters or flashes
- sudden onset, painless peripheral vision loss - described as "shadow coming across vision"
- decreased visual acuity - blurred or distorted
O/E:
- reduced peripheral visual fields +/- central vision (if macula has detached too)
- Fundoscopy - red reflex lost + pale retinal folds
- (RAPD - if optic nerve involved)
56
Retinal detachment - Management
Immediate ophthalmology referral
1. Laser therapy OR Cryotherapy
2. Surgery to reattach retina
57
Posterior vitreous detachment - pathology + most common aetiology
- when the vitreous body comes away from the retina - common in older age
- vitreous humour = gel inside the vitreous chamber of the eye, it maintains the structure of the eyeball and keeps the retina pressed on the choroid
- with age it becomes less firm and less able to maintain its shape
58
Posterior vitreous detachment - clinical features
- Sudden onset of floaters and flashes
- painless
- blurred vision
- (can be asymptomatic)
59
Posterior vitreous detachment - main investigation
Dilated fundus examination using a slit lamp
60
Posterior vitreous detachment - Management
No treatment necessary - symptoms will improve as the brain adjusts
- however, can predispose to retinal tears and retinal detachment - important to rule these out and if necessary then surgery needed to fix this
61
What is retinitis pigmentosa?
a genetic condition causing degeneration of the photoreceptors in the retina - particularly the rods
62
Retinitis pigmentosa - presentation + O/E
Usually symptoms start in childhood:
- Night blindness
- Peripheral vision loss
(rods degenerate more than cones - rods are responsible for night vision and peripheral vision)
O/E:
- Fundoscopy - pigmentation ("bone-spicule" pigmentation)
63
Conjunctivitis ("pink eye") - Presentation + bacterial VS viral
Symptoms:
- Red, bloodshot eye
- itchy or gritty sensation
- no pain
.
- Bacterial --> purulent discharge ("eyes stuck together in morning")
- Viral --> clear discharge (associated with other viral symptoms + preauricular lymph nodes)
64
Causes of an acute PAINFUL red eye
- Acute angle-closure glaucoma
- Anterior uveitis
- Scleritis
- Corneal abrasions or ulceration
- Keratitis
- Foreign body
- Traumatic or chemical injury
65
Causes of an acute PAINLESS red eye
- Conjunctivitis
- Episcleritis
- Subconjunctival haemorrhage
66
Conjunctivitis - Management
1. Usually self-limiting - 1-2 weeks
2. Hygeine advice to stop spread - avoid close contact + clean eyes with cooled boiled water and cotton wool
3. Chloramphenicol eye drops - for bacterial conjunctivitis
4. Fusidic acid - used in pregnant women
(5. allergic conjunctivitis - antihistamines)
(6. contact lens should not be worn during an episode of conjunctivitis)
67
Which infection usually causes conjunctivitis in neonates?
- Gonococcal infection - can cause serious complications (e.g. permanent vision loss)
- requires urgent ophthalmology assessment
68
Episcleritis - Presentation + O/E (appearance)
Acute-onset unilateral features:
- localised or diffuse redness (often a patch of redness in the lateral sclera)
- no pain
O/E:
- dilated episcleral vessels
69
Episcleritis VS Scleritis - symptoms + how to differentiate using phenylephrine eye drops
Episcleritis - no pain, no photophobia or discharge, and normal visual acuity
- Scleritis - these symptoms are present
.
Phenylephrine:
- Episcleral vessels - causes blanching (redness disappears)
- Scleral vessels - will not impact redness (as it is deeper structure)
70
Episcleritis - management
1. Usually self-limiting - 1-2 weeks
2. Simple analgesia (eg. ibuprofen) + lubricating eye drops
3. more severe cases - steroid eye drops
71
Subconjunctival haemorrhage - Presentation + appearance (what typically precipitates a subconjunctival haemorrhage.)
- bright red blood underneath conjunctiva
- painless + does not affect vision
- Precipitating event - coughing fit or heavy lifting
72
Subconjunctival haemorrhage - Management
1. Reassure pt that it is a self-limiting condition - 2 to 3 weeks + it might change colour to yellow/green, like a bruise, but this is normal
2. if mild irritation - lubricating eye drops
(3. if recurrent - check for underlying cause --> eg. high BP, bleeding disorders)
73
Vitreous haemorrhage - Clinical features + O/E
Symptoms:
- sudden, painless vision loss or floaters
- +/- decreased visual acuity
O/E:
- Fundoscopy - absent or diminished red reflex
(image shows vitreous hemorrhage on fundoscoy, pt has a background of treated diabetic retinopathy)
- Slit-lamp examination - assess for retinal tears/detachment
- B-scan ultrasonography - used if fundus is obscured by the haemorrhage on fundoscopy
74
Vitreous haemorrhage - Management
1. Observation if mild - usually resolves spontaneously
2. Treatment of underlying cause - eg. diabetic retinopathy (photocoagulation) OR wet AMD (anti-VEGF injections)
3. Vitrectomy - if severe or persistent
75
Diabetic retinopathy - Pathophysiology
Due to chronic hyperglycaemia:
- **Blot haemorrhages** (due to increased vascular permeability)
- **Hard exudates** (yellow-white deposits of lipids and proteins in the retina)
- **Microaneurysms** - damage to blood vessel walls leads
- **Cotton wool spots** (due to damage to nerve fibres in the retina)
- **Intraretinal microvascular abnormalities (IRMA)** (dilated and tortuous capillaries in the retina)
- **Neovascularization** can occur too
76
Grading of diabetic retinopathy (3 main grades + separate type)
**1. Background** - microaneurysms, retinal haemorrhages, hard exudates, and cotton wool spots
**2. Non-proliferative/Pre-proliferative** - + venous bleeding, multiple blot hemorrhages, and IMRAs
**3. Proliferative** - neovascularization (can causes bleeds into vitreous - leading to vision loss)
(Diabetic maculopathy also exists separately - exudates within the macular + macular oedema)
77
Diabetic retinopathy - Clinical features + O/E (fundoscopy)
Symptoms:
- early stages often asympomatic
- as progresses - pt may experience blurred vision, floaters, dark areas in their visual field, and eventually vision loss
Dilated Fundoscopy:
- microaneurysms
- cotton wool spots
- hard exudates
- intraretinal microvascular abnormalities in NPDR
- Neovascularisation +/- vitreous haemorrhage in PDR
78
Diabetic retinopathy - Management
- Non-proliferative - close monitoring and careful diabteic control
Proliferative:
1. **Laser photocoagulation** - to suppress new vessels
2. **Anti-VEGF intravitreal injections** - reduce vascular leakage and neovascularization
3. **Corticosteroids (eg. dexamethasone implant)** - an option of macular oedema
4. **Surgery (vitrectomy)** - only if severe vitreous hemorrhage or retinal detachment
79
What does this image show?
diabetic retinopathy previously treated with pan-retinal laser photocoagulation
80
Hypertensive retinpoathy - features on fundoscopy
- **Silver wiring** (walls of arterioles become thickened and sclerosed - reflect more light on examination)
- **AV nipping** (where arterioles cause compression of the veins where they cross)
- **Cotton wool spots** (caused by ischaemia and infarction of the retina)
- **Hard exudates** (caused by damaged vessels leaking lipids/proteins onto the retina)
- **Retinal haemorrhages** (caused by damaged vessels rupturing)
- **Papilloedema** (caused by ischaemia to the optic nerve - results in optic nerve swelling)
81
Hypertensive retinopathy - Keith-Wagener Classification
- Stage 1: Mild narrowing of the arterioles
- Stage 2: Focal constriction of blood vessels and AV nipping
- Stage 3: Cotton-wool patches, exudates and haemorrhages
- Stage 4: Papilloedema
82
What muscles are involved in pupil constriction and dilation + which NS (symp or parasymp) is involved in each?
Sphincter pupillae (circular muscles) --> pupil constriction
- stimulated by parasympathetic NS (using acetylcholine as a neurotransmitter)
.
Dilator pupillae (radial muscles) --> pupil dilation
- stimulated by sympathetic NS (using adrenaline as a neurotransmitter)
83
Causes of mydriasis (dilated pupil)
- Congenital
- Stimulants (e.g., cocaine)
- Anticholinergics (e.g., oxybutynin)
- Trauma
- Third nerve palsy
- Holmes-Adie syndrome
- Raised intracranial pressure
- Acute angle-closure glaucoma
84
Causes of miosis (constricted pupil)
- Horner syndrome
- Cluster headaches
- Argyll-Robertson pupil (neurosyphilis)
- Opiates
- Nicotine
- Pilocarpine
85
Third nerve palsy (oculomotor) - clinical features
- Ptosis (full ptosis)
- Dilated non-reactive pupil - if compressive cause
- Divergent strabismus (squint) in affected eye - "down and out" position
86
Third nerve palsy - why is the affected eye in a "downwards and out" position?
- 3rd nerve (oculomotor) supplies all extraocular muscles except the lateral rectus (6) and superior oblique (4)
- therefore, the lat. rectus and sup. oblique (which are still working) pull the eye "down and out"
87
Which muscle is responsible for ptosis in a 3rd nerve palsy?
**Levator palpebrae superioris**
- responsible for lifting upper eyelid
- supplied by the oculomotor nerve (CN III)
88
Third nerve palsy - why is the pupil dilated and non-reactive?
oculomotor nerve carries parasympathetic fibres that innervate the sphincter pupillae (circular muscles) of the iris
89
What are the two categories of third nerve pasly based on the presence of pupil involvement
1. Ischaemic (microvascular):
- Pupil sparing - as parasympathetic fibres are spared
- Causes - diabetes, ischaemia
- tend to be more benign and spontaneously resolve
2. Compressive (mass lesion):
- Pupil involved - as parasympathetic fibres are compressed
- Causes - tumour, PCOM tumour, cavernous sinus thrombosis
(the oculomotor nerve travels directly from the brainstem to the eye in a straight line - travels through cavernous sinus and close to the posterior communicating artery)
(The parasympathetic fibres/pupillary fibres are on the outside of the nerve, therefore compression/tumour affects them but ischaemia does not)
90
Horner's syndrome - what NS does it affect?
Sympathetic
91
Horner's syndrome - clinical features
- Ptosis (partial ptosis)
- Miosis (constricted pupil)
- Anhidrosis (loss of sweating) - ipsilateral
- (enophthalmos - rare)
92
Ptosis in third nerve palsy VS Ptosis in Horner's syndrome
- 3rd nerve palsy - full ptosis (due to paralysis of levator palpabrae superioris)
- Horner's - partial ptsosis
93
Horner's syndrome - where is the location of the lesion if anhidrosis is present? (pre-ganglionic or post-ganglionic)
Pre-ganglionic lesions cause anhidrosis
94
Horner's syndrome - investigations
Cocaine eye drops:
- acts on eye to stop noradrenaline re-uptake at the NMJ (meaning there is more noradrenaline available)
- this causes a normal eye to dilate as noradrenaline stimulates the dilator muscles of the iris
- in Horner's syndrome, the nerves are not releasing noradrenaline - so blocking re-uptake makes no difference, and there is no pupil reaction
(alternatively, low-dose adrenaline eye drops (0.1%) will dilate the pupil in Horner's syndrome, but not a normal pupil)
95
Explain why noradrenaline has no effect on the pupil in Horner's syndrome, but adrenaline causes a Horner's syndrome pupil to dilate.
Noradrenaline
- in Horner's syndrome, the postganglionic sympathetic nerve terminals are damaged or absent, so there is little or no noradrenaline to potentiate at the synaptic cleft.
- As a result, cocaine fails to cause significant pupil dilation in the affected eye
Adrenaline:
- directly stimulates α1-adrenergic receptors on the iris dilator muscle, bypassing the need for intact sympathetic nerve terminals or endogenous noradrenaline.
- in Horner's syndrome, due to denervation hypersensitivity, the α1 receptors on the dilator muscle are more responsive to adrenergic agonists like adrenaline
- This results in significant pupil dilation in the affected eye, even in the absence of functional sympathetic nerve input
96
Holmes-Adie pupil - caused by damage to what fibres and why does this cause the symptoms of holmes adie pupil (dilated pupil that reacts poorly to light and relatively well to accommodation) ?
- Post-ganglionic parasympathetic fibres
- arise from the ciliary ganglion (where pre-ganglionic parasympathetic fibres (from the Edinger-Westphal nucleus) synapse)
- they innervate the iris sphincter muscle (pupil constriction) + the ciliary muscle (lens accommodation for near vision)
97
Holmes-Adie pupil - clinical features
- Dilate pupil that responds poorly to light (causing aniscoria)
- Relatively good response to accommodation
O/E:
- **Tonic pupillary response** - when exposed to light the affected pupil demonstrates slow and prolonged constriction followed by slow redilation ("tonic" pupil)
- **Responsive to accommodation** - the pupils constrict well when focusing on a near object - this occurs due to the selective involvement of parasympathetic fibres innervating the iris sphincter muscle
98
What is tonic pupillary response?
when exposed to light the affected pupil demonstrates slow and prolonged constriction followed by slow redilation ("tonic" pupil)
99
What are the 2 types of stye (hordeolum)?
Infection or inflammation of the eyelids - particularly the oil glands - causes a tender red lump along the eyelid that may contain pus
1. Hordeolum externum - infection of the glands of Zeis (sebaceous glands at the base of the eyelashes) or glands of Moll (sweat glands at the base of the eyelashes)
2. Hordeolum internum - infection of the Meibomian glands - they are deeper, tend to be more painful
100
Stye - treatment
1. hot compresses and analgesia
2. topical antibiotics (eg. chloramphenicol) - if associated with conjunctivitis or persistent symptoms
101
Chalazion (Meibomian cyst) - what is it?
occurs when a Meibomian gland (oil gland) becomes blocked and swells - often called a Meibomian cyst
- presents with a swelling in the eyelid
- treatment - warm compresses and gentle massage towards the eyelashes (to encourage drainage)
102
Entropion - what is it + management
- Entropion = when the eyelid turns inwards with lashes pressed against the surface of the eye
- this causes pain and can result in corneal damage and ulceration
.
management:
1. taping eyelid down + lubricating drops (to prevent drying out)
2. definitive --> surgical
103
Ectropion - what is it + complication + management
- Ectropion = when the eyelid turns outwards, exposing the inner aspect
- usually affects the bottom lid - can result in exposure keratopathy, as eyeball is exposed and not adequately lubricated and protected
.
management:
1. regular lubricating eye drops to protect surface of eye
2. surgery - if more severe
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Trichiasis - what is it + management
- Trichiasis = inward growth of the eyelashes
- It results in pain and can cause corneal damage and ulceration
.
management:
1. removing affected eyelashes
2. recurrent cases - electrolysis, cryotherapy, or laser treatment to prevent from regrowing
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Periorbital cellulitis - what is it + presentation
- eyelid and skin infection in front of the orbital septum
- presents with swollen, red, hot skin around the eyelid and eye
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Perioribital cellulitis - key differential + management
- must be differentiated from orbital cellulitis (sight and life-threatening)
- management - systemic antibiotics (oral or IV)
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Orbital cellulitis - what is it + symptoms
Orbital cellulitis = an infection around the eyeball involving the tissues behind the orbital septum (posterior to orbital septum)
- Symptoms - pain with eye movement, reduced eye movements, vision changes, abnormal pupil reactions, and proptosis
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Orbital cellulitis - management
1. emergency admission under ophthalmology and intravenous antibiotics
2. surgical drainage if abscess forms
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What is keratitis + what is the most common cause of it?
Keratitis = inflammation of the cornea
--> Herpes simplex virus (HSV 1) is most common cause (herpes simplex keratitis)
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Herpes simplex keratitis - primary VS recurrent
- Herpes simplex keratitis can be primary or recurrent
- recurrence is caused by the virus travelling to the trigmeinal ganglion, where it becomes latent (dormant) and can reactivate later
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Herpes simplex keratitis - manifestations
- Epithelial keratitis (most common) - only epithelial layer of cornea affected
- Stromal keratitis - stroma is the layer between epithelium and endothelium
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Herpes simplex keratitis - clinical features + O/E
Symptoms:
- painful red eye
- photophobia
- watery discharge (epiphora)
- reduced visual acuity
O/E:
- Slit lamp examination - required to diagnose
- Fluorescein staining - dendritic corneal ulcer (dendritic describes the branching appearance of the ulcer)
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Herpes simplex keratitis - Management
1. Refer for urgent assessment and management by an ophthalmologist
2. Topical or oral antivirals (eg. aciclovir)
3. Corneal transplant - option to treat permanent scarring and vision loss after keratitis
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What is squint (strabismus) + what are the 2 types?
- Squint (strabismus) = misalignment of the eyes
1. Concomitant (common) = due to imbalance in extraocular muscles
(convergent is more common than divergent)
2. Paralytic (rare) = due to paralysis of extraocular muscles
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What can squint (strabismus) progress into if left untreated?
Amblyopia (lazy eye)
- brain favours the dominant eye and ignores inputs from the weak eye
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What are these definitions + match the relevant term to the photo
- Esotropia
- Exotropia
- Hypertropia
- Hypotropia
- Esotropia: inward positioned squint (affected eye towards the nose)
- Exotropia: outward positioned squint (affected eye towards the ear)
- Hypertropia: upward moving affected eye
- Hypotropia: downward moving affected eye
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Causes of squint (strabismus)
Usually idiopathic
- other: hydrocephalus, cerebral palsy, space occupying lesions (eg. retinoblastoma), trauma
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Manifest squint VS Latent squint
- Manifest squint (heterotropia): where the eyes are visibly misaligned when the eyes are open and being used
- Latent squint (heterophoria): eyes are misaligned when eyes are closed or covered, but appear normal when open
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How do you test for squint (strabismus)?
1. Corneal light reflex (Hirschberg test)
- hold a pen torch 50cm in front of child's face
- reflected light on corneas should be symmetrical
- asymmetry of reflected light suggests a squint
2. Cover test (manifest squint)
- ask pt to focus on an object in front of them and cover one eye
- in a manifest squint when the straight eye is covered, the squinting eye will have to move to align with the fixation objection
3. Cover/Uncover test (Latent squint)
- ask pt to focus on an object in front of them and cover one eye
- then remove cover and observe this eye
- in latent squint the eye will drift under the cover, on removing cover, the eye will straighten to regain binocular vision
4. Alternate cover test
- Move the cover slowly back and forwards between the eyes (not allowing for binocular vision to occur until test is over)
- each time cover is moved, observe that eye for any movement
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What is the management of squint (strabismus) and when should treatment be started?
1. Occlusive patch (covers good eye and forces weaker eye to develop)
2. Atropine drops in good eye (causes vision to be blurred, forces weaker eye to develop)
(treatment needs to start before 8yrs of age as visual fields finish developing - the earlier the better)
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What is hyperopia (farsightedness) + main cause
- distant objects seen more clearly than near ones - *because light focuses behind the retina rather than directly on it*
- the eye is too short, or the cornea/lens is too flat, leading to insufficient focusing power
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What is myopia (nearsightedness) + main cause
- near objects are seen more clearly than distant ones - *because light focuses in front of the retina*
- eye is too long, or the cornea/lens is too steep, leading to excessive focusing power
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Treatment of hypermetropia (farsightedness) and myopia (nearsightedness)
Glasses OR Contact lenses:
- Hyperopia - Convex (plus) lenses are used to help focus light onto the retina
- Myopia - Concave (minus) lenses are used to diverge light, allowing it to focus on the retina
(Surgery: LASIK reshapes cornea to increase (hyperopia) or decrease (myopia) curvature
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How does the shape of the eye differ in hypermetropia compared to myopia?
Hypermetropia: Shorter axial length, shallow anterior chamber, flatter cornea/lens.
Myopia: Longer axial length, deeper anterior chamber, steeper cornea/lens.
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Why does hypermetropia increase the risk of acute angle-closure glaucoma (AACG)?
Hypermetropic eyes often have a shallow anterior chamber and narrow drainage angles, increasing the likelihood of angle closure.
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Pseudosquint
- A pseudosquint (also known as pseudostrabismus) refers to the appearance of a squint (strabismus) when the eyes are actually properly aligned
- This condition is typically caused by facial or structural features around the eyes rather than an actual misalignment
- It is common in children and does not require treatment.
.
- causes: wide nasal bridge
(this is why corneal light reflex is an important test for strabismus (squint)
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Main risk factor for bacterial keratitis
Contact lens wearer
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What topical medication used in the management of eye conditions should be avoided in herpes simplex keratitis
topical steroids - increases herpes load - worsens condition
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What term is used to describe the redness of the white part of the eye
Ciliary injection
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3 types of cataracts
- Nuclear - affects central nucleus of lens
- Cortical - affects outer edge (cortex) of lens
- Posterior subcapsular - affects back surface of lens
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Why should all children with cataracts be urgently referred?
To rule out a tumour - commonly associated with retinoblastoma
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Name of this sign and what is the most serious cause?
Leukocoria (aka. white pupillary reflex)
- retinoblastoma (malignant tumour of retina)
(congenital cataract is also a cause)
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Why is it important to check if glaucoma patients have asthma?
Due to medication side effects - timolol (topical beta-blocker) can cause bronchoconstriction or reduce effectiveness of salbutamol
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Why is acute angle closure glaucoma worse in the evening (eg. low light)?
- Pupil dilates due to low light
- further narrows the anterior chamber and drainage angle to the trabecular meshwork (peripheral iris moves forward)
