Ophthalmology conditions Flashcards
1
Q
AMD
A
Progressive disease affecting the macula classified by a number of physical characteristics, in particular the number and consistency of drusen
Most common cause of blindness in the UK
2
Q
AMD risk factors
A
Age - AMD increases with age
Smoking
Caucasian
Concomitant diseases - CVD, HTN
Ocular characteristics - light iris, hyperopia
Genetics - complement factor H, gene variant Y402H
3
Q
Dry AMD
A
Less aggressive form, accounts for between 80-90% of all AMD
Initially no apparent symptoms but drusen present
Visual loss caused by atrophy or conversion to wet AMD
4
Q
Wet AMD
A
New vessels develop from the choroid layer and grow into the retina (neovascularisation)
Vessels can leak fluid or blood, causing oedema and faster vision loss
VEGF stimulates the development of new vessels
5
Q
AMD vs glaucoma
A
Glaucoma - associated with peripheral vision loss and halos around lights
AMD - associated with central vision loss and a wavy appearance to straight lines
6
Q
AMD presentation
A
Unilateral
Gradual loss of central vision
Reduced visual acuity
Crooked or wavy appearance to straight lines (metamorphopsia)
Gradually worsening ability to read small text
Wet AMD presents more acutely than dry AMD → can progress to complete vision loss within 2-3 years & bilateral disease
7
Q
AMD examination
A
Reduced visual acuity using a Snellen chart
Scotoma (enlarged central area of vision loss)
Amsler grid test - used to assess for the distortion of straight lines seen in AMD
Drusen may be seen in fundoscopy
8
Q
AMD Ix
A
Slit lamp examination - detailed view of the retina and macula
Optical CT - used to diagnose and monitor AMD
Fluorescein angiography - assess retina blood supply → shows oedema & neovascularisation in wet AMD
9
Q
AMD management
A
Require specialist ophthalmology assessment and management
No specific treatment for dry AMD, reducing risk of progression:
- avoiding smoking
- controlling BP
- vitamin supplementation has some evidence in slowing progression
Wet AMD - anti-VEGF medications (eg. ranibizumab) block VEGF & slow the development of new vessels
- injected directly into the vitreous chamber of the eye, usually about once a month
10
Q
Charles Bonnet syndrome
A
Causes a person whose vision has started to deteriorate to see things that aren’t real
Brain doesn’t receive as much information as it used to and responds by filling in the gaps with fantasy patterns or images that it’s stored
Reassuring patients is essential to help them cope with hallucinations
11
Q
Uveitis classification
A
Anatomical location - anterior (iris), intermediate (ciliary body), posterior (choroid)
Granulomatous vs non-granulomatous
Acute, recurrent or chronic
- recurrent - more than 3 months
- chronic - less than 3 months
12
Q
Uveitis aetiology
A
Autoimmune - sarcoid, SLE, MS, Behcets, seronegative spondyloarthropathies, IBD
Infectious - CMV, HSV, HZV, candida, toxoplasma
Drug induced - bisphosphonates
Traumatic
13
Q
Anterior uveitis clinical features
A
Symptoms - blurring of vision, pain, photophobia, redness of eye, floaters
Signs - keratic precipitates, cells in anterior chamber, fibrin in anterior chamber, flare in anterior chamber, posterior synechae (posterior part of the iris can get stuck to the lens during inflammation), cells in vitreous, choroiditis lesions, macular oedema
14
Q
Uveitis investigations
A
Infectious vs non infectious
FBC, U&Es, LFT, Q Gold (TB), treponemal antibody (syphilis)
Other investigations dependent on suspected cause
15
Q
Uveitis management
A
Anterior uveitis - topical steroids/subconjunctival steroids, cycloplegics
- cycloplegics - dilate the pupil & reduce pain associated with ciliary spasm
- topical steroids SE: ocular hypertension → glaucoma, posterior subcapsular cataract
Intermediate and posterior uveitis
- local treatment: periocular steroids, intravitreal steroid implants
- systemic treatment: pulse therapy, oral steroids, immunosuppression, aetiology specific antibiotic/antifungal/antiviral
- SE of steroids: insomnia, weight gain, osteoporosis, hyperglycaemia, immunosuppression, hypertension
16
Q
Anterior uveitis complications
A
Posterior synechiae
Pupillary membrane
Ocular hypertension/glaucoma
Hypotony → no treatment so will lead to blindness
Cataract
Cystoid macular oedema
17
Q
Glaucoma
A
Glaucoma - refers to optic nerve damage (characteristic optic head changes), associated with corresponding visual field defects, with or without raised intraocular pressure
Raised pressure caused by a blockage in aqueous humour trying to escape the eye
Main cause of irreversible blindness in the world
Two types: open-angle glaucoma, acute angle-closure glaucoma
18
Q
Open-angle glaucoma pathophysiology
A
Gradual increase in resistance to flow through the trabecular meshwork
Pressure slowly builds within the eye
Raised intraocular pressure causes cupping of the optic disc → cup-disk ratio > 0.5 is abnormal
19
Q
Open-angle glaucoma risk factors
A
Increasing age
Family history
Black ethnic origin
Myopia (nearsightedness)
Eye injuries/eye operations
Ocular hypertension
20
Q
Open-angle glaucoma presentation
A
Rise in intraocular pressure may be asymptomatic for a long time & diagnosed by routine eye testing
Glaucoma affects the peripheral vision first → gradual onset of peripheral vision loss (tunnel vision)
Fluctuating pain
Headaches
Blurred vision
Halos around lights, particularly at night
21
Q
Measuring intraocular pressure
A
Non-contact tonometry: estimates intraocular pressure by opticians; involves shooting a ‘puff of air’ at the cornea
Goldmann applanation tonometry - gold-standard to measure intraocular pressure → involves a device mounted on a slip lamp that makes contact with the cornea & applies various pressures
22
Q
Open-angle glaucoma diagnosis
A
Goldmann applanation tonometry
Slit lamp
Visual field assessment
Gonioscopy
Central corneal thickness
23
Q
Open-angle glaucoma management
A
360 degrees selective laser trabeculoplasty → laser directed at the trabecular meshwork, improving drainage
- may delay/prevent the need for eye drops
Next line: prostaglandin analogue eye drops (latanoprost) - increase uveoscleral outflow
- SE: eyelash growth, eyelid pigmentation, iris pigmentation
Other eye drop options: beta-blockers, carbonic anhydrase inhibitors, sympathomimetics
24
Q
Open-angle glaucoma surgery
A
360 degree selective laser trabeculoplasty (SLT) first line to people with an IOP > 24mmHg
Trabeculectomy may be considered in refractory cases
25
Acute angle closure glaucoma
Iris bulges forward and seals off the trabecular meshwork from the anterior chamber → prevents aqueous humour from draining & leads to continual increase in intraocular pressure
The pressure builds in the posterior chamber, pushing the iris forward & exacerbating angle closure
Ophthalmological emergency
26
Acute angle closure glaucoma risk factors
Long-sightedness
Increasing age
Family history
Female
Chinese and east asian ethnic origin
Shallow anterior chamber
Certain medications - adrenergic medication, anticholinergic medications, tricyclic antidepressants
27
Acute angle-closure glaucoma presentation
Appears generally unwell
Severely painful red eye
Blurred vision
Halos around lights
Associated headache, nausea & vomiting
Signs: red eye, hazy cornea, decreased visual acuity, mid-dilated pupil, fixed size pupil, hard eyeball on gentle palpation
28
Acute-angle closure glaucoma initial management
Immediate admission
Lie patient flat without a pillow
Pilocarpine eye drops
Acetazolamide 500mg orally
Analgesia & anti-emetic
29
Acute-angle closure secondary care management
Specialist medical options - pilocarpine eye drops, acetazolamide IV, timolol, brimonidine
Laser iridotomy = definitive treatment
- relieves pressure pushing iris forward against the cornea & opens the pathway for the aqueous humour to drain
30
Central retinal artery occlusion
Sudden, painless loss of vision caused by occlusion of the central retinal artery
Less common than retinal vein occlusion
More proximal an occlusion is, the worse effect on vision
31
CRAO aetiology
Atherosclerosis
Embolism
Inflammatory
Thrombophilia
32
CRAO clinical features
Sudden-onset painless loss of vision typically occurring over seconds
History of amaurosis fugax (transient loss of vision)
O/E - pale retina with a ‘cherry red spot’ at the macula, may also have a RAPD
33
CRAO investigations
Fundoscopy & thorough H&E
Imaging - OCT & fluorescein angiography may also be utilised
34
CRAO management
Vision unlikely to improve with treatment beyond 90-100 minutes - only 30% of patients will have any improvement in vision after presentation
Aim is to reperfuse the ischaemic retina as quickly as possible:
- ocular massage - aiming to dislodge the embolus
- vasodilation with isosorbide dinitrate
- anterior chamber paracentesis - reduce IOP to help dislodge the embolus
35
CRVO
Central retinal vein (or one of its branches) is occluded by a thrombus
More common than central retinal artery occlusion
36
CRVO risk factors
Atherosclerotic - age, smoking, obesity, hypertension, diabetes
Haematological - protein S, protein C or antithrombin deficiency, factor V Leiden, multiple myeloma, glaucoma, antiphospholipid syndrome
37
CRVO clinical features
Sudden, painless loss of vision/visual field defects
Ischaemic CRVO → must worse reduced visual acuity (6/60 or worse)
O/E - classic fundoscopy description is ‘stormy sunset’ with findings that include:
- numerous flame haemorrhages
- dot & blot haemorrhages
- cotton wool spots
- retinal oedema
- dilated/tortuous retinal veins
- visual field defects
38
CRVO investigations
Bloods - FBC, ESR, CRP, U&Es, LFTs, lipid profile, clotting screen
Further screening for thrombophilia if pt has a family history of clotting disorders
39
CRVO management
Immediate referral to ophthalmology
Conservative management
Retinal neovascularisation - laser photocoagulation
Macular oedema - intravitreal anti-VEGF injections
40
CRVO complications
Neovascularisation
Vitreous haemorrhage - new vessels are fragile and can bleed
Hyphaema - neovascularisation in the iris can lead to bleeding in the anterior chamber
41
Episcleritis
Benign and self-limiting inflammation of the episclera, the outermost layer of the sclera
Relatively common in young & middle-aged adults, often associated with inflammatory disorders
42
Episcleritis clinical features
Localised/diffuse redness (often a patch of redness in the lateral sclera
No pain
Dilated episcleral vessels
No photophobia/discharge
Normal visual acuity
Applying phenylephrine eye drops → causes blanching episcleral vessels → causes redness to disappear
43
Episcleritis management
Self-limiting & will resolve in 1-2 weeks
Symptoms may be relieved with analgesia & lubricating eye drops
More severe cases → steroid eye drops
44
Scleritis
Inflammation of the sclera
Most severe type = necrotising scleritis → lead to perforation of the sclera
45
Scleritis aetiology
Idiopathic
Underlying systemic inflammatory condition - RA, vasculitis
Infection - pseudomonas or staph aureus
46
Scleritis clinical features
Gradual onset, can be unilateral or bilateral
Red, inflamed sclera
Congested vessels
Severe pain
Pain with eye movement
Photophobia
Epiphora (excessive tear production)
Reduced visual acuity
Tenderness to palpation of the eye
47
Scleritis management
Urgent assessment and management by an ophthalmologist
Oral NSAIDs
Steroids - topical or systemic
Immunosuppression appropriate to underlying systemic condition
Antimicrobials for infectious scleritis
48
Diabetic retinopathy
Involves damage to the retinal blood vessels due to prolonged high blood sugar levels
49
Diabetic retinopathy pathophysiology
Hyperglycaemia damages the retinal small vessels & endothelial cells
Increased vascular permeability → leading blood vessels, blot haemorrhages & hard exudates (deposits of lipids & proteins)
Damage to the blood vessel walls leads to microaneurysms and venous beading
Damage to nerve fibres → cotton wool spots
Intraretinal microvascular abnormalities (IRMA) refer to dilated and tortuous capillaries in the retina
Neovascularisation
50
Diabetic retinopathy clinical features
Early stages may be asymptomatic
Floaters/dark spots in the vision
Blurred or distorted vision
Difficulty seeing at night
Sudden loss of vision
51
Diabetic retinopathy grading
Background - microaneurysms, retinal haemorrhages, hard exudates & cotton wool spots
Pre-proliferative - venous beading, multiple blot haemorrhages, intraretinal microvascular abnormality (IMRA)
Proliferative - neovascularisation and vitreous haemorrhage
52
Diabetic maculopathy
Exudates within the macula
Macular oedema
53
Diabetic retinopathy complications
Vision loss
Retinal detachment
Vitreous haemorrhage
Rubeosis iridis (new blood vessel formation in the iris)
Optic neuropathy
Cataracts
54
Diabetic retinopathy management
Non-proliferative diabetic retinopathy = close monitoring and careful diabetic control
Treatment options:
- pan-retinal photocoagulation (PRP) - extensive laser treatment across the retina to suppress new vessels
- anti-VEGF injections
- surgery (eg. vitrectomy) may be required in severe disease
Intravitreal implant containing dexamethasone → option for macular oedema
55
Hypertensive retinopathy
Damage to the small blood vessels in the retina relating to hypertension
56
Hypertensive retinopathy features
Silver wiring/copper wiring - walls of the arterioles become thickened & sclerosed
AV nipping - arterioles cause compression of the veins
Cotton wool spots
Hard exudates
Retinal haemorrhages
Papilloedema due to ischaemia to the optic nerve, resulting in the optic nerve swelling
57
Hypertensive retinopathy mx
Focused on controlling BP & managing risk factors
58
Conjunctivitis
Inflammation of the conjunctiva
May be bacterial, viral or allergic
59
Conjunctivitis aetiology
Allergic conjunctivitis - type I hypersensitivity reaction to allergens in the environment (eg. pollen, dust mites, pet dander)
Viral conjunctivitis - adenoviruses, can also be herpes simplex
Bacterial conjunctivitis - staph aureus, strep pneumoniae, H, influenzae, Moraxella catarrhalis, STIs
60
Conjunctivitis clinical features
Red, bloodshot eye
Itchy or gritty sensation
Discharge
- bacterial: purulent, typically worse in the morning & eyes may be stuck together
- viral: serous discharge
- allergic: serous discharge
No pain, photophobia or reduced visual acuity
61
Conjunctivitis management
Allergic - avoid allergens, antihistamines, topical mast-cell stabilisers
Viral - self-limiting, symptom relief & good hygiene practice
Bacterial - generally self-limiting, topical abx if severe
Patients should be advised to seek medical attention if condition worsens/fails to improve after a week of treatment
62
Optic neuritis
Inflammation of the optic nerve, often resulting in visual impairment and ocular discomfort
63
Optic neuritis aetiology
Demyelinating lesions - MS
Autoimmune disorders
Infectious conditions - particularly those affecting the CNS
64
Optic neuritis clinical features
Visual loss
Periocular pain - pain around the eye, often aggravated by eye movement
Dyschromatopsia - impaired colour discrimination, especially involving red-green spectrum
65
Optic neuritis ix
Visual function tests - visual acuity, colour vision, visual field
MRI head and spine
66
Optic neuritis mx
IV methylprednisolone
67
Cataracts
Characterised by an opacity in the lens, which is typically caused by denaturation of lens proteins
68
Cataracts risk factors
Age
Smoking
Diabetes mellitus
Systemic corticosteroid use
Others: alcohol consumption, UV exposure, trauma, previous eye surgery, radiation exposure
69
Cataracts clinical features
Gradual painless loss of vision
Difficulty reading/watching television
Difficulty recognising faces
Haloes around lights, particularly at night
Children → can present as a squint
Signs - loss of red reflex, brown/white appearance of lens on slit-lamp
70
Cataracts ix
Slit-lamp biomicroscopy
71
Cataracts mx
Surgical intervention → pseudophakia
- removal of the lens affected by the cataract & its replacement with an artificial lens
- most common surgical technique is phacoemulsification
72
Complications of cataract surgery
Endophthalmitis - severe pain, loss of vision, hyperaemia, presenting within days of surgery. Immediate ophthalmological intervention is required
Posterior lens capsule opacification - few weeks post-surgery, characterised by blurry vision & visible white opacity. Can be easily treated with outpatient laser procedure
Rare → retinal detachment, macular oedema, glaucoma & corneal oedema
73
Blepharitis
Various conditions which cause chronic inflammation of the eyelid margins
74
Blepharitis aetiology
Staphylococcus infection
HSV or VZV infection
Meibomian gland dysfunction
Seborrheic dermatitis
Rosacea
75
Blepharitis clinical features
Painful, gritty, itchy eyes
Eyelids sticking together upon waking
Dry eye symptoms
Erythema, crusting or scaling at eyelid margins
Visibly blocked Meibomian gland orifices
76
Blepharitis management
Lid hygiene - at least twice a day
Avoidance of contact lens use during flare-ups
77
Stye
Hordeolum externum - abscess at an eyelash follicle, commonly caused by staphylococcus
Hordeolum internum - abscess of the Meibomian gland
- can lead to a chalazion if the gland becomes blocked
78
Stye clinical features
Painful, red hot lump that points outwards causing localised inflammation
79
Stye management
Warm compresses
OTC pain relief
Topical antibiotic ointments
Persistent cases → surgical intervention may be required to drain the abscess
80
Chalazion
Occurs when a Meibomian gland becomes blocked and swells, often called a Meibomian cyst
81
Chalazion clinical features
Swelling in the eyelid
Initially painful, but evolves into a non-tender swelling that points inwards
82
Chalazion management
Warm compresses
Gentle massage towards the eyelashes (encourage drainage)
Rarely → surgical drainage
83
Thyroid eye disease
Complication of Grave’s disease, which is an autoimmune hyperthyroidism
Inflammatory process results in swelling of the extraocular muscles and orbital fat, which leads to multiple ocular complications
84
Thyroid eye disease pathophysiology
Evidence suggests an autoimmune reaction to TSH receptors results in lymphocyte infiltration into orbital tissues → initiates an inflammatory process
Inflammatory phase of TED typically lasts 6-24 months & results in the swelling of extraocular muscles & orbital fat
- TED only responsive to medical management
After the inflammatory phase → inactive fibrotic phase
- nonresponsive to medical therapy
85
TED RFs
Smoking
Family history of Grave’s disease & other autoimmune disease
Female sex
Poor thyroid control
86
TED clinical features
Ocular pain - often worse on movement
Dry, red eyes
‘bulging eyes’
Painful eyelids
Proptosis/exophthalmos
Lid retraction & lid lag
Chemosis
Orbital fat prolapse
Exposure keratopathy
87
TED mx
Good control of thyrotoxicosis & other medical therapies, such as steroids or other immunosuppressants
Sight-threatening TED → urgent surgical orbital decompression may be required, followed IV corticosteroids
Conservative therapy → artificial tears, ointments & prisms
88
TED complications
Exposure keratopathy - where corneal damage & infection occur as the patient is unable to close their eyes
Compressive optic neuropathy - retro-orbital swelling begins to compress on the optic nerve
Diplopia
89
Preseptal cellulitis
Infection of tissue anterior to the orbital septum
Much more common than orbital cellulitis & 80% of cases occur in children < 10 years
90
Preseptal cellulitis clinical features
Erythematous swollen eyelid
Mild fever
Erythema surrounding the orbit
Normal eye movements
Normal optic nerve function
91
Preseptal cellulitis ix
Blood tests - FBC, CRP
Swabs - sent for M, C & S
CT orbit is the gold standard investigation to differentiate from orbital cellulitis
92
Preseptal cellulitis mx
Young or systemically unwell children should be admitted for IV antibiotics
Otherwise, treatment is with oral antibiotics & daily outpatient review
93
Orbital cellulitis
Sight and life threatening emergency
Describes infection of the structures behind the orbital septum
94
Orbital cellulitis risk factors
Trauma
Surgical - ocular, adnexal or sinus
Sinus disease - ethmoidal sinusitis is most common site of infection that spreads to the orbit
Other facial infections - preseptal, dental abscess or dacryocystitis
95
Orbital cellulitis clinical features
Periocular pain and swelling
Fever
Malaise
Erythematous, swollen and tender eyelid
Chemosis
Proptosis
Restricted eye movements +/- diplopia
96
Orbital cellulitis ix
Blood tests - FBC, CRP
Swabs sent for M, C & S
CT orbit
97
Orbital cellulitis mx
Admission for IV antibiotics
Close monitoring with input from the ophthalmology, ear, nose and throat & medical teams
98
Infective keratitis
Inflammation of the cornea
99
Infective keratitis aetiology
Viral - herpes simplex → most common cause of keratitis
Bacterial - Pseudomonas or Staphylococcus
Fungal - candida or aspergillus
Contact lens-induced acute red eye (CLARE)
Exposure keratitis (caused by inadequate eyelid coverage)
100
HSV keratitis
Can cause inflammation in any part of the eye but most commonly affects the epithelial layer of the cornea
Primary or recurrent
- recurrent = virus travelling to the trigeminal ganglion, where it becomes latent & can reactivate later
Inflammation of stroma (layer between the epithelium and endothelium) = stromal keratitis → associated with stromal necrosis, vascularisation & scarring
101
HSV keratitis clinical features
Red, painful eye
Photophobia
Epiphora
Visual acuity may be decreased
Fluorescein staining -> epithelial ulcer
102
HSV keratitis ix
Slit lamp examination
Fluorescein staining shows a dendritic corneal ulcer
Corneal scrapings can be used for viral testing
103
HSV keratitis mx
Urgent assessment & management by an ophthalmologist
Topical/oral antivirals
Corneal transplant is an option to treat permanent scarring & vision loss after keratitis
104
Retinal detachment
Neurosensory layer of the retina separates from the retinal pigment epithelium, usually due to retinal tear
Allows vitreous fluid to get into the neurosensory retina & fill the space between the layers
105
Retinal detachment risk factors
Lattice degeneration (thinning of the retina)
Posterior vitreous detachment
Trauma
Diabetic retinopathy
Retinal malignancy
Family history
106
Retinal detachment clinical features
Painless
Peripheral vision loss - sudden & shadow coming across the vision
Blurred or distorted vision
Flashes and floaters
107
Retinal detachment mx
Detailed assessment to detect retinal tears & retinal detachment → immediate ophthalmology
Management of retinal tears aims to create adhesions between the retina & choroid:
- laser therapy
- cryotherapy
Management of retinal detachment aims to reattach the retina & reduce traction/pressure that may cause it to detach again:
- vitrectomy - removing the vitreous fluid, fixing the tear & inserting gas/oil into the eye to hold the retina in place
- scleral buckling - silicone ‘buckle’ to put pressure on the sclera from outside the eye, squashing the eye inwards to reconnect the layers of the retina
- pneumatic retinopexy - injecting a gas bubble into the vitreous body & positioning patient so the gas bubble presses the separated layer back into place
108
Pre-chiasmal field defects
Occur due to a lesion anterior to the optic chiasm
Unilateral & commonly occur due to damage of the retina/optic nerve → typically present with a scotoma/unilateral anopia
109
Scotoma
Area of reduced vision in an otherwise normal visual field
Physiological scotoma = blind spot due to the optic nerve
Central scotoma = involves the macula leading to a defect in central vision
Abnormalities of the peripheral retina (retinal detachment) can lead to a peripheral enlarging scotoma
110
Anopia
Absence of sight
One-half of vision = hemianopia
Complete anopia refers to the complete absence of vision
Pre-chiasmal field defects = anopia is unilateral (damage to optic nerve)
111
Optic chiasm field defects
Characterised by bitemporal hemianopia
Loss of vision in both temporal fields (outer half of the visual field)
Pituitary tumour most common cause due to close proximity & subsequent compression
112
Post-chiasmal field defects
May occur from a lesion anywhere along the visual pathway from the optic chiasm to the visual cortex in the occipital lobe
Bilateral
Commonly associated with stroke due to disruption of blood supply to the optic radiations/occipital cortex
113
Homonymous hemianopia
Visual field defect involving either the two right or the two left halves of the visual fields of both eyes
Vascular causes - cerebral infarction or cerebral haemorrhage
Children - most common cause is a tumour
Right is due to lesion on left and vice versa
114
Superior homonymous quadrantanopia
Visual field defect involving the two right/two left upper quadrants of the visual fields in both eyes
Lesion involving the temporal lobe optic radiations → stroke, tumour or demyelination
Accompanying features - aphasia, memory deficits, complex seizures, auditory & visual hallucinations
115
Inferior homonymous quadrantanopia
Visual field defect involving the two right or two left lower quadrants of the visual fields in both eyes
Causes may include stroke, tumour or demyelination
Accompanying features: finger agnosia, acalculia, right-left disorientation, neglect & inattention
116
Macular sparing
Refers to the preservation of central vision
Lesion of the occipital lobe causes isolated homonymous hemianopia with macular sparing
- reason for this is due to bilateral representation of the macula in the occipital cortex (receives input from both the right and left occipital lobes)
117
Abnormal pupil shape
Trauma to sphincter muscles in the iris (eg. during surgery)
Anterior uveitis can cause adhesions in the iris → irregular pupil shape
Acute angle-closure glaucoma → vertical oval pupil shape
Rubeosis iridis (neovascularisation in the iris) can distort shape of iris & pupil → associated with diabetic retinopathy
118
Mydriasis (dilated pupil) causes
Congenital
Stimulants - cocaine
Anticholinergics - oxybutynin
Trauma
Third nerve palsy
Holmes-Adie syndrome
Raised IP
Acute angle-closure glaucoma
119
Miosis (constricted pupil)
Horner syndrome
Cluster headaches
Argyll-Robertson pupil (neurosyphilis)
Opiates
Nicotine
Pilocarpine
120
3rd nerve palsy (eye findings)
Ptosis
Dilated non-reactive pupil - 3rd nerve carries parasympathetic fibres that innervate the circular muscles of the iris
Divergent strabismus in the affected eye, with a ‘down and out’ position of the affected eye
Can be idiopathic
3rd nerve palsy that does not affect the pupil suggests a microvascular cause:
- diabetes
- hypertension
- ischaemia
Full 3rd nerve palsy is caused by compression of the nerve:
- trauma
- tumour
- cavernous sinus thrombosis
- PCA aneurysm
- raised IP
121
Horner syndrome
Triad of ptosis, miosis & anhidrosis (loss of sweating)
Caused by damage to the sympathetic nervous system supplying the face
Location of Horner syndrome can be determined by the anhidrosis:
- central lesions - anhidrosis of the arm, trunk & face
- stroke, MS, swelling (tumours), syringomyelia
- pre-ganglionic lesions - anhidrosis of the face
- Pancoast tumour, trauma, thyroidectomy, top rib (cervical rib)
- post-ganglionic lesions - no anhidrosis
- carotid aneurysm, carotid artery dissection, cavernous sinus thrombosis, cluster headache
Cocaine eye drops can be used to test for Horner - no pupil reaction seen
Low-adrenalin eye drops will dilate the pupil in Horner
122
Argyll-Robertson pupil
Specific finding in neurosyphilis
Constricted pupil that accommodates when focusing on a near object but does not react to light
‘Prostitute’s pupil’
