Ophthalmology Conditions Flashcards
What is the action of atropine?
Parasympatholytic
Anticholinergic
Blocks the response of the iris sphincter muscles and accommodative muscles of the ciliary body
What are mydriatics and cycloplegics and examples?
Dilate the pupil and paralyse the ciliary muscle
Atropine
Cyclopentolate
Tropicamide
Phenylephirine
What are uses of mydriatics and cycloplegics?
Dilate pupil for visualisation of the retina
Management of children with amblyopia - lazy eye
Use in refraction of children for prescription of glasses
What is the action of cyclopentolate?
Parasympatholytic
Anticholinergic
Blocks response of iris sphincter muscles and accommodative muscles of ciliary body
What is the action of tropicamide?
Parasympatholytic
Anticholinergic
Blocks response of iris and ciliary muscle
What is the action of phenylephirine?
Sympathetic agonist
Stimulation of iris dilation muscle
What are the side effects of mydriatic/cycloplegic drops?
Whitening of eyelids due to vasoconstriction (resolves when drops wear off)
Atropine can cause redness of face and warm sensation to touch (so consider lower dose)
Sting eyes for few seconds after instillation
Cannot drive until blurring effect has worn off
What are the uses of fluorescein drops?
Diagnostically to highlight defects in corneal epithelium
Diagnostically to assess tear drainage in children with congenital nasolacrimal duct obstruction
Investigation when measuring IOP (tonometry)
Administered with local anaesthetic as 0.25% solution with oxybuprocaine HCl or proxymetacaine HCl
What is the mechanism of fluorescein drops?
Precursor of eosins
Temporarily stains any cell it enters
Marks damaged areas
Skin discolouration may last 6-12 hours
Contraindicated in an allergy
How long can atropine last?
1-2 weeks
How long can cyclopentolate last?
Effect in 25-75 mins
Recovery over 6-24 hrs
How long can tropicamide last?
Effect within 15-20 mins
Recovery over 4-8 hours
How long can phenylephirine drops last?
3-6 hours
When are mydriatic and cycloplegic drops contraindicated?
Untreated narrow angle glaucoma
Atropine - not in HTN
Avoid phenylephirine in children
What is glaucoma?
Optic nerve damage caused by a significant rise in intraocular pressure
Due to blockage in aqueous humour trying to escape
Pressure due to resistance to flow through the trabecular meshwork into the canal of Schlemm
What is the pathophysiology of open angle glaucoma?
Gradual increase in resistance through the trabecular meshwork
Slow and chronic onset, as pressure slowly builds up in eye
Increased pressure causes cupping of optic disc Normal indent (optic cup) becomes larger due to pressure (>0.5 of the sixe of the optic disc - abnormal)
What are some of the risk factors for open-angle glaucoma?
Increasing age
Family history
Black ethnic origin
Nearsightedness (myopia)
What is the presentation of open-angle glaucoma?
Can be asymptomatic for long period of time
Diagnosed on routine check
Affects peripheral vision first, closes in until tunnel vision
Can present with gradual onset of fluctuating pain
headache
blurred vision
halos appearing around lights, particularly at night time
How can intraocular pressure be measured?
Non-contact tonometry - puff of air at cornea and measuring corneal response
Goldmann applanation tonometry - gold standard
Special device mounted on slip lamp, makes contact with cornea and applies different pressures
What investigations enable a diagnosis of open angle glaucoma?
Goldmann applanation tonometry
Fundoscopy to check for optic disc cupping and optic nerve health
Visual field assessment to check for peripheral vision loss
What is the management of open-angle glaucoma?
Treatment started at an IOP of 24mmHg or above
First line - latanoprost prostaglandin eye drops
Increase uveosacral outflow
Or
Beta blockers, timolol
Carbonic anhydrase inhibitors, dorzolamide
Sympathomimetics, brimonidine
Trabeculectomy surgery when eye drops ineffective:
new channel from anterior chamber, through sclera to under conjunctiva
causes a bleb under conjunctiva (reabsorbed)
What are some of the types of glaucoma?
Open angle
Acute angle
Developmental - congenital or Reiters
Secondary - trauma, uveitic, steroid
What occurs in acute angle closure glaucoma?
Iris bulges forwards
Seals off trabecular meshwork, so cannot drain
Aqueous humour cannot leave anterior chamber
Pressure builds up in posterior chamber, causing pressure behind the iris
Worsens closure of angle
What are the risk factors for angle closure glaucoma?
Increasing age
Females affected 4x more often than males
Family history
Chinese and East Asian ethnic origin, rare in black
Shallow anterior chamber
What medications can precipitate acute angle closure glaucoma?
Adrenergic medications e.g. noradrenalin
Anticholinergic medications e.g. oxybutynin and solifenacin
TCAs e.g. amitriptyline as have anticholinergic effects (inhibits parasympathetic effect, causing glaucoma in those with narrow anterior chambers by dilating pupil and causing pupillary block)
What is seen on examination in acute angle glaucoma?
Severely painful red eye Teary Hazy cornea Decreased visual acuity Dilatation of the affected pupil Fixed pupil size Firm eyeball on palpation
Halos around lights
Associated headache, nausea, vomiting
What is the initial management of acute angle glaucoma?
Same day assessment
Lie patient on back, no pillow
Give pilocarpine eye drops - 2% for blue, 4% brown eyes
Give acetazolamide (carbonic anhydrase inhibitor reduces production of aqueous humour)
Give analgesia
Anti-emetic if needed
What secondary management of acute angle glaucoma is required?
Pilocarpine Acetazolamide IV/PO Hyperosmotic agents e.g. glycerol, mannitol to increase osmotic gradient between blood and fluid Timolol - beta-blocker Dorzolamide Brimonidine
Definitive treatment - laser iridotomy; hole in iris for humour to flow from posterior chamber to anterior
Relieves pressure pushing iris against the cornea
What is the leading cause of blindness in the UK?
Age related macular degeneration
What are the two types of age related macular degeneration?
Wet - 10% cases
Dry - 90%
Wet carries a worse prognosis
What is a key finding in association with macular degeneration?
Drusen on fundoscopy
Yellow deposits of proteins and lipids that appear between the retinal pigment epithelium and Bruch’s membrane
Normal drusen - <63 micrometres and hard
Large and greater numbers early sign, common to both wet and dry
What other features, aside from drusen are common to both wet and dry AMD?
Atrophy of the retinal pigment epithelium
Degeneration of the photoreceptors
What are the layers of the macula?
Choroid layer at bottom - contains blood vessels
Bruch’s membrane
Retinal pigment epithelium
Photoreceptors
What is the pathophysiology of wet AMD?
Development of new vessels growing from the choroid layer into the retina
These vessels can leak fluid/blood, cause oedema
VEGF released
What are the risk factors for AMD?
Age Smoking White or chinese Family history CVD, HTN Ocular characteristics - light iris
What is the presentation of AMD?
Gradual worsening central visual field loss
Reduced visual acuity
Crooked or wavy appearance to straight lines
What is the importance of the presentation of wet AMD?
Presents more acutely
Presents with loss of vision over days
Progresses to full loss of vision over 2-3 years
Often progresses to bilateral disease
What is seen on examination in AMD?
Snellen - reduced acuity
Scotoma - central patch of vision loss
Amsler grid test - distortion of straight lines
Fundoscopy - Drusen
Slit lamp biomicroscopic fundus exam
Optical coherence tomography - cross section of retina for wet AMD
Fluorescein angiography - second line for wet AMD
What is the management of dry AMD?
Focus on lifestyle measures to slow progression
Avoid smoking
Control BP
Vitamin supplements - zinc and antioxidants (not recommended to smokers due to increase in lung ca)
What is the management of wet AMD?
Anti-VEGF e.g.
ranibizumab, bevacizumab, pegaptanib
slows development of new vessels
injected into vitreous chamber once a month
Photodynamic therapy with Verteperfin - light activated compound, taken up by dividing cells inc neovascular tissue
Injected IV, activated by illumination, is sparing of healthy tissue
Need to be started within 3 months to be beneficial
If untreated can become functionally blind within 2 years
Is a treatable disease
How large is the macula?
5.5mm in diameter with the fovea at the centre
What is the function of the retinal pigment epithelium RPE?
Outer blood retinal barrier
Prevents leak of ECF from choriocapillaries to subretinal space
Actively pumps ions and water out of subretinal space
Absorbs stray light
Storage, metabolism and transport of Vitamin A in visual cycle
What are signs of dry AMD?
Drusen
RPE hyperplasia and atrophy
What is drusenoid RPE detachment?
Soft drusen enlarge, become more numerous and coalesce giving a localised elevation of the RPE
Lifts it away from Bruch’s membrane
Results in hypoxic state and inflammation
What occurs in advanced stages of dry AMD?
Confluent drusen
Central and paracentral degeneration of the macula
Atrophy of choriocapillaries, RPE and photoreceptors
Geography atrophy - map like area of atrophy extending from foveal centre
What is the classification of wet AMD?
Based on location of lesion in relation to fovea:
subfoveal
juxtafoveal
extrafoveal
What is the fundus fluorescein angiogram classification?
For Wet AMD
Characterised by angiographic
Classic - CNV clearly visible
Occult - obscured, not visible
What clinical features have been associated with an even greater risk of developing wet AMD?
More than 5 drusen
Large - soft and confluent drusen
Pigment clumping in the RPE
Systemic hypertension
What is Charles Bonnet syndrome?
Visual hallucinations due to visual loss
Common in those with wet AMD
What is hypertensive retinopathy?
Damage to small blood vessels in retina
Chronic hypertension or malignant HTN
What is silver/copper wiring?
Walls of the arterioles become thickened and sclerosed increasing reflection of light
What is arteriovenous nipping?
Arterioles cause compression of the veins where they cross
Due to sclerosis and hardening of the arterioles
What are cotton wool spots?
Due to ischaemia and infarction in the retina, causing damage to nerve fibres
Appear as fluffy white patches on the retina
Result of accummulation of axoplasmic material within the nerve fibre layer
What are the findings in hypertensive retinopathy?
Cotton wool spots
Retinal haemorrhages - rupture and release of blood into the retina
Papilloedema - ischaemia to optic nerve, causes optic nerve swelling and blurring of disc margins
Silver wiring
Hard exudates
Arteriovenous nipping
What is the pathophysiology of diabetic retinopathy?
Hyperglycaemia damages retinal small vessels and endothelial cells.
Increased vascular permeability leads to leakage from the blood vessels, blot haemorrhages and hard exudates.
Damage to blood vessel wall - microaneurysms and venous bleeding.
Damage to nerve fibres in retina - cotton wool spots
Intraretinal microvascular abnormalities - dilated and tortuous capillaries
Shunt between arterial and venous vessels
Neovascularisation - growth factors released in the retina, development of new blood vessels
What is the classification of diabetic retinopathy?
Non-proliferative - background, can develop into proliferative
Proliferative - new blood vessels have developed, vitrous haemorrhages
Diabetic maculopathy
What are the findings of non-proliferative diabetic retinopathy?
Mild - microaneurysms
Moderate - microaneurysms, blot haemorrhages, hard exudates, cotton wool spots, venous bleeding
Severe - blot haemorrhages, microaneurysms in 4 quadrants
venous beating in 2 quadrants
intraretinal microvascular abnormality
What are the findings in diabetic maculopathy?
Ischaemic maculopathy
Macular oedema
What are the complications of diabetic retinopathy?
Retinal detachment
Vitreous haemorrhage - bleeding into the vitreous humour
Rebeosis iridis - new blood vessel formation in the iris
Optic neuropathy
Cataracts
What is the management of diabetic retinopathy?
Laser photocoagulation
Anti VEGF medications - ranibizumab, bevacizumab
Vitreoretinal surgery
What does damage to retinal capillaries lead to in diabetic retinopathy?
Microvascular occlusion
Microvascular leakage
What are predictive risk factors for progression of diabetic retinopathy?
Duration of DM Hyperglycaemia HTN. hyperlipidaemia Nephropathy Pregnancy
Obesity, smoking, alcohol, physical inactivity
What is rubeosis iridis?
Neovascularisation - new blood vessels found on the surface of the iris
often associated with diabetes in advanced proliferative retinopathy
What are cataracts?
When the lens in the eye becomes cloudy and opaque, describes any opacity or reduction in clarity of the crystalline lens
Lens focuses light onto the retina
How are congenital cataracts screened for?
They occur before birth
Screened for red reflex during neonatal examination
What are the risk factors for cataracts?
Most develop over years with advanced age in the presence of risk factors
Increasing age Smoking Alcohol Diabetes Steroids Hypoglycaemia
What is the difference in the loss of vision in cataracts compared with other pathologies?
Cataracts cause generalised reduction in visual acuity, starbursts around light
Glaucoma - peripheral loss of vision, halos around lights
Macular degeneration - central loss of vision, crooked or wavy appearance to straight lines
What is the clinical presentation of cataracts?
Usually asymmetrical, as both eyes affected separately
Very slow reduction in vision
Progressive blurring of vision
Change of colour of vision, colours becoming more brown or yellow
Starbursts around lights, particularly at night time
Loss of red reflex - can appear white or grey, show up on photographs
What is the management of cataracts?
Surgery - drill and break lens into pieces, remove and implant artificial lens into the eye
or lens extraction by phacoemulsification - ultrasound energy
Cataracts can mean other conditions e.g. AMD or diabetic retinopathy can go undetected, until after surgery and still have poor visual acuity
What is endophthalmitis?
Rare but serious complication
Inflammation of inner contents of the eye
Usually due to infection
Treated with intravitreal antibiotics
Otherwise loss of vision and loss of the eye
What are the causes of cataracts?
Congenital Age Drugs - systemic steroids or steroid eye drops Systemic disease - diabetes, down's Other ocular disease - uveitis Trauma
What are the complications of cataract surgery?
Per-operatively - posterior capsular rupture, vitreous loss
Early-post op - endophthalmitis
Late post-op - posterior capsule opacification
What can cause abnormal pupil shape?
Trauma to sphincter muscles in the iris, e.g. cataract surgery
Anterior uveitis causing adhesions
Acute angle glaucoma causing ischaemic damage - vertical oval pupil
Rubeosis iridis - neovascularisation of the iris
in diabetic retinopathy
Coloboma - congenital malformation, hole in the iris causing irregular pupil shape
Tadpole pupil - spasm in a segment of the iris, temporary, associated with migraines
What are causes of mydriasis - dilated pupil?
Third nerve palsy Holmes-Aide syndrome Raised ICP Congenital Trauma Stimulants such as cocaine Anticholinergics
What are causes of miosis - constricted pupil?
Horner's syndrome Cluster headaches Argyll Robertson pupil - neurosyphilis Opiates Nicotine Pilocarpine
What is the presentation of a third nerve palsy?
Ptosis - levator palpebrae superioris
Dilated non-reactive pupil
Divergent strabismus - down and out eye
Oculomotor supplies all muscles except lateral rectus and superior oblique - so down and out from these
What are causes of a third nerve palsy?
Oculomotor nerve travels through cavernous sinus close to posterior communicating artery
Therefore cavernous sinus thrombosis or posterior communicating aneurysm can compress
Idiopathic Tumour Trauma Cavernous sinus thrombosis Posterior communicating aneurysm Raised ICP
What is the difference between a sparing and full third nerve palsy?
Sparing - microvascular because parasympathetic fibres spared - spares the pupil - diabetes, HTN, ischaemia
Full - surgical third due to physical compression
What is the triad of Horner’s?
Ptosis
Miosis
Anhidrosis
May also have enopthalmos - sunken eye
Light and accommodation not affected
What are the causes of Horner’s?
Central - 4 Ss
Stroke, MS, swelling (tumour), syringomyelia
Pre-ganglionic - 4Ts
Tumour (pancoast), trauma, thyroidectomy, top rib - cervical rib growing above first rib
Post-ganglionic - 4Cs
Carotid aneurysm, carotid artery dissection, cavernous sinus thrombosis, cluster headache
What is congenital Horner’s associated with?
Heterochromia - difference in colour of the iris on the affected side
What is the pathway of nerves affected in Horner’s?
Sympathetic arise from spinal cord
These are pre-ganglionic
Enter into sympathetic ganglion at the base of the neck
Exit as post-ganglionic, travel to the head, run alongside internal carotid artery
How can Horner’s be tested for?
Cocaine eye drops
Stops noradrenalin re-uptake at the NMJ
Causes normal eye to dilate as more noradrenaline available so causes dilation, but in Horner’s there is no release initially
So no reaction
Or - adrenaline eye drops won’t dilate a normal pupil, but will dilate a Horner’s
What is a Holmes Adie pupil? (tonic pupil)
Unilateral dilated pupil
Sluggish to react to light
Slow dilation of the pupil following constriction, over time pupil will get smaller
Damage to post-ganglionic parasympathetic fibres
Holmes Adie syndrome also has absent ankle and knee reflexes
What is Argyll Robertson pupil?
Specific to neurosyphilis
Constricted pupil, accommodates when focusing on near object but does not react to light
What is blepharitis?
Inflammation of the eyelid margins
What is the presentation of blepharitis?
Gritty, itchy, dry sensation in the eyes
Associated with dysfunction of the Meibomian glands
What is the management of blepharitis?
Hot compress
Gentle cleaning of eyelid margins to remove debris
Lubricating eye drops:
Hypromellose
Polyvinyl alcohol
Carbomer
What is a stye?
Infection of glands of zeis or glands of moll
Sebaceous glands at the base of the eyelashes
What is the management of a stye?
Hot compresses and analgesia
Topical antibiotics e.g. chloramphenicol if associated with conjunctivitis or persist
What is a chalazion?
Blockage of Meibomian gland
Swelling in the eyelid, typically not tender
What is the treatment of chalazion?
Hot compress, analgesia
Topical antibiotics if actuely inflamed
What is the presentation of a stye?
Tender red lump along eyelid
May contain pus
What is entropion?
Eyelid turns inwards with the lashes against the eyeball
Results in pain, can cause corneal damage and ulceration
What is the management of entropion?
Taping eyelid down
Use regular lubricating drops to prevent eye drying out
Definitive management with surgical intervention
What rheumatology pathology is common in uveitis?
Ank spon
What are the features of ank spon?
HLA-B27 associated
Apical fibrosis Anterior uveitis Aortic regurgitation Achilles tendonitis AV node block Amyloidosis And cauda equina syndrome
Peripheral arthritis
What should be asked in a patient with acute red eye?
Vision - normal or reduced
Painful or painless
Check IOP
What causes painful red eye?
Conjunctivitis Scleritis Keratitis Corneal foreign body Episcleritis
What are causes of painless red eye?
Subconjunctival haemorrhage
What is crucial to the history of subconjunctival haemorrhage?
Hypertension
On any anticoagulation
Check INR - if raised, needs to be addressed ASAP
What is ectropion?
Eyelid turns outwards
Inner aspect of the eyelid exposed, usually affects bottom lid
Can lead to exposure keratopathy as eyeball is exposed
What is trichiasis?
Inward growth of the eyelashes, can result in corneal damage and ulceration
What is the management of trichiasis?
Remove the eyelash - epilation
Recurrent cases may require electrolysis, cryotherapy or laser treatment to prevent lash regrowing
What is periorbital cellulitis?
Eyelid and skin infection in front of the orbital septum
In front of the eye
Presents with swelling, redness, hot skin around the eyelids and eye
What is the treatment of periorbital cellulitis?
Systemic antibiotics
May require observation if vulnerable to prevent development into orbital
What is orbital cellulitis and its clinical features?
Infection around the eyeball, behind the orbital septum
Sight threatening emergency
Pain on eye movement Reduced eye movements Changes in vision Abnormal pupil reactions Forward movement of the eyeball - proptosis
What is the treatment of orbital cellulitis?
Medical emergency
Requires admission
IV antibiotics
Surgical drainage if abscess
MRI/CT helpful in diagnosis and planning treatment
How does the lens change shape?
Ciliary body contract –> pull suspensory ligaments –> flatten lens –> less refraction
vice versa if ciliary body relax
What are common causes of cataracts in younger patients?
Trauma
Drugs - steroids, amiodarone, allopurinol
Systemic disease - Diabetes, myotonic dystrophy, neurofibromatosis type 2
What is conjunctivitis?
Inflammation of the conjunctiva
the tissue that covers the inside of eyelids and sclera
What are the main types of conjunctivitis?
Bacterial
Viral
Allergic
What is the main presentation of conjunctivitis?
Unilateral or bilateral Red eyes Bloodshot Itchy or gritty sensation Discharge from the eye
Does not cause pain, photophobia or reduced visual acuity
Vision may be blurry due to discharge
What are the features of bacterial conjunctivitis?
Purulent discharge
Inflamed conjunctiva
Typically worse in the morning, eye stuck together
Starts in one eye, spread to the other
What are the features of viral conjunctivitis?
Clear discharge
Other symptoms of viral infection e.g. dry cough, sore throat, blocked nose
Contagious
Preauricular lymph nodes
What is the management of conjunctivitis?
Usually resolves without treatment after 1-2 weeks
Good hygiene
Avoid contact lenses
Abc - chloramphenicol and fusidic acid
What is a consideration in conjunctivitis under 1 month?
Neonatal conjunctivitis
Gonococcal infection
Can cause loss of sight
Complications e.g. pneumonia
What is allergic conjunctivitis and its management?
Contact with allergens
Causes swelling of conjunctival sac and eyelid
Significant watery discharge, itchy
Antihistamines
Topical mast cell stabilisers - preventing mast cells releasing histamines
What is anterior uveitis?
Inflammation in the anterior uvea - iritis
What is the uvea?
Iris, ciliary body, choroid
What is the difference between acute and chronic uveitis?
Chronic - more granulomatous - more macrophages, less severe
Lasts more than 3 months
What conditions are associate with acute anterior uveitis?
HLA B27 conditions
Ankylosing spondylitis
Inflammatory bowel disease
Reactive arthritis
What conditions are associated with chronic anterior uveitis?
Sarcoidosis Syphilis Lyme's disease TB Herpes virus
What is the presentation of anterior uveitis?
Unilateral
Starts spontaneously
Without a hx of trauma or precipitating events
May occur with a flare of an associated disease e.g. reactive arthritis
Dull aching painful red eye
Ciliary flush - ring of red spreading from cornea
Reduced visual acuity
Floaters, flashes
Miosis - constriction due to sphincter contraction
Photophobia - ciliary muscle spasm
Pain on movement
Excessive tears
Posterior synechiae - adhesions pulling iris, abnormally shaped
Hypopyon - collection of white blood cells in anterior chamber
What is the management of anterior uveitis?
Referral for same day assessment due to emergency red eye
Refer to rapid access clinic for topical steroids
Steroids
Cycloplegic-mydriatic medications e.g. cyclopentolate or atropine
(antimuscarinic, block iris sphincter and ciliary body)
Immunosuppressants e.g. DMARDs, TNF inhibitors
Laser therapy, cryotherapy, vitrectomy
What is episcleritis?
Inflammation of episclera
Outermost layer of sclera
Underneath conjunctiva
Who is episcleritis seen in?
Young and middle aged adults
Not usually due to infection
Associated with inflammatory disorders e.g. RA or IBD
What is the presentation of episcleritis?
Acute onset, unilateral Typically not painful Can have mild pain Segmental redness - lateral sclera Foreign body sensation Dilated episcleral vessels Watering of eye No discharge
What is the management of episcleritis?
Usually self limiting Will recover in 1-4 weeks Lubricating eye drops Simple analgesia Cold compresses Systemic NSAIDs naproxen
What are the most common causes of ophthalmia neonatorum?
Conjunctivitis in the first 30 days of life
Bacteria - strep, staph
Neisseria gonorrhoea
Chlamydia
What is scleritis?
Inflammation of the full thickness of the sclera
Most severe is necrotising scleritis, can lead to perforation of the sclera
What are associated systemic conditions with scleritis?
Rheumatoid arthritis SLE Inflammatory bowel disease Sarcoidosis Granulomatosis with polyangiitis
What is the presentation of scleritis?
Acute onset 50% cases bilateral Severe pain Pain with eye movement Photophobia Eye watering Reduced visual acuity Abnormal pupil reaction to light Tenderness to palpation
Severe 8-9/10 boring pain
May have diffuse or nodular swelling
What is the management of scleritis?
Consider underlying systemic condition
NSAIDs - topical/systemic
Steroids
Immunosuppression - appropriate to the underlying condition e.g. methotrexate for RA
Refer to eye emergency dept
What can complicate the management of scleritis?
Scleromalacia perforans - diffuse scleral thickening seen in rheumatoid Keratitis - persistent ulceration Uveitis Cataract formation Glaucoma
What causes scleritis?
Immune complex dependent microangiopathy
What are corneal abrasions and common causes?
Scratches or damage to the cornea, cause of red, painful eye
Contact lenses - assoc. infection with pseudomonas Foreign bodies Fingernails Eyelashes Entropion - inward turning eyelid
What is an important differential to consider with corneal abrasions?
Herpes keratitis
Requires antiviral drops
What is the presentation of corneal abrasions?
History of contact lenses or foreign body Painful red eye Foreign body sensation Watering eye Blurring vision Photophobia
How can a corneal abrasion be diagnosed?
Fluorescein stain
Collects in abrasions - yellow-orange colour
Slit-lamp examination
What is the management of corneal abrasions?
Same day assessment
Mild in primary care
Removal of foreign bodies Simple analgesia Lubricating eye drops Antibiotic drops - chloramphenicol FU after 24 hours
Chemical abrasions - immediate irrigation for 20-30 minutes, urgent referral
Mild uncomplicated usually heal over 2-3 days
What are some of the causes of keratitis?
Inflammation of the cornea
Viral infection - herpes Bacterial - pseudomonas, staph Fungal - candida, aspergillus CLARE - contact lens acute red eye Exposure keratitis - inadequate eye lid covering, e.g. ectropion
Where does herpes simplex keratitis most commonly affect?
The epithelial layer of the cornea
If inflammation of the stroma - stromal keratitis
What complications is stromal keratitis associated with?
Stromal necrosis
Vascularisation and scarring
Can lead to corneal blindness
What is the presentation of herpes keratitis?
Painful red eye Photophobia Vesicles around the eye Foreign body sensation Watering eye Reduced visual acuity
Fever, vesicular lid lesions
Follicular conjunctivitis
Preauricular lymphadenopathy
How can herpes keratitis be diagnosed?
Staining with fluorescein
Shows dendritic corneal ulcer (branching and spreading of the ulcer)
Slit-lamp examination
Corneal swabs, scrapings
What is the management of herpes keratitis?
Same day assessment
Aciclovir - topical or oral
Ganciclovir eye gel
Topical steroids for stromal keratitis
Corneal transplant may be required after infection to treat corneal scarring caused by stromal keratitis
What causes herpes simplex keratitis?
Type 1 HSV common important cause of ocular disease
Usually acquired in early life from close contact e.g kissing
Primary infection may cause a conjunctivitis, then resolution and latency in trigeminal ganglion
Risk of reactivation if immunosuppression, systemic illness
What is herpes zoster ophthalmicus?
Ophthalmic shingles
Affects ophthalmic division of the trigeminal nerve
Prodromal period, unwell
Pain and vesicles in nerve distribution
Lid swelling, may be bilateral
Keratitis
Iritis
Secondary glaucoma
What bacteria can cause bacterial keratitis?
Staph epidermidis
Staph aureus
Strep pneumonia
Pseudomonas
What are predisposing causes of bacterial keratitis?
Keratoconjunctivitis sicca - dry eye
Breach in corneal epithelium e.g. trauma or surgery
Contact lens wear
Prolonged use of topical steroids
What is the presentation of bacterial keratitis?
Pain - severe
Purulent discharge
Visual loss
Hypopyon - mass of white cells collected in anterior chamber
White corneal opacity - site of polymorphonuclear infiltration of the stroma
What are other types of keratitis?
Fungal
Interstitial - any vascular keratitis that affects the corneal stroma without epithelial involvement
What are causes of a painful eye with vision loss?
Angle closure glaucoma Corneal ulcer/keratitis Uveitis Endophthalmitis Retrobulbar optic neuritis Orbital cellulitis Giant cell arteritis
What are causes of a painless eye with fleeting vision loss?
Embolic retinal artery occlusion
Migraine and aurea
Raised intracranial pressure
Prodromal in GCA
What are causes of a painless eye with persistent vision loss?
Vitreous haemorrhage Retinal artery occlusion Retinal detachment AMD Other macular disease Optic neuritis Ischaemic optic neuropathy Orbital disease affecting the optic nerve Intracranial disease affecting the visual pathway
What are some causes of ocular pain?
Discomfort - blepharitis, dry eye, conjunctivitis, allergy
Pain on movement - optic neuritis
Pain around the eye - GCA, migraine, cellulitis, headache
Severe pain - keratitis, abrasion, foreign body, uveitis, angle closure glaucoma, endophthalmitis, scleritis, myositis of extraocular muscles
What are causes of diplopia?
Neurogenic - nerve palsies, failure to control squint, visual field defects
Myogenic - thyroid eye disease, myasthenia, myositis, myopathy
Orbital - trauma, SOLs
Monocular - corneal disease, cataracts
What are the causes of myopia?
(Short sightedness)
Parallel rays of light brought to a point of focus before they reach the retina
Eye too long/large - axial
Optical focusing apparatus of the eye is too powerful
What are the causes of hypermetropia?
Long sightedness
Eye is too short
Focusing apparatus too weak (lens and cornea)
Treated with a convex lens
What is aphakia?
After a cataract extraction, the eye is rendered highly hypermetrophic
Because the lens provides one third of the refractive power of the eye
How can aphakia be corrected?
Insertion of an intraocular lens at the time of surgery
Contact lenses
Aphakic spectacles
What is the risk of orbital cellulitis?
Can spread to cause a brain abscess
What tumours may produce signs of orbital disease?
Lacrimal gland tumours
Optic nerve gliomas - in neurofibromatosis type 1
Meningiomas
Lymphomas
Rhabdomyosarcomas
Mets e.g. neuroblastomas in kids, breast, lung, prostate
What can cause ptosis?
Mechanical - large lid lump, lid oedema, downward tethering due to scarring, structural abnormalities
Neurological - third nerve palsy, Horner’s, Marcus Gunn jaw winking syndrome
Myogenic - myasthenia gravis, muscular dystrophy, ophthalmoplegia
What is myasthenia gravis?
Autoimmune disease of the voluntary muscles
Weakness triggered by periods of muscle activity
Relieved by rest
Circulating antibodies block the action of acetylcholine at post synaptic nicotinic neuromuscular kunctions
What tests are completed to diagnose myasthenia gravis?
Repeated upgaze, downgaze movements
results in fatigue and increased ptosis
Look fown for 15s then look at elevated target, lid overshoots then falls
Ice applied reduces ptosis
Weakness of eyelid closure
What can cause evaporative dry eye?
Inadequate meibomian oil delivery
Ectropion - not adequately apposed
Incomplete lid closure e.g. seventh nerve palsy
Infrequent blinking - parkinson’s
What can cause ectopia lentis (disorder of lens position)?
Weakness of zonule - subluxation
After ocular trauma
Homocystineuria - lens displaced downwards
Marfan’s
What signs are seen on examination in uveitis?
Visual acuity reduced
Eye inflamed - mostly around the limbus - ciliary flush
What may a patient complain of with macular dysfunction?
Blurred central vision
Distorted vision - metamorphopsia
Reduction or enlargement of an object
Loss of the central visual field
What can macular oedema be associated with?
Intraocular surgery
Uveitis
Retinal vascular disease - diabetic retinopathy and retinal vein occlusion
Retinitis pigmentosa
What is a retinoblastoma?
Commonest malignant tumour of the eye in childhood
Due to germinal mutations or somatic mutations
If the eye can be salvaged - systemic chemo and local treatment e.g. cryo
Removal of the eye
What are the features of a retinoblastoma?
White pupillary reflex
Squint due to reduced vision
Occasionally if advanced; painful red eye
What is the cause of cotton wool spots?
At margins of ischaemic retinal infarct
Due to obstruction of axoplasmic flow, build up of axonal debris in the nerve fibre layer of the retina
What are the stages of diabetic retinopathy?
None - no signs, vision normal
Background - signs of leakage, microaneurysms, haemorrhage, exudates away from the macula
Maculopathy - exudates, haemorrhage in macula region, central oedema, vision reduced, sight threatening
Preproliferative retinopathy - evidence of arteriolar occlusions, RMA, cotton wool spots, veins irregular, vision normal
Proliferative retinopathy - release of vasoproliferative substance, new vessel growth on disc or retina, vision normal, sight threatening
Advanced retinopathy - bleeding into vitreous, pulling of overlying pigment epithelium
What is a subconjunctival haemorrhage?
One of the small blood vessels in the conjunctiva ruptures
Releases blood into space between sclera and conjunctiva
What can cause subconjunctival haemorrhages?
Idiopathic - otherwise healthy
After a period of strenuous activity e.g. heavy coughing, weight lifting, straining when constipated
Trauma to the eye
What factors can predispose a patient to subconjunctival haemorrhage?
Hypertension Bleeding disorders e.g. thrombocytopenia Whooping cough Medications e.g. warfarin, NOACs, antiplatelets Non accidental injury
What is the presentation of a subconjunctival haemorrhage?
Patch of bright red blood underneath the conjunctiva In front of the sclera Painless Does not affect vision May be history of strenuous event
What is the management of a subconjunctival haemorrhage?
Harmless, resolve spontaneously
Within 2 weeks
Investigate precipitating factors
If there is foreign body sensation, lubricating eye drops can help
What is the vitreous body?
Gel inside the eye that maintains the structure of the eyeball, keeps the retina pressed on the choroid
Made up of collagen and water
What is posterior vitreous detachment?
Vitreous gel comes away from the retina, very common, particularly in older patients
What is the presentation of posterior vitreous detachment?
Painless condition Can be completely asymptomatic Spots of vision loss Floaters Flashing lights
What is the management of posterior vitreous detachment?
No treatment necessary
Symptoms improve over time as brain adjusts
Can predispose a patient to developing retinal tears or detachment
Exclude and assess risk of this, thorough assessment of the retina
What is retinal detachment?
Sight-threatening emergency
Outer retina relies on blood vessels of the choroid for its blood supply
Retina separates from choroid underneath
Usually due to retinal tear
Allows vitreous fluid to get under the retina, fills space
What are the risk factors for retinal detachment?
Posterior vitreous detachment Diabetic retinopathy Trauma to the eye Retinal malignancy Older age Family history
What is the presentation of retinal detachment?
Painless Peripheral vision loss Sudden, shadow like curtain coming across vision Blurred or distorted vision Flashes and floaters
What is the management of retinal detachment?
Reattach retina, reduce traction or pressure which may cause it to recur
Vitrectomy - removing relevant parts of vitreous body and replacing with oil or gas
Scleral buckling - silicone buckle to put pressure on outside of eye/sclera so outer eye indents and brings choroid inwards to make contact with retina
Pneumatic retinopexy - inject gas bubble into vitreous body and position patient so gas bubble creates pressure and flattens retina
What is the management of retinal tears?
Create adhesions between the retina and choroid
Laser therapy
Cryotherapy
What occurs in central retinal vein occlusion?
When a blood clot forms in the retinal veins
Central retinal vein runs through optic nerve, drains blood from retina
One of four branched veins blocked causes problems in area, whereas central vein causes problems for whole retina
Blood in retina = leakage of fluid and blood
Causes macular oedema and retinal haemorrhages
Damages retinal tissue
Loss of vision
Release of VEGF to stimulate neovascularisation
What is the presentation of central retinal vein occlusion?
Sudden painless loss of vision
What are the risk factors for central retinal vein occlusion?
Hypertension High cholesterol Diabetes Smoking Glaucoma Systemic inflammatory conditions such as SLE
What is seen on fundoscopy in central retinal vein occlusion?
Flame and blot haemorrhages
Optic disc oedema
Macula oedema
What other investigations are useful in central retinal vein occlusion?
Full medical history FBC for leukaemia ESR for inflammatory disorders BP for hypertension Serum glucose for diabetes
What is the management of central retinal vein occlusion?
Referral immediately
Treatment of macular oedema and prevent complications e.g. neovascularisation, galucoma
Laser photocoagulation
Intravitreal steroids e.g. dexamethasone intravitreal implant
Anti-VEGF therapies e.g. rituximab, bevacizumab
What are the risk factors of central retinal artery occlusion?
Risk factors for atherosclerosis Older age Family history Smoking Alcohol consumption Hypertension Diabetes Poor diet Inactivity Obesity
Who is at a higher risk of central retinal artery occlusion secondary to giant cell arteritis?
White patients over 50
Particularly females
And those already affected by GCA or polymyalgia rheumatica
What is the presentation of central retinal artery occlusion?
Sudden painless loss of vision
Relative afferent pupillary defect
Fundoscopy - pale retina, cherry-red spot, due to lack of perfusion
What is the relative afferent pupillary defect?
Pupil in the affected eye constricts more when light is shone in the other eye, compared to when it is shone in the affected eye.
Because the input is not being sensed by the ischaemic retina, but is being sensed by the normal retina causing consensual reflex
What is the management of central retinal artery occlusion?
Referral immediately
Check for GCA - ESR and temporal artery biopsy, give steroids - prednisolone 60mg
If presents shortly after symptoms, try to dislodge thrombus:
Occular massage
remove fluid from anterior chamber to reduce IOP
Inhaling carbogen (5% carbon dioxide, 95% oxygen) to dilate artery
sublingual isosorbide Dinitrate to dilate the artery
Long term management reduce reversible risk factors
What is optic neuritis?
Inflammation of the optic nerves
What are some of the types of optic neuritis and causes?
Acute demyelinating - most common, due to MS
Ischaemic - GCA, diabetic papillopathy
Corticosteroid-responsive - autoimmune diseases, SLE
Infections - TB, mycoplasma,
Lyme’s
Nutritional - B12 deficiency
Drugs - Amiodarone, ethambutol, isoniazid, methanol intoxication
What are the differentials for optic neuritis?
Posterior scleritis
Maculopathy
Retinopathy
Big blind spot syndrome
What is the usual presentation of optic neuritis?
Visual impairment
Pain around the eye
Dyschromatopsia - impairment of colour vision
Light flashes
Increased symptoms with raised body temperature
Decreased pupillary light reaction in the affected eye
What are the investigations for optic neuritis?
Full ophthalmological examination
Testing visual acuity, contrast and colour vision, visual field testing
MRI - developing MS
Bloods - FBC, ESR, TFTs, autoantibodies, syphilis
Serological testing
CXR - infection
LP
What is the management of optic neuritis?
Consider corticosteroids in acute phase - methylprednisolone
What does Hutchinson’s sign indicate?
Lesion to the tip of the nose
Increased chance of ocular involvement
Treatment is with aciclovir
What are the stages of thyroid eye disease?
Inflammatory phase
Followed by ‘inactive’ fibrotic phase
Sight loss can occur when delay in start of treatment
Onset of hyperthyroidism and TED usually within 18 months of each other
How does blepharitis present?
Bilateral Burning watery eyes (with foreign body sensation if cornea involved) Worse in morning - eyes may stick Red inflamed eyelid Crusts/scales along eyelashes Tear film deficiency
Why are corticosteroids used for uveitis?
Reduce inflammation
Prevent adhesions
What complications are associated with uveitis?
Relapse
Posterior synechiae (adhesions from lens to iris)
Cataract
Glaucoma (due to steroids)
What must you examine for if a patient has uveitis?
Back pain - ank spond Rash/bite - lyme Resp. Symptoms - Sarcoidosis GI symptoms - IBD Cold sore - herpes Oral/genital ulcers - Behcet's
What features are associated with intermediate uveitis?
Painless floaters
Decreased vision
Minimal redness and pain
What is affected in posterior uveitis?
Retina and choroid
What happens in herpetic keratitis?
What is the hallmark feature on examination?
Virus travel along trigeminal nerve to ophthalmic division to corneal nerve
Dendritic ulcer pattern seen
What investigations would you request for someone with a corneal abrasion?
None normally needed
CT = 1st choice
X-ray if metallic FB
MRI contraindicated for metallic FB
Fluorescein examination
What are the ADR’s associated with anti-VEGF injections?
Retinal detachment
Endophthalmitis
Allergic reaction
What is retinitis pigmentosa?
Inherited eye disease that is characterised by black pigmentation and gradual degeneration of the retina
How does retinitis pigmentosa present?
Night blindness
Ring scotoma - loss of all peripheral vision –> tunnel vision –> blindness
Black bone spicule pigmentation of the peripheral retina
Mottling of retinal pigmented epithelium
Waxy looking disc
What is the pathogenesis of retinitis pigmentosa?
Photoreceptor death - rods first
Cell death lead to inflammation of vitreous humour
Why do you not get a relative afferent pupillary defect in Retinitis Pigmentosa?
Some cases X linked - more men
Peak ages - 7.5, 17 and >50yo
How is Retinitis pigmentosa managed?
Visual rehab
Counselling
No way to stop disease progression
What is the pathogenesis of thyroid eye disease?
Autoimmune reaction to thyroid stimulating hormone receptors
Infiltration of lymphocytes into orbital tissue, release of cytokines
Hyperosmotic shift causing oedema
What are the risk factors of thyroid eye disease?
Current smoking Female sex Middle age Autoimmune thyroid disease Uncontrolled thyroid function Radio-iodine therapy
What is the presentation of thyroid eye disease?
Occular irritation Ache - worse in mornings Red eyes Diplopia - restricted ocular mobility Change in appearance of eyes, bulging eyes Dry or watery Mild photophobia Dyschromatopsia - colour deficiency
Proptosis - lid retraction, lid lag, orbital fat prolapse
Exposure keratopathy - photophobia, tearing, grittiness, pain, due to incomplete lid closure
What are the investigations for thyroid eye disease?
TSH
Free thyroxine - T4
Anti-TSH receptor autoantibodies, TPO
Thyroid uptake scan
What are some complications of thyroid eye disease?
Superior limbic keratoconjunctivitis
Conjunctival injection - over rectus muscles - enlargement of conjunctival vessels
Glaucoma may result from decreased episcleral venous outflow
Strabismus - presents as hypotropia or esotropia due to involvement of inferior and medial rectus
Optic nerve compression
What is examined in thyroid eye disease?
Visual acuity Ishihara colour assessment Exophthalmometry Assess lid lag, lid retraction Corneal exposure Intraocular pressure Orthoptic assessment
What is the clinical activity score for thyroid eye disease?
Pain - feeling on globe, or with movement
Redness - eyelids, conjunctiva
Swelling - lids, chemosis (swelling of conjunctiva)
Impaired function - decrease in eye movements, acuity
What are the types of thyroid eye disease?
Type I - minimal inflammation and restrictive myopathy – mainly fat expansion
Type II - significant orbital inflammation and restrictive myopathy
What is the treatment of thyroid eye disease?
Optimise endocrine control Stop smoking Avoid radioiodine Lubricants (Ocular Hypotensives) NSAIDS Selenium, rituximab Steroids Steroid sparing agents Radiotherapy Surgery - orbital decompression, strabismus surgery, blepharoplasty Botulinum toxin to reduce upper lid swelling Prisms to control diplopia
What is a squint (strabismus)?
Eyes don’t point in the same direction
Misalignment of the visual axis of the eyes
What are the different causes of proptosis?
Protrusion of the eye
Displaced directly forwards in a SOL within the extraocular muscle cone - intra-conal lesion e.g. optic nerve sheath meningioma
Displaced to one side - extra-conal lesion
e.g. tumour of lacrimal glands displaces to nasal side
Transient proptosis - valsalva manoeuvre increases cephalic venous pressure
Presence of pain with proptosis suggests infection
What cause cause pupil irregularity and alter pupil reactions?
Anterior uveitis - posterior synechiae - appearance
Sequelae of intraocular surgery
Blunt trauma to the eye - may rupture sphincter muscle - trauma mydriasis
Acute and severe rise in intraocular pressure e.g. glaucoma
What can cause a disruption of the sympathetic pathway and Horner’s?
Syringomyelia - expanding cavity in the spinal cord, sometimes extends into medulla
Small cell carcinoma of the lung apex - cervical chain
Neck injury
Cavernous sinus disease - catching sympathetic carotid plexus in the sinus
What are the features of Horner’s?
Small pupil on affected side
Loss of dilator function
Recession of the globe into the orbit - enophthalmos
Lack of sweating if the pathway is affected proximal to the base of the skull
What are important clues of raised intracranial pressure?
Headache worse on waking and coughing
Nausea, retching
Diplopia - sixth nerve palsy
If due to e.g. SOL - visual field loss, cranial nerve palsy
Hx of head trauma suggesting subdural haemorrhage, history of medications e.g. oral contraceptives, tetracyclines
What are the visual signs of raised intracranial pressure?
Optic disc swollen, edges blurred, superficial capillaries are dilated
Large blind spot
Abnormal neurological signs may indicate space occupying lesion
What is idiopathic intracranial hypertension?
Usually presents in overweight women
Headache, obscurations of vision and sixth nerve palsies
Raised intracranial pressure and disc swelling present
Treatment with medications e.g. oral acetazolamide
Ventriculoperitoneal shunting
Optic nerve decompression
What is the presentation of giant cell arteritis?
Autoimmune vasculitis
Sudden loss of vision Scalp tenderness e.g. on combing Pain on chewing, jaw claudication Shoulder pain Malaise
What are the investigations for GCA?
ESR and CRP usually grossly elevated
Temporal artery biopsy
BP check, blood glucose check
What is the management of GCA?
High dose steroids immediately, oral and IV
Dose tapered over ensuing weeks
What are causes of a pale optic disc?
Compression of optic nerve Retinal artery occlusion Glaucoma RICP Optic neuritis Inherited optic nerve/retinal disease Toxic optic neuropathy Tobacco/alcohol
What are most common causes of compression of the optic chiasm?
Causing a bitemporal hemianopia - compression of the nasal retina (temporal field)
Pituitary tumour
Meningioma
Craniopharyngioma
What defect do lesions of the optic tract and radiation cause?
Usually vascular or neoplastic
Homonymous hemianopia
Loss confined to the right or left hand side of the field in both eyes
What are the types of squint?
Congenital/acquired - onset before/after 6 months
Concomitant/incomitant
Manifest/latent
What is the function of the different extraoccular muscles?
Superior rectus - abduction and elevation
Lateral rectus - abduction
Inferior rectus - abduction and depression
Inferior oblique - adduction and elevation
Medial rectus - adduction
Superior oblique - adduction and depression
Define Hyphaema
When blood enters anterior chamber between cornea and iris
How does a Hyphaema present?
Decrease/ Loss of vision (may improve as gravity pulls the blood down)
Red tinge to eye
Name 5 causes of a Hyphaema
Intraocular Surgery Blunt trauma Lacerating Trauma Leukaemia Retinoblastoma
How are Hyphaemas managed?
Small - Outpatient basis, antifibrinolytics, corticosteroids, mitotics, asparin
Non resolving - surgical clean out
Pain relief - avoid aspirin and NSAIDs due to platelet interaction
Name three requirements of the accommodation reflex
Eyes converging
Pupil size reducing
Lens changing shape and pattern
Name six causes of sudden visual loss
CRAO Anterior Ischaemic Optic Neuropathy Vitreous Haemorrhage Retinal Vein Occlusion Retinal Detachment Optic Neuritis
Give 5 causes of Endopthalmitis
Trauma, Eye Surgery, VEGF injections, Endogenous seeding, Extension of Corneal infection
Describe the likely pathogens of Endopthalmitis with each cause
Surgery - Coag neg Staph (epidermis),
Trauma - bacillus cereus,
Endogenous - S.Aureus,Klebsiella
Orbital Cellulitis is generally a clinical diagnosis. What investigations could you do, and what would they show?
FBC - leukocytosis
Blood cultures - negative
LP (if focal signs)
Swabs
CT sinus and orbit - extension
Orbital Cellulitis is an emergency and requires urgent antibiotics and four hourly monitoring. What are the Abx of choice?
1) Co Amoxiclav
If pen allergic - Clindamycin and Metronidazole
MRSA - Vancomycin
What is the immediate management for Ocular Chemical Injury?
1) Check pH with universal indicator
2) Administer topical anaesthetic and remove contact lenses
3) 1L saline irrigation continued until pH is 7
4) Rechecked every 15 minutes
If the Chemical Injury of the eye was moderate or severe, how would it be managed?
Dexamethasone 1-2 hourly
Vitamin C (topically and orally)
Citrate and Tetracyclines
Name three associations of Anterior Uveitis and Chronic Anterior Uveitis respectively
Anklyosing Spondylitis, IBD, Reactive Arthritis
Sarcoidosis, Syphilis, TB
What can be seen on examination of a Keratitic eye?
Oedema
White cell infiltration
Epithelial defect
What is Presbyopia?
Gradual loss of accommodation response due to decline in elasticity, becoming apparent when amplitude is insufficient to carry out near tasks
How does Presbyopia present?
Difficulty carrying out near tasks
Accommodative lag (from distance to near vice versa)
Tiring with continuous close work
How is Presbyopia treated?
OTC glasses are normally sufficient
If pre-existing refractive error - prescription glasses
If Presbyopia happens prematurely, what is the likely cause?
Accommodative Insufficiency (Associated with encephalitis and enclosed head trauma)
Inability to maintain binocular enlargment as object becomes closer (aka eye strain)
Define Anterior Ischaemic Optic Neuropathy
Loss of vision as a result of damage to optic nerve from ischaemia
Involves the 1mm head of optic nerve (AKA disc)
How does Arteritic Anterior Ischaemic Optic Neuropathy present?
Rapid onset unilateral visual loss and decreased acuity
Chalky white pallor of optic disc
Amaurosis fugax?
GCA signs?
How is Arteritic Ischaemic Optic Neuropathy investigated?
GCA - ESR/CRP, Temporal Artery Biopsy
MRI/USS - between Arteritic and non
OCT
Describe the management options for Arteritic Anterior Ischaemic Optic Neuropathy
IV Methylpred for 3 days (switch to oral and taper)
MAB against IL6 (Tocilizumab)
Methotrexate
Vitreous haemorrhage is one of the most common causes of sudden painless visual loss. Describe the possible aetiologies
Proliferative diabetic retinopathy (fragile vessels)
Posterior vitreous detachment
Ocular Trauma
How does Vitreous Haemorrhage present?
- Sudden painless visual loss
- Red Hue (may turn green after breakdown)
- New onset floaters/cobwebs
- May be worse in the morning if blood settles during sleep
Name four investigations for Vitreous Haemorrhage
IOP
Slit Lamp - Red Cells in anterior vitreous
Rule out retinal detachment
USS
Describe the general management of Vitreous Haemorrhage
Exclude retinal detachment
Rest with head elevated and re- evaluate in 3-7 days for source
Name four definitive treatment options for Vitreous Haemorrhage
Laser Photocoagulation (for proliferative vasculopathies)
Anterior Retinal Cryotherapy
Vitrectomy
VEGF
Diplopia can be monocular or binocular, what is the difference?
Monocular - doesn’t disappear with one eye closed, likely opthalmological aetiology
Binocular - with one eye closed it disappears, likely neurological aetiology
Describe the anatomical course of CNIII
Emerges from midbrain Travels close to PCA Pierces dura near tentorium cerebelli Lateral cavernous sinus Superior orbital fissure
Name four causes of Oculomotor nerve lesions
Diabetes
GCA
Raised ICP
PCA Aneurysm
How do Oculomotor nerve lesions present?
Fixed dilated pupil that doesn’t accommodate
Ptosis
Unopposed lateral deviation
Intortion on looking down
Microvascular - pupil sparing
How do Oculomotor nerve lesions present (sympathetics involved)?
Pupil will be fixed but not dilated
Trochlear Nerve lesions are rare, give three causes
Orbital trauma
Diabetes
Infarction secondary to hypertension
Name 6 causes of Diplopia
CNIII lesion CNIV lesion CNVI lesion Orbital Blow Out # Thyroid Eye Disease MG
How do Trochlear Nerve Lesions present?
Vertical Diplopia
Weakness of downward and intortion
Compensatory head tilt away from affected side
How does a CNVI lesion appear?
Inability to look laterally
Give three causes of a CNVI lesion
MS
Pontine Cerebrovascular incident
Raised ICP (due to long course)
Describe the pathophysiology of an Orbital Blow Out Fracture
Usually from an object <5cm
Force transmits along rim and into orbital floor
Force is transmitted into three buttresses (infraorbital, displacement of zygomaticofrontal suture, fracture of zygomatic arch)
Name five clinical features of Orbital Blow Out Fractures
Periorbital bruising Surgical Emphysema Vertical Diplopia (worse on looking up) Endopthalmos Infraorbital Paraesthesia
What investigations should you do for a suspected Orbital Blow Out?
Plain XRay - Facial, Occipitomental, Submentovertical (droplet sign in maxillary sinus)
CT
How are Orbital Blow Out Fractures managed?
Don’t blow nose for 10 days
Some can be managed with just broad spec abx
Surgery
The onset of Thyroid Eye Disease is normally within 18 months of diagnosis. Describe the pathophysiology
Initial inflammatory phase lasting 6-24 months (expansion of extraocular muscles and orbital fat resulting in proptosis and optic neuropathy)
Followed by inactive fibrotic phase
Infiltration of lymphocytes stimulate cytokine release and polysaccharide release from fibroblasts - leads to oedema
What are the important receptors in Thyroid Eye Disease?
TSH
IGF1
Name four risk factors for Thyroid Eye Disease
Current smoker
Female
Middle Aged
Radioiodine therapy
Describe the pathophysiology of Myasthenia Gravis
- Receptor sites at NMJ are destroyed
- Not enough stimulation to trigger action potential
- Increased fatiguability with use (reduced ACh) and improvement with rest
Name some signs of Myasthenia Gravis
Ptosis
Cogan Lid Twitch (down gaze followed by up gaze, eye saccades and lid overshoots)
Incomitant strabismus
Raised eyebrows
Pupils never involved
Name three diagnostic tests for MG
Tensilon Test (inhibits AChesterase, only useful when they have measurable findings)
Repetitive Nerve Stimulation Test (decline in compound muscle action potentials within the first 4-5 stimuli)
Single Fibre EMG
Name two laboratory tests for MG
Serum Anti ACh Receptor Titre
Serum Anti Muscle Specific Kinase AB titre
What is the main differential for MG?
Lambert Eaton Syndrome
Improvement of symptoms with repeated stimulation
Describe the management of MG
Med - Steroids, Pyridostigmine, Immunomodulators (if refractory)
Surgery - Removal of thymus
What is Amaurosis Fugax?
How does Amaurosis Fugax present?
Hypoperfusion of optic nerve, normally secondary to carotid artery atherosclerosis and secondary thromboemboli
Precedes stroke so urgent investigations required
Curtain descending down over vision
If provoked by gaze - optical lesion
Other than carotid pathology, give three causes of Amaurosis Fugax
GCA
Retinal Migraine
Papilledema
How is Amaurosis Fugax investigated?
Inflammatory markers
Carotid imaging and cardiac evaluation
MRI/MRA
How is Amaurosis Fugax managed?
TIA - stroke work up
GCA - Emperic steroids and temporal artery biopsy
Antiplatelets/Anticoag
What is Papilledema?
Optic disc swelling secondary to raised ICP
Oedema, continued pressure and optic nerve atrophy
Name three investigations you would do to define the underlying cause of Papilledema
BP
CT/MRI
LP with opening pressure
Name three ways Papilloedema can present
Asymptomatic
Signs of raised ICP
Abducens Palsy
The gold standard management for Papilloedema is to treat underlying cause and reduced ICP. How should IIH be managed?
Weight reduction
Acetazolamide
?CSF Shunt, Duran Venous Stenting
Dry eyes can cause a gritty, foreign body sensation worse at the end of the day. What are some red flags?
Severe eye pain
Significant visual loss
Photophobia
What is the treatment of dry AMD?
Supplementation with Vitamin C, Vitamin E, Zinc, Copper, Lutein and Zeaxanthin
What is pan-retinal photocoagulation used for?
Proliferative diabetic retinopathy
Sacrificing the peripheral retina to reduce the production of VEGF by the ischaemic retina and preventing neovascularisation
What is an important investigation and complication of rubeosis iridis?
Serious complication of severe proliferative diabetic retinopathy - new vessels grow on the iris and in the anterior chamber.
These vessels have the potential to cause a raised intraocular pressure and a secondary glaucoma and therefore measuring this patient’s intraocular pressure is very important.
What are two important sign’s in thyroid eye disease?
Lid retraction (Dalrymple's sign) Lid lag on down gaze (Von Graefe's sign)
What is the treatment of endopthalmitis?
The treatment is intravitreal vancomycin as the most common causative organisms after surgery are gram positive.
Cultures are taken from the vitreous, either by a tap, or by doing a vitrectomy and antibiotic therapy should be tailored according to culture and sensitivities.
What can be given for the treatment of allergic conjunctivitis?
mast cell stabilisers such as Sodium Cromoglycate
What is a systemic cause of cataracts?
Myotonic dystrophy
What is the treatment for gonorrhoeal conjunctivitis in infants?
Ceftriaxone IV, bacitracin ointment and hourly saline lavage
