Ophthalmology Flashcards
Red eye - Acute angle closure glaucoma
What are the features?
Acute angle closure glaucoma
-severe pain (may be ocular or headache)
-decreased visual acuity, patient sees haloes
-semi-dilated pupil
-hazy cornea
What are 3 factors that predispose to acute angle glaucoma
In acute angle-closure glaucoma (AACG) there is a rise in IOP secondary to an impairment of aqueous outflow. Factors predisposing to AACG include:
hypermetropia (long-sightedness)
pupillary dilatation
lens growth associated with age
Give 8 features of acute angle glaucoma
Features
-severe pain: may be ocular or headache
-decreased visual acuity
-symptoms worse with mydriasis (e.g. watching TV in a dark room)
-hard, red-eye
-haloes around lights
-semi-dilated non-reacting pupil
-corneal oedema results in dull or hazy cornea
-systemic upset may be seen, such as nausea and vomiting and even abdominal pain
What are 2 investigations for acute angle glaucoma?
Investigations
-tonometry to assess for elevated IOP
-gonioscopy (literally looking, oscopy, at the angle, gonio): a special lens for the slit lamp that allows visualisation of the angle
What is the management of acute angle glaucoma?
The management of AACG is an emergency and should prompt urgent referral to an ophthalmologist. Emergency medical treatment is required to lower the IOP with more definitive surgical treatment given once the acute attack has settled.
There are no guidelines for the initial medical treatment emergency treatment. An example regime would be:
combination of eye drops, for example:
-a direct parasympathomimetic (e.g. pilocarpine, causes contraction of the ciliary muscle → opening the trabecular meshwork → increased outflow of the aqueous humour)
-a beta-blocker (e.g. timolol, decreases aqueous humour production)
-an alpha-2 agonist (e.g. apraclonidine, dual mechanism, decreasing aqueous humour production and increasing uveoscleral outflow)
-intravenous acetazolamide
reduces aqueous secretions
some guidelines also recommend the use of topical steroids to reduce inflammation
Definitive management
laser peripheral iridotomy
creates a tiny hole in the peripheral iris → aqueous humour flowing to the angle
Red eye - anterior uveitis
What are the features?
Anterior uveitis
-acute onset
-pain
-blurred vision and photophobia
-small, fixed oval pupil, ciliary flush
What is anterior uveitis?
Anterior uveitis is one of the important differentials of a red eye. It is also referred to as iritis. Anterior uveitis describes inflammation of the anterior portion of the uvea - iris and ciliary body. It is associated with HLA-B27 and may be seen in association with other HLA-B27 linked conditions
Give 10 features of anterior uveitis
-acute onset
-ocular discomfort & pain (may increase with use)
-pupil may be small +/- irregular due to -sphincter muscle contraction
-photophobia (often intense)
-blurred vision
- red eye
-lacrimation
-ciliary flush: a ring of red spreading outwards
-hypopyon; describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level
-visual acuity initially normal → impaired
Give 5 associated conditions with anterior uveitis
Associated conditions
-ankylosing spondylitis
-reactive arthritis
-ulcerative colitis, Crohn’s disease
-Behcet’s disease
-sarcoidosis: bilateral disease may be seen
What is the management of anterior uveitis?
Management
urgent review by ophthalmology
cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate
steroid eye drops
Red eye - scleritis
What are the features?
Scleritis
severe pain (may be worse on movement) and tenderness
may be underlying autoimmune disease e.g. rheumatoid arthritis
what is scleritis? give 4 risk factors
Scleritis describes full-thickness inflammation of the sclera. It generally has a non-infective cause and typically causes a red, painful eye.
Risk factors
rheumatoid arthritis: the most commonly associated condition
systemic lupus erythematosus
sarcoidosis
granulomatosis with polyangiitis
give 4 features of scleritis
Features
-red eye
-classically painful (in comparison to episcleritis), but sometimes only mild pain/discomfort is present
-watering and photophobia are common
-gradual decrease in vision
What is the management of scleritis
Management
-same-day assessment by an ophthalmologist
-oral NSAIDs are typically used first-line
-oral glucocorticoids may be used for more -severe presentations
-immunosuppressive drugs for resistant cases (and also to treat any underlying associated diseases)
What is episcleritis? what are 2 associated conditions
Episcleritis is describes the acute onset of inflammation in the episclera of one or both eyes.
The majority of cases are idiopathic, associated conditions include:
-inflammatory bowel disease
-rheumatoid arthritis
Give 4 features of episcleritis? how can you distinguish between scleritis and episcleritis?
Features
-red eye
-classically not painful (in comparison to scleritis), but mild pain/irritation is common
watering and mild photophobia may be present
-in episcleritis, the injected vessels are mobile when gentle pressure is applied on the sclera
-in scleritis, vessels are deeper, hence do not move
phenylephrine drops may be used to differentiate between episcleritis and scleritis
-phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels
-if the eye redness improves after phenylephrine a diagnosis of episcleritis can be made
-approximately 50% of cases are bilateral
What is the management of episcleritis
Management
-conservative
-artificial tears may sometimes be used
Red eye - conjunctivitis
What are the features?
Conjunctivitis
purulent discharge if bacterial, clear discharge if viral
Conjunctivitis
-what is seen in bacterial vs viral conjunctivitis
Bacterial conjunctivitis
-Purulent discharge
-Eyes may be ‘stuck together’ in the morning)
Viral conjunctivitis
-Serous discharge
-Recent URTI
-Preauricular lymph nodes
Describe the management of infective conjunctivitis
Management of infective conjunctivitis
-normally a self-limiting condition that usually settles without treatment within 1-2 weeks
-topical antibiotic therapy is commonly offered to patients, e.g. Chloramphenicol. Chloramphenicol drops are given 2-3 hourly initially whereas chloramphenicol ointment is given qds initially
-topical fusidic acid is an alternative and should be used for pregnant women. Treatment is twice daily
Contact lens users:
-topical fluoresceins should be used to identify any corneal staining
-treatment as above
-contact lens should not be worn during an episode of conjunctivitis
advice should be given not to share towels
school exclusion is not necessary
Give 5 features of allergic conjunctivitis
Features
-Bilateral symptoms conjunctival erythema, conjunctival swelling (chemosis)
-Itch is prominent
-the eyelids may also be swollen
-May be a history of atopy
-May be seasonal (due to pollen) or perennial (due to dust mite, washing powder or other allergens)
Describe the management of allergic conjunctivitis?
Management of allergic conjunctivitis
-first-line: topical or systemic antihistamines
-second-line: topical mast-cell stabilisers, e.g. Sodium cromoglicate and nedocromil
Red eye - subconjunctival haemorrhage
-What is in the history?
History of trauma or coughing bouts
Red eye - endophthalmitis
-What are the features
Typically red eye, pain and visual loss following intraocular surgery
Corneal abrasions
-give 5 features
Corneal abrasions refer to any defect of the corneal epithelium and most commonly come about from a recent history of local trauma (e.g. fingernails, branches).
Features
-eye pain
-lacrimation
-photophobia
-foreign body sensation and conjunctival injection
-decreased visual acuity in the affected eye
What is the investigation and mamagement of a corneal abrasion?
Investigation
fluorescein staining
examination typically reveals a yellow-stained abrasion (representative of the de-epithelialized surface) which is usually visible to the naked eye
visualisation is enhanced by the use of a cobalt blue filter (available on an ophthalmoscope) or a Wood’s lamp
Management
a topical antibiotic is recommended for these patients in order to prevent secondary bacterial infection.
What is a corneal ulcer and what are 2 risk factors?
A corneal ulcer describes a defect in the cornea, typically secondary to an infective cause. The term corneal abrasion is typically used for corneal defects secondary to physical trauma.
Risk factors
-contact lens use
-vitamin A deficiency: a particular problem in the developing world
What are 4 features of corneal ulcer?
Features
-eye pain
-photophobia
-watering of the eye
-focal fluorescein staining of the cornea
What is keratitis?
Keratitis describes inflammation of the cornea. Microbial keratitis is not like conjunctivitis - it is potentially sight threatening and should therefore be urgently evaluated and treated.
What are 8 types of keratitis?
Causes
bacterial
-typically Staphylococcus aureus
-Pseudomonas aeruginosa is seen in contact lens wearers
fungal
amoebic
acanthamoebic keratitis
-accounts for around 5% of cases
-increased incidence if eye exposure to soil or contaminated water
-pain is classically out of proportion to the findings
parasitic: onchocercal keratitis (‘river blindness’)
Remember, other factors may causes keratitis:
-viral: herpes simplex keratitis
-environmental
photokeratitis: e.g. welder’s arc eye
exposure keratitis
-contact lens acute red eye (CLARE)
Give 4 features of keratitis
Features
-red eye: pain and erythema
-photophobia
-foreign body, gritty sensation
-hypopyon may be seen
What is the management of suspected keratitis in contact lens wearers?
Referral
contact lens wearers
assessing contact lens wearers who present with a painful red eye is difficult
an accurate diagnosis can only usually be made with a slit-lamp, meaning same-day referral to an eye specialist is usually required to rule out microbial keratitis
What is the management and complications of keratitis?
Management
-stop using contact lens until the symptoms have fully resolved
-topical antibiotics
-typically quinolones are used first-line
cycloplegic for pain relief
e.g. cyclopentolate
Complications may include:
-corneal scarring
-perforation
-endophthalmitis
-visual loss
Give 5 features of herpes simplex keratitis
Herpes simplex keratitis most commonly presents with a dendritic corneal ulcer.
Features
-red, painful eye
-photophobia
-epiphora
-visual acuity may be decreased
-fluorescein staining may show an epithelial ulcer
What is the management of herpes simplex keratitis?
Management
-immediate referral to an ophthalmologist
-topical aciclovir
What are 5 features of corneal foreign body?
Features
-eye pain
-foreign body sensation
-photophobia
-watering eye
-red eye
Give 5 indications for referral of corneal foreign body?
Indications for referral to ophthalmology
-Suspected penetrating eye injury due to high-velocity injuries (e.g. drilling, lawn moving or hammering) or sharp objects (e.g. as glass, knives, pencils or thorns)
-Significant orbital or peri-ocular trauma has occurred.
-A chemical injury has occurred (irrigate for 20-30 mins before referring)
-Foreign bodies composed of organic material (such as seeds, soil) should be referred to ophthalmology as these are associated with a higher risk of infection and complications
-Foreign bodies in or near the centre of the cornea
-Any red flags e.g. severe pain; irregular, dilated or non-reactive pupils; significant reduction in visual acuity.
What is herpes zoster ophthalmicus? give 2 features?
Herpes zoster ophthalmicus (HZO) describes the reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve. It accounts for around 10% of case of shingles.
Features
-vesicular rash around the eye, which may or may not involve the actual eye itself
-Hutchinson’s sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement
What is the management of herpes zoster ophthalmicus?
Management
oral antiviral treatment for 7-10 days
-ideally started within 72 hours
-intravenous antivirals may be given for very severe infection or if the patient is immunocompromised
-topical antiviral treatment is not given in HZO
topical corticosteroids may be used to treat any secondary inflammation of the eye
ocular involvement requires urgent ophthalmology review
What are 3 complications of herpes zoster ophthalmicus?
Complications
-ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
-ptosis
-post-herpetic neuralgia
What is hyphema and what is the management?
Hyphema (blood in the anterior chamber of the eye) - especially in the context of trauma warrants urgent referral to an ophthalmic specialist for assessment and management. The main risk to sight comes from raised intraocular pressure which can develop due to the blockage of the angle and trabecular meshwork with erythrocytes. Strict bed rest is required as excessive movement can redisperse blood that had previously settled; therefore high-risk cases are often admitted. Even isolated hyphema will require daily ophthalmic review and pressure checks initially as an outpatient.
What needs to be assessed for in hyphema? what are the features to look out for and the management of this?
An assessment should also be made for orbital compartment syndrome, e.g. secondary to retrobulbar haemorrhage. This is true ophthalmic emergency
features
-eye pain/swelling
-proptosis
-‘rock hard’ eyelids
-relevant afferent pupillary defect
management
-urgent lateral canthotomy (before diagnostic imaging) to decompress the orbit
What is transient monocular visual loss?
Sudden loss is a frightening symptom for patients. It may represent an ongoing issue or only be temporary. The term transient monocular visual loss (TMVL) describes a sudden, transient loss of vision that lasts less than 24 hours.
What are the 4 most common causes of sudden loss of vision?
The most common causes of a sudden painless loss of vision are as follows:
-ischaemic/vascular (e.g. thrombosis, embolism, temporal arteritis etc). This includes recognised syndromes e.g. occlusion of central retinal vein and occlusion of central retinal artery
-vitreous haemorrhage
-retinal detachment
-retinal migraine
Ischaemic/vascular cause of sudden loss of vision
-What is this AKA?
-What may this represent and therefore what is the treatment?
-what is ischaemic optic neuropathy caused by?
Ischaemic/vascular
-often referred to as ‘amaurosis fugax’
wide differential including large artery disease (atherothrombosis, embolus, dissection), small artery occlusive disease (anterior ischemic optic neuropathy, vasculitis e.g. temporal arteritis), venous disease and hypoperfusion
-may represent a form of transient ischaemic attack (TIA). It should therefore be treated in a similar fashion, with aspirin 300mg being given
a-ltitudinal field defects are often seen: ‘curtain coming down’
-ischaemic optic neuropathy is due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve
CRVO
-What are 3 causes
-What is seen on fundoscopy?
Central retinal vein occlusion
-incidence increases with age, more common than arterial occlusion
-causes: glaucoma, polycythaemia, hypertension
-severe retinal haemorrhages are usually seen on fundoscopy
CRVO
-What is this a differential for?
-Give 5 risk factors
Central retinal vein occlusion (CRVO) is a differential for sudden painless loss of vision.
Risk factors
-increasing age
-hypertension
-cardiovascular disease
-glaucoma
-polycythaemia
What are the features seen in CRVO? what is a key differential and what does this cause?
Features
-sudden, painless reduction or loss of visual acuity, usually unilaterally
fundoscopy
-widespread hyperaemia
-severe retinal haemorrhages - ‘stormy sunset’
A key differential is branch retinal vein occlusion (BRVO) - this occurs when a vein in the distal retinal venous system is occluded and is thought to occur due to blockage of retinal veins at arteriovenous crossings. It results in a more limited area of the fundus being affected.
What is the management of CRVO?
Management
-the majority of patients are managed conservatively
indications for treatment in patients with CRVO include:
-macular oedema - intravitreal anti-vascular endothelial growth factor (VEGF) agents
-retinal neovascularization - laser photocoagulation
CRAO
-What is this due to
-What are 3 main features?
Central retinal artery occlusion
-due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)
-features include afferent pupillary defect, ‘cherry red’ spot on a pale retina, sudden, painless unilateral visual loss
What is the management of CRAO?
Management is difficult and the prognosis is poor
-any underlying conditions should be identified and treated (e.g. intravenous steroids for temporal arteritis)
-if a patient presents acutely then Intraarterial thrombolysis may be attempted but currently, trials show mixed results.
Vitreous haemorrhage
-Give 3 causes
-Give 2 main features
-Once the bleeding stops how quickly does the blood clear?
Vitreous haemorrhage
causes: diabetes, bleeding disorders, anticoagulants
features may include sudden visual loss, dark spots
Vitreous haemorrhage is bleeding into the vitreous humour. It is one of the most common causes of sudden painless loss of vision. It causes disruption to vision to a variable degree, ranging from floaters to complete visual loss. The source of bleeding can be from disruption of any vessel in the retina as well as the extension through the retina from other areas. Once the bleeding stops, the blood is typically cleared from the retina at an approximate rate of 1% per day.
How common is vitreous haemorrhage? what are the three most common causes?
Epidemiology
-Spontaneous vitreous haemorrhage has an incidence of around 7 cases per 100000 patient-years
-Incidence by age and sex varies according to the incidence of the underlying causes
Common causes (collectively account for 90% of cases):
-proliferative diabetic retinopathy (over 50%)
-posterior vitreous detachment
-ocular trauma: the most common cause in children and young adults
What are 3 symptoms and 2 signs of vitreous haemorrhage
Patients typically present with an acute or subacute onset of:
-painless visual loss or haze (commonest)
-red hue in the vision
-floaters or shadows/dark spots in the vision
Signs:
-decreased visual acuity: variable depending on the location, size and degree of vitreous haemorrhage
-visual field defect if severe haemorrhage
What are 5 investigations for vitreous haemorrhage
Investigations:
-dilated fundoscopy: may show haemorrhage in the vitreous cavity
-slit-lamp examination: red blood cells in the anterior vitreous
-ultrasound: useful to rule out retinal tear/detachment and if haemorrhage obscures the retina
-fluorescein angiography: to identify neovascularization
-orbital CT: used if open globe injury
What are the signs of symptoms of posterior vitreous detachment?
May precede retinal detachment
Posterior vitreous detachment
Flashes of light (photopsia) - in the peripheral field of vision
Floaters, often on the temporal side of the central vision
Give 4 features of retinal detachment
-Dense shadow that starts peripherally progresses towards the central vision
-A veil or curtain over the field of vision
-Straight lines appear curved
-Central visual loss
What is a retinal detachment?
Retinal detachment occurs when the neurosensory tissue that lines the back of the eye comes away from its underlying pigment epithelium. It is a reversible cause of visual loss, provided it is recognised and treated before the macula is affected. If left untreated and symptomatic, retinal detachment will inevitably lead to permanent visual loss.
Give 5 risk factors of retinal detachment?
Risk factors
-diabetes mellitus
occurs as a result of breaks in the retina due to traction by the vitreous humour
these tears may proceed to detachment if left untreated
-myopia
-age
-previous surgery for cataracts (accelerates posterior vitreous detachment)
-eye trauma e.g. boxing
Give 6 features of retinal detachment? what can be seen on fundoscopy 2?
Features
-new onset floaters or flashes, as these indicate pigment cells entering the vitreous space or traction on the retina respectively
-sudden onset, painless and progressive visual field loss, described as a curtain or shadow progressing to the centre of the visual field from the periphery should also raise suspicion of detachment
-if the macula is involved, central visual acuity and visual outcomes become much worse
-peripheral visual fields may be reduced, and central acuity may be reduced to hand movements if the macula is detached
-the swinging light test may highlight a relative afferent pupillary defect if the optic nerve is involved
fundoscopy
-the red reflex is lost and retinal folds may appear as pale, opaque or wrinkled forms
-if the break is small, however, it may appear normal
What is the management of patient with new onset flashes/floaters?
Management
any patients with new onset flashes and floaters should be referred urgently (<24 hours) to an ophthalmologist for assessment with a slit lamp and indirect ophthalmoscopy for pigment cells and vitreous haemorrhage
Give 4 risk factors for age related macular degeneration
Risk factors
Advancing age itself is the greatest risk factor for ARMD
-the risk of ARMD increases 3 fold for patients aged older than 75 years, versus those aged 65-74.
-smoking
current smokers are twice as likely as non-smokers to have ARMD related visual loss, and ex-smokers have a slightly increased risk of developing the condition, (OR 1.13).
-family history is also a strong risk factor for developing ARMD
first degree relatives of a sufferer of ARMD are thought to be four times more likely to inherit the condition.
other risk factors for developing the condition include those associated with an increased risk of ischaemic cardiovascular disease, such as hypertension, dyslipidaemia and diabetes mellitus.
What are the two forms of macular degeneration? what are each characterised by? which is most common?
Traditionally two forms of macular degeneration are seen:
dry macular degeneration
90% of cases
also known as atrophic
characterised by drusen - yellow round spots in Bruch’s membrane
wet macular degeneration
10% of cases
also known as exudative or neovascular macular degeneration
characterised by choroidal neovascularisation
leakage of serous fluid and blood can subsequently result in a rapid loss of vision
carries the worst prognosis
Recently there has been a move to a more updated classification:
early age-related macular degeneration (non-exudative, age-related maculopathy): drusen and alterations to the retinal pigment epithelium (RPE)
late age-related macular degeneration (neovascularisation, exudative)
Give 5 features of macular degeneration?
Patients typically present with a subacute onset of visual loss with:
-a reduction in visual acuity, particularly for near field objects
-gradual in dry ARMD
-subacute in wet ARMD
-difficulties in dark adaptation with an overall deterioration in vision at night
fluctuations in visual disturbance which may vary significantly from day to day
-they may also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects
-visual hallucinations may also occur resulting in Charles-Bonnet syndrome
What are 3 clinical signs of macular degeneration?
Signs:
-distortion of line perception may be noted on Amsler grid testing
-fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.
-in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.
What are 3 investigations of ARMD?
Investigations:
-slit-lamp microscopy is the initial investigation of choice, to identify any pigmentary, exudative or haemorrhagic changes affecting the retina which may identify the presence of ARMD. This is usually accompanied by colour fundus photography to provide a baseline against which changes can be identified over time.
-fluorescein angiography is utilised if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy. This may be complemented with indocyanine green angiography to visualise any changes in the choroidal circulation.
-optical coherence tomography is used to visualise the retina in three dimensions because it can reveal areas of disease which aren’t visible using microscopy alone.
What are 3 treatment of ARMD?
Treatment
the AREDS trial examined the treatment of dry ARMD in 3640 subjects. It showed that a combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third. Patients with more extensive drusen seemed to benefit most from the intervention. Treatment is therefore recommended in patients with at least moderate category dry ARMD.
vascular endothelial growth factor (VEGF)
-VEGR is a potent mitogen and drives increased vascular permeability in patients with wet ARMD
-a number of trials have shown that use of anti-VEGF agents can limit progression of wet ARMD and stabilise or reverse visual loss
-evidence suggests that they should be instituted within the first two months of diagnosis of wet ARMD if possible
-examples of anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,. The agents are usually administered by 4 weekly injection.
laser photocoagulation does slow progression of ARMD where there is new vessel formation, although there is a risk of acute visual loss after treatment, which may be increased in patients with sub-foveal ARMD. For this reason anti-VEGF therapies are usually preferred.
How common is diabetic retinopathy? What is the pathophysiology?
Diabetic retinopathy is the most common cause of blindness in adults aged 35-65 years-old.
Pathophysiology
Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage to endothelial cells and pericytes
Endothelial dysfunction leads to increased vascular permeability which causes the characteristic exudates seen on fundoscopy. Pericyte dysfunction predisposes to the formation of microaneurysms. Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia
What are the three classifications of diabetic retinopathy?
Patients are typically classified into those with non-proliferative diabetic retinopathy (NPDR), proliferative retinopathy (PDR) and maculopathy.
What are the 3 stages of non-proliferative diabetic retinopathy? what signifies each one?
Mild NPDR
-1 or more microaneurysm
Moderate NPDR
-microaneurysms
-blot haemorrhages
-hard exudates
-cotton wool spots (‘soft exudates’ - represent areas of retinal infarction), venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR
Severe NPDR
-blot haemorrhages and microaneurysms in 4 quadrants
-venous beading in at least 2 quadrants
-IRMA in at least 1 quadrant
Give three key features of proliferative diabetic retinopathy? 3
Key features
-retinal neovascularisation - may lead to vitrous haemorrhage
-fibrous tissue forming anterior to retinal disc
-more common in Type I DM, 50% blind in 5 years
Give 4 key features of maculopathy?
Key features
-based on location rather than severity, anything is potentially serious
-hard exudates and other ‘background’ changes on macula
-check visual acuity
-more common in Type II DM
What management is given to all patients with any diabetic retinopathy?
All patients
optimise glycaemic control, blood pressure and hyperlipidemia
regular review by ophthalmology
What is the management of maculopathy and non-proliferative diabetic retinopathy?
Maculopathy
-if there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors
Non-proliferative retinopathy
-regular observation
-if severe/very severe consider panretinal laser photocoagulation
what are 3 management options for proliferative retinopathy?
Proliferative retinopathy
Panretinal laser photocoagulation
-following treatment around 50% of patients develop a noticeable reduction in their visual fields due to the scarring of peripheral retinal tissue
-other complications include a decrease in night vision (rods are predominantly responsible for vision in low light conditions, the majority of rod cells are located in the peripheral retina), a generalised decrease in visual acuity and macular oedema
intravitreal VEGF inhibitors
often now used in combination with panretinal laser photocoagulation
examples include ranibizumab
strong evidence base suggests they both slow progression of proliferative diabetic retinopathy and improve visual acuity
if severe or vitreous haemorrhage: vitreoretinal surgery
Describe the classification of hypertensive retinopathy
The table below shows the Keith-Wagener classification of hypertensive retinopathy
Stage Features
I Arteriolar narrowing and tortuosity
Increased light reflex - silver wiring
II Arteriovenous nipping
III Cotton-wool exudates
Flame and blot haemorrhages
These may collect around the fovea resulting in a ‘macular star’
IV Papilloedema
What is open-angle glaucoma?
Glaucomas are optic neuropathies associated with raised intraocular pressure (IOP). They can be classified based on whether the peripheral iris is covering the trabecular meshwork, which is important in the drainage of aqueous humour from the anterior chamber of the eye. In primary open-angle glaucoma (POAG), the iris is clear of the meshwork. The trabecular network functionally offers an increased resistance to aqueous outflow, causing increased IOP. It is now recognised that a minority of patients with raised IOP do not have glaucoma and vice versa.
What are 7 risk factors for primary open-angle glaucoma?
Risk factors:
increasing age
-affects < 1’5 in individuals under 55 years of age
-but up to 10% over the age of 80 years
genetics
-first degree relatives of an open-angle glaucoma patient have a 16% chance of developing the disease
Afro Caribbean ethnicity
myopia
hypertension
diabetes mellitus
corticosteroids
What are 3 features of POAG?
POAG may present insidiously and for this reason is often detected during routine optometry appointments. Features may include
-peripheral visual field loss - nasal scotomas progressing to ‘tunnel vision’
-decreased visual acuity
-optic disc cupping
What are 4 signs on fundoscopy of POAG?
Fundoscopy signs of POAG
1. Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen
2. Optic disc pallor - indicating optic atrophy
3. Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
4. Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages
How is the diagnosis of POAG made and what are 6 investigations?
Diagnosis:
-Case finding and provisional diagnosis is done by an optometrist
-Referral to the ophthalmologist is done via the GP
-Final diagnosis is done by investigations as below
Investigations:
-automated perimetry to assess visual field
slit lamp examination with pupil dilatation to assess optic nerve and fundus for a baseline
-applanation tonometry to measure IOP
-central corneal thickness measurement
-gonioscopy to assess peripheral anterior chamber configuration and depth
-Assess risk of future visual impairment, using risk factors such as IOP, central corneal thickness (CCT), family history, life expectancy
Give 4 steps of management of POAG?
NICE guidelines
1: offer 360° selective laser trabeculoplasty (SLT) first-line to people with an IOP of ≥ 24 mmHg NICE
-360° SLT can delay the need for eye drops and can reduce but does not remove the chance they will be needed at all
-a second 360° SLT procedure may be needed at a later date
2: prostaglandin analogue (PGA) eyedrops should be used next-line NICE
3:the next line of treatments includes:
-beta-blocker eye drops
-carbonic anhydrase inhibitor eye drops
-sympathomimetic eye drops
4: surgery in the form of a trabeculectomy may be considered in refractory cases.
Prostaglandin analogues in POAG:
-How does this work?
-How is this given?
-what are 2 adverse effects?
Prostaglandin analogues (e.g. latanoprost) Increases uveoscleral outflow
Once daily administration
Adverse effects include brown pigmentation of the iris, increased eyelash length
Beta blocker drops in POAG
-How does this work?
-Who should this be avoided in?
Beta-blockers (e.g. timolol, betaxolol) Reduces aqueous production
Should be avoided in asthmatics and patients with heart block
Sypathomimetics in POAG
-how does this work?
-When to avoid this
-What is an adverse effect?
Sympathomimetics (e.g. brimonidine, an alpha2-adrenoceptor agonist)
Reduces aqueous production and increases outflow
Avoid if taking MAOI or tricyclic antidepressants
Adverse effects include hyperaemia
Carbonic anhydrase inhibitor in POAG
-How does this work
-What is an adverse effect?
Carbonic anhydrase inhibitors (e.g. Dorzolamide)
Reduces aqueous production
Systemic absorption may cause sulphonamide-like reactions
Miotics in POAG
-How does this work?
-What are 3 adverse effects?
Miotics (e.g. pilocarpine, a muscarinic receptor agonist)
Increases uveoscleral outflow
Adverse effects included a constricted pupil, headache and blurred vision
Optic neuritis
-Give three causes
-Give 5 features
Causes
-multiple sclerosis: the commonest associated disease
-diabetes
-syphilis
Features
-unilateral decrease in visual acuity over hours or days
-poor discrimination of colours, ‘red desaturation’
-pain worse on eye movement
-relative afferent pupillary defect
-central scotoma
What is the investigations/management/prognosis of optic neuritis?
Investigation
MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases
Management
high-dose steroids
recovery usually takes 4-6 weeks
Prognosis
MRI: if > 3 white-matter lesions, 5-year risk of developing multiple sclerosis is c. 50%
RAPD
-How is this found
-What is this caused by?
-What is the finding?
Also known as the Marcus-Gunn pupil, a relative afferent pupillary defect is found by the ‘swinging light test’. It is caused by a lesion anterior to the optic chiasm i.e. optic nerve or retina
Finding
the affected and normal eye appears to dilate when light is shone on the affected
Give 2 causes of RAPD
Causes
retina: detachment
optic nerve: optic neuritis e.g. multiple sclerosis
Give the afferent and efferent pathway of the pupillary light reflex
Pathway of pupillary light reflex
afferent: retina → optic nerve → lateral geniculate body → midbrain
efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve
What is an argyll-robertson pupil? give 2 features? what are 2 causes?
Argyll-Robertson pupil is one of the classic pupillary syndrome. It is sometimes seen in neurosyphilis. A mnemonic used for the Argyll-Robertson Pupil (ARP) is Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)
Features
small, irregular pupils
no response to light but there is a response to accommodate
Causes
diabetes mellitus
syphilis
What is holmes-adie pupil? what is holmes adie syndrome?
Holmes-Adie pupil is a benign condition most commonly seen in women. It is one of the differentials of a dilated pupil.
Overview
unilateral in 80% of cases
dilated pupil
once the pupil has constricted it remains small for an abnormally long time
slowly reactive to accommodation but very poorly (if at all) to light
Holmes-Adie syndrome
association of Holmes-Adie pupil with absent ankle/knee reflexes
What are 4 features of horners syndrome?
Horner’s syndrome
Features
-miosis (small pupil)
-ptosis
-enophthalmos* (sunken eye)
-anhidrosis (loss of sweating one side)
What are 3 causes of horners syndrome?
Spinal cord lesion above T1: stroke / tumours syringmyelia/MS/encephalitis
Damage to 2nd order neurone: pancoast tumour/thyroidectomy/trauma/cervical rib
Damage to 3rd order neurone: dissection of internal carotid artery/carotid aneurysm/cavernous sinus thrombosis/cluster headache
What are 3 tests for horners syndrome?
Distinguishing between causes
-heterochromia (difference in iris colour) is seen in congenital Horner’s
-anhidrosis
-pharmacologic tests
can be useful to confirm the diagnosis of Horner syndrome and localise the lesion
apraclonidine drops (an alpha-adrenergic agonist) can be used: causes pupillary dilation in Horner’s syndrome due to denervation supersensitivity but produces mild pupillary constriction in the normal pupil by down-regulating the norepinephrine release at the synaptic cleft
How to distinguish cause of horners syndrome being central/pre-ganglionic/post-ganglionic
Central lesions i.e. spinal cord - anhydrosis of face,arm and trunk
Pre-ganglionic lesions - anhydrosis of face
Post-ganglionic lesions - no anhydrosis
Give 8 causes of mydriasis?
Causes of mydriasis (large pupil)
third nerve palsy
Holmes-Adie pupil
traumatic iridoplegia
phaeochromocytoma
congenital
Drug causes of mydriasis
topical mydriatics: tropicamide, atropine
sympathomimetic drugs: amphetamines, cocaine
anticholinergic drugs: tricyclic antidepressants
Anisocoria may result in apparent mydriasis, due to the difference with the other pupil.
Cataracts:
-Who is this most common in?
A cataract is a common eye condition where the lens of the eye gradually opacifies i.e. becomes cloudy. This cloudiness makes it more difficult for light to reach the back of the eye (retina), thus causing reduced/blurred vision. Cataracts are the leading cause of curable blindness worldwide.
Epidemiology
Cataracts are more common in women than in men
The incidence of cataracts increases with age. One study found that 30% of individuals aged 65 and over had a visually-impairing cataract in either one or both eyes
Give 9 causes of cataracts
Causes
Normal ageing process: most common cause
Other possible causes
Smoking
Increased alcohol consumption
Trauma
Diabetes mellitus
Long-term corticosteroids
Radiation exposure
Myotonic dystrophy
Metabolic disorders: hypocalcaemia
What are 4 symptoms and 1 sign of cataracts?
Patients typically present with a gradual onset of:
-Reduced vision
-Faded colour vision: making it more difficult to distinguish different colours
-Glare: lights appear brighter than usual
-Halos around lights
Signs:
A Defect in the red reflex: the red reflex is essentially the reddish-orange reflection seen through an ophthalmoscope when a light is shone on the retina. Cataracts will prevent light from getting to the retina, hence you see a defect in the red reflex.
What are 2 investigations of cataracts?
Investigations:
-Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
-Slit-lamp examination. Findings: visible cataract
Give 4 different classifications of cataracts?
Classification
-Nuclear: change lens refractive index, common in old age
-Polar: localized, commonly inherited, lie in the visual axis
-Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
-Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy
What is the management of cataracts?
Management
Non-surgical: In the early stages, age-related cataracts can be managed conservatively by prescribing stronger glasses/contact lens, or by encouraging the use of brighter lighting. These options help optimise vision but do not actually slow down the progression of cataracts, therefore surgery will eventually be needed.
Surgery: Surgery is the only effective treatment for cataracts. This involves removing the cloudy lens and replacing this with an artificial one. NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice. Also whether both eyes are affected and the possible risks and benefits of surgery should be taken into account. Prior to cataract surgery, patients should be provided with information on the refractive implications of various types of intraocular lenses. After cataract surgery, patients should be advised on the use of eye drops and eyewear, what to do if vision changes and the management of other ocular problems. Cataract surgery has a high success rate with 85-90% of patients achieving 6/12 corrected vision (on a Snellen chart) postoperatively.
Give 4 complications following surgery for cataracts
Complications following surgery
-Posterior capsule opacification: thickening of the lens capsule
-Retinal detachment
-Posterior capsule rupture
-Endophthalmitis: inflammation of aqueous and/or vitreous humour
Give 5 eyelid problems encountered in GP
Eyelid problems commonly encountered include:
-blepharitis: inflammation of the eyelid margins typically leading to a red eye
-stye: infection of the glands of the eyelids
-chalazion (Meibomian cyst)
-entropion: in-turning of the eyelids
-ectropion: out-turning of the eyelids
Give 2 different types of stye. What is the management?
Different types of stye are recognised:
-external (hordeolum externum): infection (usually staphylococcal) of the glands of Zeis (sebum producing) or glands of Moll (sweat glands).
-internal (hordeolum internum): infection of the Meibomian glands. May leave a residual chalazion (Meibomian cyst)
management includes hot compresses and analgesia. CKS only recommend topical antibiotics if there is an associated conjunctivitis
What is a chalazion? what is the management?
A chalazion (Meibomian cyst) is a retention cyst of the Meibomian gland. It presents as a firm painless lump in the eyelid. The majority of cases resolve spontaneously but some require surgical drainage
What is blepharitis?
Blepharitis is inflammation of the eyelid margins. It may due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis). Blepharitis is also more common in patients with rosacea
The meibomian glands secrete oil on to the eye surface to prevent rapid evaporation of the tear film. Any problem affecting the meibomian glands (as in blepharitis) can hence cause drying of the eyes which in turns leads to irritation
Give 6 features of blepharitis
Features
-symptoms are usually bilateral
-grittiness and discomfort, particularly around the eyelid margins
-eyes may be sticky in the morning
-eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis
-styes and chalazions are more common in patients with blepharitis
-secondary conjunctivitis may occur
Give 3 management points for blepharitis
Management
softening of the lid margin using hot compresses twice a day
‘lid hygiene’ - mechanical removal of the debris from lid margins
-cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used
-an alternative is sodium bicarbonate, a teaspoonful in a cup of cooled water that has recently been boiled
artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film
Lacrimal duct problems
-What is dacrocystitis? what are the features 2 and management?
-How common is congenital lacrimal duct obstrution? what are the features 2 and management?
Dacryocystitis is infection of the lacrimal sac
Features
watering eye (epiphora)
swelling and erythema at the inner canthus of the eye
Management is with systemic antibiotics. Intravenous antibiotics are indicated if there is associated periorbital cellulitis
Congenital lacrimal duct obstruction affects around 5-10% of newborns. It is bilateral in around 20% of cases
Features
watering eye (even if not crying)
secondary infection may occur
Symptoms resolve in 99% of cases by 12 months of age
What is nasolacrimal duct obstruction? what is the management?
Nasolacrimal duct obstruction is the most common cause of a persistent watery eye in an infant. It is caused by an imperforate membrane, usually at the lower end of the lacrimal duct. Around 1 in 10 infants have symptoms at around one month of age
Management
teach parents to massage the lacrimal duct
symptoms resolve in 95% by the age of one year. Unresolved cases should be referred to an ophthalmologist for consideration of probing, which is done under a light general anaesthetic
Papilloedema:
-What is this?
-What features may be seen at fundoscopy? 6
Papilloedema describes optic disc swelling that is caused by increased intracranial pressure. It is almost always bilateral.
The following features may be observed during fundoscopy:
venous engorgement: usually the first sign
loss of venous pulsation: although many normal patients do not have normal pulsation
blurring of the optic disc margin
elevation of optic disc
loss of the optic cup
Paton’s lines: concentric/radial retinal lines cascading from the optic disc
Give 5 causes and 2 rare causes of papilloedema?
Causes of papilloedema
space-occupying lesion: neoplastic, vascular
malignant hypertension
idiopathic intracranial hypertension
hydrocephalus
hypercapnia
Rare causes include
hypoparathyroidism and hypocalcaemia
vitamin A toxicity
Give 7 causes of blurred vision
Blurred vision may be defined as a loss of clarity or sharpness of vision. The vast majority of patients with blurred vision will have long-term refractive errors. Like a lot of terms, it can mean different things to different patients/doctors, therefore, it’s important to assess for associated symptoms such as visual loss, double vision, floaters.
Causes
refractive error: most common
cataracts
retinal detachment
age-related macular degeneration
acute angle closure glaucoma
optic neuritis
amaurosis fugax
Give 3 investigations of patients complaining of blurred vision?
Assessment
-visual acuity with a Snellen chart
pinhole occluders are a useful way to check for whether the blurred vision is due to a refractive error or not
if the blurring improves with a pinhole occluder then likely cause is a refractive error
-visual fields
-fundoscopy
Squint, how are these divided?
Squint (strabismus) is characterised by misalignment of the visual axes. Squints may be divided into concomitant (common) and paralytic (rare). It is important to detect as uncorrected may lead to amblyopia (the brain fails to fully process inputs from one eye and over time favours the other eye).
What is a concomitant vs a paralytic squint?
Concomitant:
Due to imbalance in extraocular muscles
Convergent is more common than divergent
Paralytic:
Due to paralysis of extraocular muscles
What are 2 tests for squint? what is the management?
Detection of a squint may be made by the corneal light reflection test - holding a light source 30cm from the child’s face to see if the light reflects symmetrically on the pupils
The cover test is used to identify the nature of the squint
ask the child to focus on an object
cover one eye
observe movement of uncovered eye
cover other eye and repeat test
Management
referral to secondary care
eye patches may help prevent amblyopia
What is retinitis pigmentosa?
-give 3 features
Retinitis pigmentosa primarily affects the peripheral retina resulting in tunnel vision
Features
night blindness is often the initial sign
tunnel vision due to loss of the peripheral retina (occasionally referred to as funnel vision)
fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
Give 6 assoc. diseases with retinitis pigmentosa?
Associated diseases
Refsum disease: cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis
Usher syndrome
abetalipoproteinemia
Lawrence-Moon-Biedl syndrome
Kearns-Sayre syndrome
Alport’s syndrome
Give 5 ocular manifestations of rheumatoid arthritis? give 2 iatrogenic eye conditions in rheumatoid?
Ocular manifestations of rheumatoid arthritis are common, with 25% of patients having eye problems
Ocular manifestations
keratoconjunctivitis sicca (most common)
episcleritis (erythema)
scleritis (erythema and pain)
corneal ulceration
keratitis
Iatrogenic
steroid-induced cataracts
chloroquine retinopathy
