Progressive visual loss Flashcards
What is glaucoma
- optic nerve damage that is caused by a significant rise in intraocular pressure.
- raised intraocular pressure is caused by a blockage in aqueous humour trying to escape the eye.
What happens in open angle glaucoma
- gradual increase in resistance through the trabecular meshwork.
- This makes it more difficult for aqueous humour to flow through the meshwork and exit the eye.
- Therefore the pressure slowly builds within the eye and this gives a slow and chronic onset of glaucoma.
What happens in acute closed angle glaucoma
- the iris bulges forward and seals off the trabecular meshwork from the anterior chamber preventing aqueous humour from being able to drain away.
- This leads to a continual build up of pressure.
- This is an ophthalmology emergency.
What are the risk factors for open angle glaucoma
Increasing age
Family history
Black ethnic origin
Nearsightedness (myopia)
What is the presentation of open angle glaucoma
- usually asymptomatic and diagnosed on routine screening
- Gradual progressive loss of peripheral vision
- gradual onset of fluctuating pain, headaches, blurred vision and halos appearing around lights, particularly at night time.
How do you measure intraocular pressure
Non-contact tonometry
What is Non-contact tonometry
- commonly used machine for estimating intraocular pressure by opticians.
- shooting a “puff of air” at the cornea and measuring the corneal response to that air.
- less accurate but gives a helpful estimate for general screening purposes.
What is Goldmann applanation tonometry
- gold standard way to measure intraocular pressure.
- special device mounted on a slip lamp that makes contact with the cornea and applies different pressures to the front of the cornea to get an accurate measurement of what the intraocular pressure is.
How do you diagnose open angle glaucoma
- Goldmann applanation tonometry
- Fundoscopy
- Visual field assessment
What might you see on fundoscopy in a patient with open angle glaucoma
- cupping of the optic disc
- optic cup greater than 0.5 the size of the optic disc is abnormal.
What is normal intraocular pressure
10-21 mmHg
What is the management of intraocular pressure
- reduce intraocular pressure
- Prostaglandin analogue eyedrops: latanoprost
- Betablockers (e.g. timolol)
- Carbonic anhydrase inhibitors (e.g. dorzolamide)
- Trabeculectomy
What are side effect of latanoprost
eyelash growth
eyelid pigmentation
iris pigmentation (browning).
When do you begin treating patients with open angle glaucoma
> 24mmHG
close monitoring prior to this
How to prostaglandin analogue treat open angle glaucome
increase uveoscleral outflow
How do Betablockers treat open angle glaucoma
reduce the production of aqueous humour
How do carbonic anhydrase inibitors treat open angle glaucoma
reduce the production of aqueous humour
What is trabeculectomy
- involves creating a new channel from the anterior chamber, through the sclera to a location under the conjunctiva
- causes a “bleb” under the conjunctiva where the aqueous humour drains.
- It is then reabsorbed from this bleb in to the general circulation.
- For when drops are not maintaining intraocular pressure
What are the risk factors for acute angle closure
- Increasing age
- Females: males 4:1
- Family history
- Chinese and East Asian ethnic origin. Unlike open angle glaucoma it is rare in people of black ethnic origin.
- Shallow anterior chamber
What medications can precipitate angle closure
- Adrenergic medications such as noradrenalin
- Anticholinergic medications such as oxybutynin and solifenacin
- Tricyclic antidepressants such as amitriptyline, which have anticholinergic effects
What is the presentation of acute angle closure
Severely painful red eye
Blurred vision
Halos around lights
Associated headache, nausea and vomiting
What will you see on examination of a patient with acute angle closure
Red eye Teary Hazy cornea Decreased visual acuity Dilatation of the affected pupil Fixed pupil size Firm eyeball on palpation
What is the management of acute angle closure
Emergency opthalmology appointment, if waiting for an ambulance:
- Lie patient on their back without a pillow
- Give pilocarpine eye drops (2% for blue, 4% for brown eyes)
- Give acetazolamide 500 mg orally
- Given analgesia and an antiemetic if required
How does pilocarpine work
- acts on the muscarinic receptors in the sphincter muscles in the iris
- causes constriction of the pupil: miotic agent.
- ciliary muscle contraction.
- These two effects cause the pathway for the flow of aqueous humour from the ciliary body, around the iris and into the trabecular meshwork to open up
How does Acetazolamide work
carbonic anhydrase inhibitor. This reduces the production of aqueous humour.
What is laser iridotomy
- definitive treatment
- laser makes a hole in the iris to allow the aqueous humour to flow from the posterior chamber into the anterior chamber.
- This relieves pressure that was pushing the iris against the cornea and allows the humour the drain.
What is age related macular disease
- degeneration in the macular that cause a progressive deterioration in vision.
- most common cause of blindness in the UK.
- drusen seen during fundoscopy.
What are the 4 layers of the macular
- choroid layer: blood vessels that provide the blood supply to the macula.
- Bruch’s membrane.
- Retinal pigment epithelium
- photoreceptors. (top layer)
What is drusen
- yellow deposits of proteins and lipids that appear between the retinal pigment epithelium and Bruch’s membrane.
- Some drusen can be normal.
- Normal drusen are small (< 63 micrometres) and hard.
- Larger and greater numbers of drusen can be an early sign of macular degeneration.
What features are common to both wet and dry AMD
- Drusen
- Atrophy of the retinal pigment epithelium
- Degeneration of the photoreceptors
What features are common to both wet and dry AMD
- Drusen
- Atrophy of the retinal pigment epithelium
- Degeneration of the photoreceptors
What happens in Wet AMD
- development of new vessels growing from the choroid layer into the retina.
- These vessels can leak fluid or blood and cause oedema and more rapid loss of vision.
- A key chemical that stimulates the development of new vessels is vascular endothelial growth factor (VEGF)
What are the risk factors of AMD
Age Smoking White or Chinese ethnic origin Family history Cardiovascular disease
What is the presentation of AMD
- Gradual worsening central visual field loss (more acute if wet)
- Reduced visual acuity
- Crooked or wavy appearance to straight lines
What may you find on examination in a patient with AMD
- Reduced acuity using a Snellen chart
- Scotoma (a central patch of vision loss)
- Amsler grid test can be used to assess distortion of straight lines
- Fundoscopy. Drusen are the key finding.
What investigations may you complete in a patient with suspected AMD
- Acuity
- Amsler Grid
- Fundoscopy
- Slit-lamp biomicroscopic fundus examination
- Optical coherence tomography
- Fluorescein angiography
What is Fluorescein angiography
- involves giving a fluorescein contrast and photographing the retina to look in detail at the blood supply to the retina. - Shows up oedema and neovascularisation
- used second line to diagnose wet AMD if optical coherence tomography does not exclude wet AMD.
What is the management of dry AMD
- opthalmology referral
- Avoid smoking
- Control blood pressure
- Vitamin supplementation has some evidence in slowing progression
What is the management of wet AMD
- Anti-VEGF injections into the vitreous chamber of the eye
- Medications such as ranibizumab, bevacizumab and pegaptanib block VEGF and slow the development of new vessels.
- slow and even reverse the progression of the disease.
- typically need to be started within 3 months to be beneficial.
What is the management of diabetic retinopathy
- Laser photocoagulation
- Anti-VEGF medications such as ranibizumab and bevacizumab
- Vitreoretinal surgery (keyhole surgery on the eye) may be required in severe disease
What are the complications of diabetic retinopathy
- Retinal detachment
- Vitreous haemorrhage
- Rebeosis iridis (new blood vessel formation in the iris)
- Optic neuropathy
Cataracts
What is a vitreous haemorrhage
bleeding in to the vitreous humour
What is diabetic maculopathy
- Macular oedema
- Ischaemic maculopathy
What is Proliferative Diabetic Retinopathy
Neovascularisation
Vitreous haemorrhage
What may you see on severe Non-proliferative Diabetic Retinopathy
- blot haemorrhages plus microaneurysms in 4 quadrants
- venous beating in 2 quadrates
- intraretinal microvascular abnormality (IMRA) in any quadrant
What may you see on moderate Non-proliferative Diabetic Retinopathy
- microaneurysms
- blot haemorhages
- hard exudates
- cotton wool spots
- venous beading
What are the different types of classification of diabetic retinopathy
- Proliferative
- Non-proliferative: often called background or pre-proliferative retinopathy as it can develop in to proliferative retinopathy
- Diabetic maculopathy
What are the two types of classification of diabetic retinopathy
- Proliferative
- Non-proliferative: often called background or pre-proliferative retinopathy as it can develop in to proliferative retinopathy
What is neovascularisation
when growth factors are released in the retina causing the development of new blood vessels.
How do cotton wool spots form
Damage to nerve fibres in the retina due to ischaemia and infarcts cause fluffy white patches to form on the retina
How do cotton wool spots form
Damage to nerve fibres in the retina causes fluffy white patches to form on the retina
What does damage to the blood vessel walls in the retina lead to
- Microaneurysms: weakness in the wall causes small bulges.
- Venous beading: walls of the veins are no longer straight and parallel and look more like a string of beads or sausages.
What are hard exudates
yellow/white deposits of lipids in the retina
caused by damaged vessels leaking lipids into the retina.
What are hard exudates
yellow/white deposits of lipids in the retina
How does hyperglycaemia lead to diabetic retinopathy
Hyperglycaemia leads to damage to the retinal small vessels and endothelial cells. Increased vascular permeability leads to leakage from the blood vessels, blot haemorrhages and the formation of hard exudate
What is hypertensive retinopathy
- Damage to the small blood vessels in the retina relating to systemic hypertension
- Can be due to chronic hypertension or can develop quickly in response to malignant hypertension.
What signs are associated with hypertensive retinopathy
- Silver wiring or copper wiring
- Arteriovenous nipping
- Cotton wool spots
- Hard exudates
- Retinal haemorrhages
- Papilloedema
What is silver wiring/copper wiring
where the walls of the arterioles become thickened and sclerosed causing increased reflection of the light.
What is Arteriovenous nipping
the arterioles cause compression of the veins where they cross. This is again due to sclerosis and hardening of the arterioles.
What are retinal haemorrhages
caused by damaged vessels rupturing and releasing blood into the retina.
What is papilloedema
caused by ischaemia to the optic nerve resulting in optic nerve swelling (oedema) and blurring of the disc margins.
What is the management of hypertensive retinopathy
- controlling the blood pressure and other risk factors such as smoking and blood lipid levels.
What are cataracts
- lens in the eye becomes cloudy and opaque.
- this reduces visual acuity by reducing the light that enters the eye.
- Develop slowly over years
- Caution: may conceal other pathology e.g. AMD
What are cataracts
- lens in the eye becomes cloudy and opaque.
- this reduces visual acuity by reducing the light that enters the eye.
- Develop slowly over years
What are the risk factors for cataracts
- Increasing age
- Smoking
- Alcohol
- Diabetes
- Steroids
- Hypocalcaemia
What is the presentation of cataracts
- Usually asymmetrical
- Very slow reduction in vision
- Progressive blurring of vision
- Change of colour of vision with colours becoming more brown or yellow
- “Starbursts” can appear around lights, particularly at night time
What is the main sign for cataracts
- Loss of red reflex: appear grey or white
- Can be seen in congenital cataracts too
What is the management of cataracts
- If symptoms manageable, nil
- cataract surgery
What does cataract surgery entail
- drilling and breaking the lens into pieces, removing the pieces and then implanting an artificial lens into the eye.
- This is usually done as a day case under local anaesthetic. It usually gives good results.
What is Endophthalmitis
- inflammation of the inner contents of the eye, usually caused by infection.
- can be treated with intravitreal antibiotics injected into the eye.
- can lead to loss of vision and loss of the eye itself.
What is Retinitis pigmentosa
- congenital inherited condition where there is degeneration of the rods and cones in the retina
- Can cause isolated retinitis pigmentosa or systemic diseases
- Generally, rods degenerate more than cones, leading to night blindness.
- They get decreased central and peripheral vision.
What is the presentaiton of Retinitis Pigmentosa
- Night blindness is often the first symptom
- Peripheral vision is lost before the central vision
- Most symptoms start in childhood
What systemic disease are associated with retinitis Pigmentosa
Usher’s Syndrome
Bassen-Kornzweig Syndrome
Refsum’s Disease
What systemic disease are associated with retinitis Pigmentosa
Usher’s Syndrome
Bassen-Kornzweig Syndrome
Refsum’s Disease
What is Usher’s Syndrome
causes hearing loss plus retinitis pigmentosa
What is Bassen-Kornzweig Syndrome
is a disorder of fat absorption and metabolism causing progressive neurological symptoms and retinitis pigmentosa
What is Refsum’s Disease
metabolic disorder of phytanic acid causing neurological, hearing and skin symptoms and retinitis pigmentosa
What treatment may be potentially initiated by a specialist to manage retinitis pigmentosa (lacks evidence)
Vitamin and antioxidant supplements Oral acetazolamide Topical dorzolamide Steroid injections Anti-VEGF injections (gene therapy)
What treatment may be potentially initiated by a specialist to manage retinitis pigmentosa
Vitamin and antioxidant supplements Oral acetazolamide Topical dorzolamide Steroid injections Anti-VEGF injections
What is posterior vitreous detachment
- the vitreous gel comes away from the retina.
- It is very common, particularly in older patients as the vitreous body becomes less firm and less able to maintain its shape
What is posterior vitreous detachement
- the vitreous gel comes away from the retina.
- It is very common, particularly in older patients as the vitreous body becomes less firm and less able to maintain its shape
What is the presentation of posterior vitreous detachment
Asymptomatic Painless Spots of vision loss Floaters Flashing lights
What is the management of posterior vitreous detachment
- No treatment, overtime the brain adjusts
What does posterior vitreous detachment predispose you to
- retinal tears and detachment
- EXCLUDE
Causes of tunnel vision
Papilloedema glaucoma retinitis pigmentosa choroidoretinitis optic atrophy secondary to tabes dorsalis hysteria
What type of screening should be done for patients with a strong FH of glaucoma
annual screening from 40yo
