Ophthalmology Flashcards
What are the paths of the neurovasculature through the orbital cavity?
Optic canal
- Optic nerve
- Ophthalmic artery
Superior orbital fissure
- Oculomotor nerve
- Trochlear nerve
- Abducens nerve
- Ophthalmic nerve (Va)
- Superior ophthalmic vein
Inferior orbital fissure
- Infraorbital nerve (branch of maxillary CN Vb)
- Inferior ophthalmic vein
- Sympathetic nerves
What is the vasculature of the eye?
Ophthalmic artery from the internal carotid supplies the eyeball.
The central retinal branch of the ophthalmic artery supplies the retina, occlusion will therefore cause blindness.
Drained by the superior and inferior ophthalmic veins, into the cavernous sinus.
What are the layers of the eyelid?
Skin and subcutaneous tissue (most superficial)
Orbicularis oculi
Orbital septum= tough sheet of fibrous tissue, blends with tarsal plates. Separates pre and post septal space.
Tarsal plates
Inferior tarsus- contains Meibomian glands slows evaporation of the eye’s tear film & prevents eyelids sticking together when closed
LPS
Superior tarsal muscle
Both open eyelids
Conjunctiva- contains goblet cells producing mucous layer of tear film.
What are the contents of the orbital cavity?
Eyeball Peri-ocular fat Extra-ocular muscles Nerves and BV Lacrimal apparatus
What are the actions of the extraocular muscles?
LPS- Elevates upper eyelid
SR- Elevates + adducts + medial rotation
IR- Depresses + adducts + lateral rotation
MR- Adducts
LR- Abducts Abducens nerve
SO- Depresses + abducts + medial rotation
Trochlear nerve
IO- Elevates + abducts + lateral rotation
Where is the visual cortex located?
Calcarine cortex of the occipital lobe.
What is the purpose of aqueous humour?
Secreted by the ciliary body from the anterior chamber.
Exerts a pressure to allow the eyeball to maintain its shape.
Provide nutrients and oxygen for ocular tissue including the avascular lens.
Removal of metabolic by-products from intraocular cells
Facilitating passage of light from intraocular cells
How is aqueous humour drained?
Through the iridocorneal angle (between cornea and iris) via the trabecular meshwork.
Then into the canal of Schlemm.
Any blockage of this pathway will increase IOP and can lead to glaucoma.
NB- Age related degeneration of the trabecular meshwork will lead to chronic open angle glaucoma.
What is the accommodation reflex?
Allows better focusing of images at closer distance.
Convergence
Change in lens thickness
Pupillary constriction
What is the uvea?
Most vascularised part of the body, found in the eye.
Pigmented layer of the eye consisting of three continuous segments- iris (anterior), ciliary body (intermediate) and choroid (posterior).
It is prone to infection- uveitis.
How do you classify uveitis?
- Establish the location- which part of the uvea is affected?
- Need to establish then whether the cause is infectious or non infectious.
- Are there any keratic (cornea) precipitates present? Either granulomatous (e.g. in TB or sarcoidosis) or non granulomatous (appear more discrete).
- Chronicity- is it acute? Recurrent (acute but >3 months apart) or chronic (<3 months apart)?
Examples of classified uveitis:
Idiopathic acute anterior uveitis with granulomatous KP
TB associated acute anterior uveitis with granulomatous KP
What are some causes of uveitis?
Mainly idiopathic.
Auto-immune: Sarcoidosis, SLE, MS, Behcets, Vogt koyangi Harada
Infectious- Viral- HIV, CMV Fungal- Candida Protozoa- Toxoplasma Bacteria- Syphyllis, TB
Drug induced- Bisphosphonates, rifabutin, antivirals
Traumatic- sympathetic ophthalmia
Sometimes although classified as idiopathic, could be due to sarcoidosis which has not manifested yet elsewhere in the body. Need a biopsy to diagnose sarcoidosis and so if early presentation in the eye, lung biopsy would be -ve, we can’t do an eye biopsy so if we still suspect sarcoidosis we treat it as sarcoidosis although it is classified as idiopathic.
What symptoms does a Px with anterior uveitis present with?
Blurring of vision (due to cell and protein leaking)
Pain
Photophobia
Redness of eye
The symptoms present are due to inflammation of the iris, where blood vessels leak out WBC into the anterior chamber. Can see these cells floating when shining a white light into the eye, in a dark room. I.e similar to the beam of light from a projector where you can see dust particles.
What signs does a Px with anterior uveitis have?
Keratic precipitates Cells in anterior chamber Fibrillin in anterior chamber Flare in anterior chamber (flare refers the beam of light you are shining through- which otherwise you wouldn’t see) Cells in vitreous Choroiditis lesions Macular oedema Hypopyan- fibrin deposition
The iris rests on the lens, so if inflamed the iris will scar and the posterior surface will stick to the lens- posterior synechiae. (Same can happen on anterior with the cornea)
If you don’t want this to stick you pull the iris away from the lens by dilating it, need to do quick since these strong adhesions are hard to overcome.
What causes keratic precipitates?
Macrophages and white cells try moving towards cooler temperatures, therefore move to the front of the eye.
Once inflammation subsides they are usually absorbed.
What are the differentials of anterior uveitis?
Acute glaucoma
Keratitis
Scleritis
Ocular trauma
What is intermediate uveitis?
Inflammation of ciliary body predominately- could still be inflammation in anterior or posterior aspect also.
What symptoms would a Px with intermediate/posterior uveitis present with?
Floaters- ciliary body inflamed-leaks WBC into the vitreous
Blurring of vision- Due to floaters or macular oedema due to inflammation.
IU treatment
Need oral steroids or systemic anti inflammatory
What signs would a Px with intermediate/posterior uveitis have?
Cells in vitreous Snow balls (clumps of WBC in vitreous) often cause the symptom of floaters. Snow banking (snowballs rest on macula) Sheathing of BV Macular oedema
What is posterior uveitis?
Inflammation of the choroid predominantly.
What symptoms would a Px with posterior uveitis present with?
Blurred vision
Could be more drastic reduction in vision- since retina lies in front on the choroid therefore inflammation of the choroid will lead to inflammation of the retina.
NB toxoplasma treated with anti toxoplasma drugs then infalmmation.
TB uveitis need to be treated with anti-TB then steroids
CMV retinitis- Normal population have CMV but become infective when immunity is lower I.e. HIV, chemotherapy, steroids.
Sarcoidosis
How would you investigate uveitis?
First differentiate if infectious or non infectious.
FBC
U+Es
LFTs
Q Gold (+ve- have been exposed to tubercular antigen- treat with a 3 month course of anti-TB since it’s an immunological repsonse to the antigen rather than infectious response)
Treponemal antibody (syphyllis- can present in any way therefore test important for diagnosis)
Which special tests can you conduct to determine the cause of uveitis?
Sarcoidosis- XR + biopsy lung SLE- anti dsDNA MS- MRI. First presenting feature of MS can be optic neuritis or intermediate uveitis. Behcets- HLA B51 Vogt Koyanagi Harada- HLA DR4/B27
Viral- Take sample for PCR
Fungal- Hx is useful and snowballs but should sample PCR.
Protozoa- IgG, IgM
Bacteria- For TB- IGRA Montoux, CXR
For syphyllis- treponemal antibodies.
How would you treat anterior uveitis?
Topical steroids/subconjucntivals
Cycloplegics - relax ciliary body (reduce pain) and cause dilatation of pupil (stops posterior synechiae from forming).
Rarely infective therefore can start treatment whilst awaiting results.
Why would we use steroids to treat uveitis?
What are the common local and systemic side effects?
Put steroid in the eyes to reduce the inflammation and reduce any systemic side effects.
Local:
Raised pressure in the eye which can lead to glaucoma- therefore give drops to prevent this.
Cataracts- surgery to fix this- reluctant to do this on younger Px as they lose the accommodation reflex with an artificial lens.
Systemic:
Osteoporosis Indigestion- gastric ulcers which may bleeds therefore give PPI. Immunosuppression Hair loss Hyperglycaemia Weight gain High dose can lead to avascular necrosis of femur Anxiety HTN Cushingoid features
Immunosuppressants take time to work so use steroids in the mean time
These have less side effects than steroids
What are the complications of anterior uveitis?
Posterior synechiae
Pupillary membrane
Ocular HTN/glaucoma- three causes- (1) Steroid drops (2) Build up of cell debris from inflamed BV can block the trabecular mesh work and so the ‘draining system’ (3) Increase in pressure can cause the anterior surface of the iris to stick to the cornea causing peripheral anterior synechiae- blocking the angle and trabecular meshwork.
Hypotony- if ciliary body not working properly due to inflammation this causes a reduced pressure, as it can’t produce the aqueous humour.
Cataract
Cystoid macular oedema
Posterior subcapsular cataracts- breadcrumb appearance from steroids
More worried about a reduced pressure since can’t do much to fix it, OST you can do is give max steroid drops to reduce inflammation and encourage ciliary body to work.
What is sympathetic opthalmia?
How does it occur?
How would you treat it?
Usually a penetrating injury of one eye where the iris pigment leaks and mixes with the blood.
The body develops an immunity against the iris pigment, and so will attack the other eye since it also contains the iris pigment. The person is at risk of losing the sight in the non injured eye.
Treat with steroids and immunosuppressants.
The bulk of the antigens are in the injured eye and so although the disease will not be cured, the symptoms will be reduced if this eye is removed.
What are the complications of intermediate/posterior uveitis?
Cataracts
Floaters
Swelling of macular- cystoid macular oedema
How would you treat intermediate/posterior uveitis?
Local-
Periocular steroids
Intravitreal steroid implants
Systemic-
Pulse therapy
Oral steroids
Immunosuppressants instead of long term steroid use
Antibiotic/antifungal/antiviral if infectious cause.
NB toxoplasma treated with anti toxoplasma drugs first then treat the inflammation.
TB uveitis need to be treated with anti-TB first then steroids
CMV retinitis- Normal population have CMV but become infective when immunity is lower I.e. HIV, chemotherapy, steroids.
What are some examples of immunotherapy used to treat uveitis?
Calcineurin inhibitiors- tacrolimus, cyclosporin. SE- BP, deranged renal function.
Cytotoxic immunosuppressants- methotrexate, azathioprine. SE- Bone marrow suppression, lymphoma.
Biologics- Infliximab, rituximab. SE- Infections, autoimmune like syndromes.
Which structures lie behind the orbit?
The internal carotid.
If a person was stabbed in the eye don’t remove the apparatus.
What is Neurofibromatosis type 1?
Born without the greater wing of the sphenoid.
Brain bulges out through this area.
Pulsatile proptosis
What is glaucoma?
What are some types of glaucoma?
Group of conditions characterised by progressive optic neuropathy with corresponding visual field defects.
With/without raised IOP.
Types include: Primary open-angle glaucoma Angle closure glaucoma Secondary glaucoma (due to uveitis, trauma etc) Congenital glaucoma
How does glaucoma affect vision?
Main cause of irreversible blindness worldwide.
Damage to optic nerve affects peripheral vision first then total sight loss (Tunnel vision) then end stage complete VF loss.
Night vision worsens.
In the early stages (before tunnel vision) the pupil responses are normal.
How does tunnel vision manifest in a Px life?
Falling over
Bumping into things
Use their head more to see things around
Night vision becomes worse
What is the pathophysiology in glaucoma?
(1)Increase in IOP-
When we measure pressure we measure the anterior chamber pressure. The ciliary body secretes aqueous humour which provides nutrition for the cornea and removes waste/toxins.
This drains from the trabecular meshwork. Problem in the draining system will increase the pressure.
(2) Poor blood/O2 supply to the nerve head therefore nerve fibres gradually die. This gives you the optic neuropathy and VF defects, which defines glaucoma. (Nerve fibres die usually as you grow older but higher with glaucoma)
NB- Loss of VF demonstrated by cupping. As nerve fibres die, the C:D increases and the BV don’t have much support so use the cup as their support.
What are the types of glaucoma?
Open or closed angle glaucoma. Each further divided into primary and secondary.
Open angle (More Common)- The angle between the iris and cornea remains wide open, slow blockage of trabecular meshwork over time. Closed angle- Sudden block in trabecular meshwork, decreased size of angle between iris and cornea, sudden increase in IOP.
What are some risk factors for open angle glaucoma?
Raised IOP Increasing age African, Hispanic, Asian FHx Myopia Diabetes, heart disease, HTN
What happens in open angle glaucoma?
Gradual increase in resistance through the trabecular meshwork
à difficult for aqueous humour to flow through the meshwork to exit the eye, hence pressure slowly builds up within the eye
Increased pressure in the eye causes cupping of the optic disc – normally the optic cup is less than half the size of the optic disc; in increased intraocular pressure the indent is wider- cupping of the optic disc occurs
How does open angle glaucoma present?
How is it diagnosed?
Largely asymptomatic
Visual loss may occur but central vision is preserved until later in disease
Diagnosis via routine ophthalmic examination at optometrists
GPs may suspect if they visualise cupped discs during ophthalmoscopy
Diagnosis-
- Ophthalmoscopy- cupped disc
- Visual fields
- Intraocular pressure- may or may not be elevated
How is open angle glaucoma managed?
First line- Prostaglandin analogue eye drop i.e. lantanoprost
Second line- beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop
More advanced consider surgery/laser
What are the risk factors for closed angle glaucoma?
Raised IOP Age Far East ethnicity/south East Asian FHx Hypermetropia Adrenergic medications Anticholinergic medications Tricyclic antidepressants eg amitriptyline- anticholinergic effects
How does acute closed angle glaucoma occur?
The iris bulges forward and seals off the trabecular meshwork from the anterior chamber
This prevents aqueous humour from being able to drain away
This results in continual build up of pressure in the eye, esp in the posterior chamber, which causes pressure behind the iris and worsens the closure of the angle
OPHTHALMIC EMERGENCY!
Can lead to permanent vision loss
How does acute closed angle glaucoma present?
Appear generally unwell in themselves Acute onset Red eye Blurred vision Halos around lights Associated headache N&V
O/E- red eye, teary, hazy cornea, decreased VA, dilatation of affected pupil, fixed pupil size, firm eyeball on palpation
How is acute closed angle glaucoma managed?
Immediately admit- if there is a delay to admission do the following
- Lie pt on their back w/o pillow
- Give pilocarpine eyedrops
- Give acetazolamide 500mg orally
- Give analgesia and anti-emetic if required
In secondary care, various medical options to reduce IOP-
- Pilocarpine
- Oral or IV acetazolamide
- Hyperosmotic agents eg glycerol or mannitol to increase osmotic gradient between the blood and fluid in the eye
- Timolol- BB- reduces production of aqueous humour
- Dorzolamide- CA inhibitor- reduced production of aqueous humour
- Brimonidine- sympathomimetic- reduces production of aqueous humour & increased uveoscleral outflow
Definitive treatment-
-Laser iridotomy- makes hole in iris to allow aqueous humour to flow from posterior chamber into anterior chamber, relieving pressure that was pushing the iris against the cornea, allows fluid to drain
What are the risk factors for other forms of glaucoma?
Raised IOP Trauma Topical steroids Ocular inflammation Surgical/iatrogenic
What is the MOA of pilocarpine in glaucoma?
Acts on muscarinic receptors in sphincter muscles in iris and causes constriction of pupil
Therefore it is a miotic agent
Also causes ciliary muscle contraction
These 2 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
What is normal IOP range?
How do you measure IOP?
10-21mmHg
Goldmann Applanation Tonometry (GAT)- gold standard test
Special device mounted on slit lamp, makes contact with cornea and applies different pressures to the front of the cornea to get an accurate measurement
Non-contact tonometry- used by opticians
Shooting a puff of air at the cornea and measuring the corneal response to the air, less accurate, but gives helpful estimate for general screening purposes
Is there any screening for glaucoma?
No
But optometrist should examine;
- Older age- >60 every 2 years, >70 every year (free through NHS)
- FHx of glaucoma- people >40 with first-degree relative with open angle glaucoma have eye test annually (free through NHS)
- People >40 of black African family origin- annual eye test (not through NHS)
How is glaucoma treated?
Incurable
Can aim to slow down the progression
Aim to reduce IOP, even normal tension glaucoma.
Can treat through medical therapy, surgery or laser treatment.
Medical therapy- B blockers Timalol.
Ocular surgeries
Lasers
How would you treat glaucoma medically?
- Use Beta-blocker like Timolol
- Mitotics like pilocarpine in angle closed glaucoma will pull the iris away from the trabecular meshwork to improve drainage of aqueous humour.
- Prostaglandin analogue like Xalatan will reduce production of aqueous humour and help with drainage; only take one a day.
- Alpha adrenergics like Alphagan will reduce production of aqueous humour.
- Carbonic anhydrase inhibitors
Adverse reaction to meds, eye drops. Stop the drops and find alternative.
How would you treat glaucoma with a laser?
Trabeculoplasty- Increases outflow of aqueous by encouraging pumping of trabecular.
-Cyclodiode- Destroys parts of the ciliary body. Used only to provide comfort in the blind eye by reducing IOP. Don’t use in healthy eye as can cause vision loss.
Goniotomy- Used in children
Peripheral Laser Iridotomy- Used in closed angle
How would you treat glaucoma surgically?
What are the associated complications?
Trabeculectomy- Making a different tract for the humour to drain by cutting through the eye. Under the top lid they’ll have a ‘bleb’- Px won’t notice.
Don’t use in young Px or uveitis since can scar easily and block the new channel.
Iritis
Blelbitis
Sudden increase/ decrease in IOP.
What are the signs and symptoms of acute angle closure glaucoma?
-Red painful eye
-N+V (may be there first)
-Blurred vision due to cornea hazy
-Halo eyes (esp in subacute closed angle glaucoma where the angle opens and close intermittently)
-Corneal Oedema- blue haze around
-Fixed and oval pupil
Ciliary injection
How is acute angle closure glaucoma treated?
- Give intraocular injections (subconjunctival) of acetozolamide- for quick reduction in IOP.
- Keep them hydrated and check IOP in 30mins then again, should reduce pressure within 1hr.
- Cornea should become clearer, now able to examine the eye.
- Adjunct topical therapy
-Then laser peripheral iridotomy in both eyes, creates a hole in the eye to allow aqueous humour drainage.
How do you take a Hx of poor vision?
Onset?
Distance/near?
Do you wear glasses?
When did you have an eye test last?
Optical components
Cornea fixed at ~40 diopter
Lens (variable) ~20 dioptres
Axial length ~23mm (distance from cornea to retina)
What is refractive error?
What causes refractive error?
Deficiency in refraction leading to blurred vision.
Either due to physiological causes
-Normal cornea but anomalous axial length. (Most common cause in people who wear glasses)
-Anomalous cornea but normal axial length.
Or
Pathological including corneal transplant, rubbing eyes, as result of corneal ulcer etc.
What are the types of refractive error?
Myopia either normal cornea but longer axial length (common) or high power cornea but normal axial length.
Hypermetropia- opposite to myopia.
Astigmatism- rugby ball cornea, have two curves in the cornea 90 degrees to each other resulting in blurred vision. Each curve produces its own image. Usually have in both eyes, won’t know unless Px is assessed.
Acquired astigmatism I.e. in corneal transplant.
What is presbyopia?
Natural decline in accommodation reflex, due to thickening and reduced elasticity of the lens.
Need for reading glasses
What are the RF for diabetic retinopathy?
Duration of diabetes Poor glycaemic control Hypertension Pregnancy Smoking Obesity Nephropathy
Is there any screening for diabetic retinopathy?
> 12yrs with diabetes gets annual screening.
What is the pathophysiology behind diabetic retinopathy?
Two mechanisms:
Leakage: Hyperglycaemia leads to loss of pericytes. Some exist in the capillary support system and so can lead to microaneurysm formation- early sign of diabetic retinopathy.
Occlusion of capillaries: Basement membrane thickens and endothelial cells undergo apoptosis due to hyperglycaemia. This, along with loss of pericytes and increased platelet aggregation leads to occlusion and ischaemia.
Retinal hypoxia upregulates VEGF.
What do microaneurysms/leakages cause?
What do occluded capillaries cause?
Microaneurysms/leakages: Lipid exudates, oedema, haemorrhages.
Occlusion of capillaries- ischaemia which can cause new vessel formation (not good as can rupture), irregular retinal veins/venous bleeding, cotton wool spots, intraretinal microvascular abnormalities (IRMA- valved branches of vessels which aim to perfuse areas of nil perfusion).
IRMA are patent and do not leak whereas neovascular vessels are leaky.
How is diabetic retinopathy classified?
Falls into either diabetic retinopathy:
Background diabetic retinopathy
Pre proliferative
Proliferative
(Will progress to the next stage if poor glycaemic control)
or
Diabetic maculopathy: Focal macular oedema Diffuse macular oedema Ischaemic maculopathy Clinically significant macular oedema (CSMO)
All changes are seen and diagnosed when observed via a slit lamp.
What are the signs of background diabetic retinopathy?
How is it managed?
Microaneurysm- saccular aneurysm
Dot and blot haemorrhages (retinal haemorrhages)
Hard exudates- lipid deposits due to leakage
Cotton wool spots (ischaemia of the nerve fibre layer)
Manage- Regular monitoring by an ophthalmologist.
What are the signs of preproliferave diabetic retinopathy?
How is it managed?
Progression from BR if poor glycaemic control, leading to ischaemia.
Leads to:
IRMA
Venous loop/bleeding
Cluster of large blot haemorrhages
Multiple cotton wool spots- in > 2-3 quadrants
Manage by follow up in 4 months.
What are the signs of proliferative retinopathy?
How is it managed?
This is a more serious form of retinopathy. As a result of progression from preproliferative if poor glycaemic control and/or other vascular problems present.
New vessels form either on the disc (NVD) or elsewhere (NVE).
May have pre-retinal haemorrhages.
Advance disease may have retinal detachment.
Manage with panretinal photocoagulation treatment within 2 weeks.
What is diabetic maculopathy?
The macula provides us with our central vision.
In diabetic maculopathy, the macula sustains damage, often from diabetic macula oedema- BV next to macula leak protein/fluid.
If this causes retina to harden or exudates become large next to the fovea this is termed CSMO.
What is focal macular oedema?
How is it managed?
Focal
Well-circumscribed areas of leakage, with oedema.
Full/partial rings of exudates often surrounding microaneurysm
Treat with focal laser- takes 3 months to take effect.
What is diffuse macular oedema?
How is it treated?
Diffuse retinal thickness with cystoid oedema (diffuse swelling)
Treat with grid laser.
What is ischaemic maculopathy?
How is it managed?
Reduced visual acuity
Normal clinical appearance
Macular ischaemia on fundus fluorescent angiogram.
Treat through observation
What is clinically significant macular oedema (CSMO)?
How is it treated?
Retinal thickening at or within 500 microns of the centre of the macula.
Hard exudates at or within 500 microns of the centre of the macula if associated with adjacent retinal thickening
Retinal thickness of >1disc area, any part of which is within 1DD of the centre of the macula.
Treat with Anti-VEGF
What is mixed maculopathy?
Combination of diffuse and ischaemic maculopathy.
What is central involving maculopathy?
How would you treat it?
Thickening involving the fovea centre >400 micron and visual acuity 6/9
Treatment: Anti VEGF therapies,
IV Iluvien (implants) for persistent DMO which is not cured by Anti-VEGF.
What are some complications of diabetic retinopathy?
Maculopathy is the most common cause of blindness in diabetes. T1DM is more likely to present with proliferative change. T2DM is more likely to present with maculopathy.
Common complications-
- Retinopathy.
- Iridopathy (ischaemic changes of iris- minor iris transillumination defects).
- Unstable refraction.
- Orbital infection
- Ocular ischaemic syndrome
Less common include recurrent stye, ocular nerve palsies etc.
How would you manage diabetic retinopathies primarily? (Prevention>Cure)
- Good glycaemic control
- BP control
- Reduce cholesterol
- Stop smoking
- Weight loss
- Exercise
Give an overview of management of the different diabetic retinopathy types.
- Background: Annual screening , Systemic disease with 9-12 months hospital FU.
- Pre Proliferative: 4-6/12 FU
- Proliferative/Active : Pan Retinal Photocoagulation(PRP) within 2/52
- Proliferative- once stable: 4-6/12 FU
- Proliferative with DMO: Macular laser to treat maculopathy first- otherwise can lose vision then PRP.
Give an overview of management of the different types of diabetic maculopathy.
- Focal: Focal laser, FU 3-4/12
- Diffuse: Grid laser, FU 3-4/12
- Central involving: > 400 micron Anti VEGF
- Ischaemic : observe
- Persistent maculopathy: IV fluocinolone (Iluvein)
What is a vitreous haemorrhage and how would you treat it?
What is rubeosis and how would you treat it?
VH- Bleeding of normal, diseased or new BV into the vitreous humour leading to sudden onset painless vision loss.
PRP same day or 2/52 later- until vision is cleared.
If persistent: vitrectomy+ endolaser+ anti VEGF.
R- Severe ischaemia leads to neovascularisation; where new vessels can grow over the iris- appears red and if trabecular meshwork is blocked on its course then can cause glaucoma.
Urgent PRP
Rubeotic glaucoma: PRP/ANTI VEGF,IOP reduction, Cyclodiode
If causes VH- VITI+ Endolaser
How would you take a Hx of Red Eye?
Vision loss- corenal ulceration, glacuma, iritis Pain- amount of pain; severe- scleritis, minimal- conjunctivitis Discharge- can indicate bacterial Onset (sudden/gradual) Duration Other Symptoms? Itching? Grittiness?
How would you examine a red eye?
- Snellen chart- Even if in A&E; need to assess VA
- Ophthalmoscope (blue light to examine the anterior chamber)
- Magnifying Aid
- Fluorescein drops to look for corneal abrasions- will pass over normal cornea but will get ‘stuck’ at defects
- Use slit lamps
What is bacterial conjunctivitis?
How is it managed?
Mild discomfort
Purulent discharge
Starts off with one eye so ask in the Hx.
Good VA
Manage by taking a swab and treat with chloramphenicol (ointment/eyedrops) QDS for 1 wk.
What is viral conjunctivitis?
How is it managed?
Gritty/mild discomfort Associated cold/cough Watery discharge Duration of several weeks Corneal involvement can be very painful Diffuse bilateral red eye Preauricular LN sometimes
Manage- Self limiting
Can take a viral swab and treat with lubricants, Abx to avoid secondary bacterial infection.
Steroid eye drops if cornea involved.
Bilateral redness
What is Chlamydial conjunctivitis?
How is it managed?
Mucopurulent discharge
More chronic- lasting weeks
Associated STI symptoms
O/E conjunctival injection, follicles (transparent collection of lymphocytes)
Manage- With chlamydial swab, referral to GUM, topical Abx and systemic azithromycin/tetracycline.
What is allergic conjunctivitis?
How is it managed?
Hx of atopy, itching and redness
Diffuse injection
Chemosis (swollen conjunctivae)
Papillae- oedema in conjunctiva under the eyelid (cobblestone like)
Manage- Topical/oral antihistamines. If severe then topical steroids.
What is ophthalmia neonatrum?
How is it managed?
Conjunctivitis of <1 month old.
Gonorrhoeal/chlamydial- passed through the delivery and can result in corneal disease/blindness.
Manage- Need urgent viral/bacterial/chlamydial swabs
Treat with topical Abx drops, admit under paediatrics and may require systemic treatment-depending on the cause.
What is episcleritis?
How is it managed?
Localised area of inflammation of episclera Acute onset Discharge Area of irritation Sector of redness Minimal discomfort Bright red eye but no associated pain Foreign body sensation Watering eye Associated with IBD and RA
Usually self limiting- resolves within 7-10 days, can prescribe lubricant drops for comfort or NSAIDs.
If recurrent then consider inflammatory screen.
What is scleritis?
How is it managed?
Inflammation of the sclera. Very painful Reduced VA Photophobia Global tenderness on palpation Diffuse redness Px may wake up with it, unable to move the eye.
Associated with: SLE RA IBD Sarcoidosis Granulomatosis with polyangiitis
Manage- Need immediate referral. Inflammatory screen looking for RA, Wegners, sarcoidosis etc.
Treat with NSAIDs, oral prednisolone or immunosuppressants if have a systemic disease.
What is keratitis?
What are the causes?
What is the most common type?
Inflammation of the cornea
Causes: Viral- HPV Bacterial- Staph, pseudomonas Fungal infection- Candida, aspergillus Contact lens acute red eye (CLARE)
Common type is Herpes simplex keratitis (HSV).
What are the types of corneal ulcers?
Bacterial
Viral- Herpes Simplex Keraitis, Herpes Zoster Ophthalmicus, Adenovirus
Other infections including fungal, acanthamoeba
