Ophthalmology: Eye Conditions 3 Flashcards
1
Q
What is the vitreous fluid/humor?
What is posterior vitreous detachment?
A
- Vitreous fluid/humor fills the vitreous chamber of the eye. It usually maintains the structure/shape of the eyeball and keeps the retina pressed against the choroid; it is made up of collagen and water.
- Posterior vitreous detachment is the separation of the vitreous membrane from the retina
2
Q
State 2 risk factors for posterior vitreous detachment- highlighting the key risk factor
A
- Increasing age (75% cases in those >65yrs): as we age, vitreous fluid becomes less viscous and hence doesn’t hold it’s shape as well; consequently, vitreous membrane is pulled away from retina
- Highly myopic (near sighted) patients: increased risk of developing it earlier in life because eye has longer axial length than normal
3
Q
Describe typical presentation of posterior vitreous detachment
A
May be asymptomatic or may have:
- Floaters (may describe as dots, strands or squiggles. Large floaters as cobweb across vision)
- Photopsia (flashing lights)
- NO PAIN
4
Q
What would you see on fundoscopy in posterior vitreous detachment?
A
Weiss ring (detachment of vitreous membrane around optic nerve forms a ring-shaped floater)
5
Q
Do patients with suspected posterior vitreous detachment need to see an ophthalmologist?
A
Yes, need to see one within 24hrs to rule out retinal tears or detachment as these can cause sight loss and require surgery to fix
6
Q
Discuss the management of posterior vitreous detachment
A
- Reassurance: symptoms will improve over time as brain adjusts & PVD on it’s own does not lead to sight loss
7
Q
What is a vitreous haemorrhage?
State some common causes
A
- Bleeding into the vitreous humour
- Common causes:
- Proliferative diabetic retinopathy (>50%)
- Posterior vitreous detachment
- Ocular trauma
8
Q
State some risk factors for vitreous haemorrhage
A
Risk factors for vitreous haemorrhage include:
- Diabetes
- Trauma
- Anticoagulants
- Coagulation disorders
- Severe short sightedness
9
Q
Discuss the presentation of vitreous haemorrhages
A
- Disruption to vision can vary
- Floaters
- Haze/red hue in vision
- Complete visual loss
- Decreased visual acuity (variable dependent on size & location of haemorrhage)
- Painless
10
Q
Discuss the management of vitreous haemorrhages
A
Management varies for individuals but some options include:
- Observation if stopped bleeding
- Treat underlying cause:
- Laser photocoagulation
- Anti-VEGF
- Vitrectomy (if not clearing after 3 months)
11
Q
State some potential complications of posterior vitreous detachment
A
Increased risk of:
- Retinal tear
- Retinal detachment
… which can both lead to vision loss
12
Q
What is retinal detachment?
What usually causes the above?
Why is it a problem?
A
- Retina separates from choroid
- Usually due to retinal tear that allows vitreous fluid to get between the retina and choroid and thus cause separation of the two layers
- Outer retina relies on choroid for it’s blood supply hence it may cause vision loss if not recognised early
13
Q
State some risk factors for retinal detachment
A
- Posterior vitreous detachment
- Diabetic retinopathy
- Trauma to the eye
- Retinal malignancy
- Older age
- Family history
- Previous surgery for cataracts
14
Q
Describe typical presentation of retinal detachment (in adults)
A
- Sudden, painless peripheral vision loss (like a shadow coming across vision)
- Floaters (pigment cells in vitreous space)
- Blurred vision
- Photopsia
- If macula affected, reduced central visual acuity
15
Q
Infants with retinal detachment often present late due to impaired ability to recognise and communicate symptoms; how may children with retinal detachment present?
A
- Squint
- White pupillary reflex (loss of red reflex)
16
Q
What might you find on examination of pt with retinal detachment?
A
- Reduced peripheral visual fields
- Reduced central vision acuity (if macula involved)
- Loss of red reflex
- Relative afferent pupillary defect (if optic nerve involved)
17
Q
Discuss the management of retinal detachment (include management of any associated retinal tears)
A
Same day (urgent) referral to ophthalmologist for assessment & management. Aim of treatment is to reattach retina and reduce any traction or pressure that might result in it detaching again.
Options for reattaching retina
- Vitrectomy: remove parts of vitreous body and replace with oil or gas
- Scleral buckling: use silicone ‘buckle’ to put pressure on sclera so that outer eye indents to force choroid inwards and into contact with detached retina
- Pneumatic retinopexy: inject gas bubble into vitreous body; gas bubble creates pressure that flattens retina against choroid
Must also treat any associated retinal tears:
- Laser therapy
- Cyrotherapy
(both create adhesions between retina and choroid)
18
Q
What is a retinal vein occlusion?
State the two types of retinal vein occlusion
A
Retinal vein occlusion is when there is impaired drainage of retinal vein(s)- usually due to a thrombus. Two types of retinal vein occlusion:
- Branch retinal vein occlusion (occurs in one of 4 retinal veins, each of which drains ¼ of retina)
- Central retinal vein occlusion (occurs in central retinal vein which the 4 retinal veins drain into- hence it drains whole of retina)
19
Q
Discuss pathophysiology of retinal vein occlusion
A
- Blockage of vein causes pooling of blood in retina
- Causes leakage of fluid and blood
- → retinal haemorrhages
- → macula oedema
- Damage to retinal tissue and loss of vision
- Increased venous pressure also decreases capillary perfusion resulting in release of VEGF which stimulates neovascularisation
20
Q
State some risk factors for retinal vein occlusion
A
- Hypertension
- Hypercholesterolaemia
- Diabetes
- Smoking
- Glaucoma
- Systemic inflammatory conditions e.g. SLE
21
Q
How does retinal vein occlusion present?
A
- Sudden, painless reduction or loss of vision (whether it is reduction or loss depends on which vein occluded. Complete loss would mean central retinal vein occlusion)
- Usually unilateral
22
Q
What would you find on fundoscopy of pts with retinal vein occlusion?
A
- Flame haemorrhages
- Blot haemorrhages
- Optic disc oedema
- Macula oedema
- Cotton wool spots
In central retinal vein occlusion “blood & thunder”
23
Q
What investigations would you do if you suspect retinal vein occlusion?
A
Investigations for risk factors
- BP: hypertension
- Glucose: diabetes
- Lipids: hypercholesterolaemia
- ESR: inflammatory disorders
- FBC: retinal vein occlusion can be presentation of leukaemia
Further ophthalmological investigations:
- OCT
- Fluorescein angiography
24
Q
Discuss the management of retinal vein occlusion
A
Same day (urgent) referral to ophthalmology for assessment & management. Management is centred around treating macular oedema and preventing complications such as neovascularisation & glaucoma. Options:
- For macular oedema:
- Intravitreal anti-VEGF therapies
- Or intravitreal steroids
- For neovascularisation:
- Pan-retinal laser photocoagulation (uses the heat from a laser to seal or destroy abnormal, leaking blood vessels in the retina)
ALSO, should manage underlying conditions/risk factors.
25
What is the main complication/thing you are worried about with retinal vein occlusions?
**Loss of vision** (can result from the development of neovascularisation, macular oedema, or macular ischaemia. The risk diminishes with time since the RVO occurred)
26
Compare the following in terms of symptoms:
* Posterior vitreous detachment
* Retinal detachment
* Vitreous haemorrhage
27
State some of the most common causes of sudden, painless loss of vision
* Ischaemic/vascular: *thrombosis, embolism, temporal arteritis (including recognised syndromes e.g. occlusion of central retinal vein and occlusion of central retinal artery)*
* Retinal detachment
* Retinal migraine
* Vitreous haemorrhage
28
What is amaurosis fugax?
* Temporary partial or complete loss of sight in one eye that is typically caused by an abrupt reduction in blood flow (ischaemia) to an eye- usually lasts few seconds to minutes
* Can be referred to as transient vision loss
* May be monocular or binocular
* Most commonly monocular due to ipsilateral carotid artery disease
29
What do pts commonly describe if there is an ischaemic/vascular aetiology to their vision loss?
“curtain coming down”
30
What might a transient loss of vision also be a form of?
May be a form of a transient ischaemic attack and if so needs treating in same way (300mg aspirin)
31
What is central retinal artery occlusion?
Blockage of central retinal artery which supplies blood to the retina
*\*branch of ophthalmic artery which is branch of internal carotid artery*
32
State some common causes of central retinal artery occlusion- highlighting the most common
* **Thromboembolism from atherosclerosis**
* Giant cell arteritis
33
* State some risk factors for central retinal artery occlusion
_Same as those for other cardiovascular disease:_
* Advancing age
* FH
* Smoking
* Alcohol
* Diabetes
* Hypertension
* Poor diet
* Inactivity
* Obesity
_Risk factors for giant cell arteritis:_
* \>50yrs
* Polymyalgia rheumatica
* Previous history
34
Describe typical presentation of central retinal artery occlusion (symptoms & signs- including fundoscopy findings)
* Sudden, painless loss of vision
* RAPD *(pupil in affected eye constricts more when light in shone in other eye as input is not being sensed by ischaemic retina in affected eye)*
* Pale retina *(due to lack of perfusion)*
* Cherry red spot *(is the macula that has a thinner surface that shows the red coloured choroid below)*
35
Discuss the management of central retinal artery occlusion
Must be referred to **ophthalmologist immediately for management.**
_Immediate management_
* **Investigate for GCA** (ESR & temporal artery biopsy); if it is GCA, treat with high dose steroids 60mg
If pt presents shortly after symptom development then there are a few things that can be tried to dislodge thrombus however none of them have strong evidence base:
* Ocular massage
* Removing fluid from anterior chamber to reduce intraocular pressure
* Inhaling carbogen (mix of 5% CO2 and 95% O2) to dilate artery
* Sublingual isosorbide dinitrate
_Further/long term management_
* Treating **reversible risk factors**
* **Secondary prevention of cardiovascular disease** (e.g. antihypertensive, statins, aspirin etc…)
36
State 1 potential complications of central retinal artery occlusion
* Partial or complete loss of sight in affected eyes
37
Diabetic retinopathy is the _____ common cause of blindness in adults aged 35-65yrs
MOST common
38
What is diabetic retinopathy?
Damage to the blood vessels in retina due to prolonged exposure to hyperglycaemia; leads to progressive deterioration in retinal health
39
Discuss the pathophysiology of diabetic retinopathy
* **Hyperglycaemia** thought to increase retinal blood flow and lead to abnormal metabolism in retinal vessel walls
* **Causes damage to endothelial cells & pericytes** *(cells that wrap around endothelial cells in capillaries)*
* Endothelial damage results in **increased vascular permeability**
* Blot haemorrhages
* Hard exudates
* Pericyte damage predisposes to **microaneurysm formation and venous beading**
* Damage to blood vessels can result in **retinal ischaemia**
* Response to this is to **release VEGF**
* Resulting in **neovascularisation**
* Damage to **nerve fibres causes cotton wool spots**
40
Discuss the classification of diabetic retinopathy
Broadly split into two categories based on fundoscopy appearance:
* **Non-proliferative** *(also referred to as pre-proliferative, background)* no new blood vessels formed
* Mild
* Moderate
* Severe
* **Proliferative:** new blood vessels developed
* **Maculopathy:** can have in non-proliferative and proliferative
41
Non-proliferative diabetic retinopathy can be split into mild, moderate and severe; state some features of each that you may see on fundoscopy
_Mild_
* Microaneurysms
_Moderate_
* Micoraneurysms
* Blot haemorrhages
* Hard exudates
* Cotton wool spots
* Venous beading
_Severe_
* Blot haemorrhages & microaneurysms in 4 quadrants
* Venous beading in at least 2 quadrants
* IRMA in at least 1 quadrant
42
What is IRMA?
* **Intraretinal microvascular abnormalities**
* **Dilated & tortuous capillaries** in retina
* Can act as shunt between arterial and venous vessels in retina
43
State some features of proliferative diabetic retinopathy on seen on fundoscopy
* Neovascularisation
* Vitreous haemorrhage
44
What might we find, on further investigations, that suggests pt has diabetic maculopathy?
Maculopathy means disease of the macula; hence, diagnosis is based on location as oppose to specific findings on fundoscopy (as in non-proliferative and proliferative)
* Macular oedema *(see on OCT, black [fluid] in macula area of retina. Hard to see on fundoscopy)*
* Ischaemic maculopathy *(use fluorescein angiogram)*
45
State some potential complications of diabetic retinopathy
* Retinal detachment
* Vitreous haemorrhage
* Rubeosis iridis
* Optic neuropathy
* Cataracts
46
What is rubeosis iridis?
Why is it a problem?
* Abnormal blood vessel formation in the iris
* Can progress to neovascular glaucoma (open or closed angle)!
47
Discuss the management of diabetic retinopathy *(think about management that applies to all pts and then stage/classification specific management)*
_All patients= optimise the following:_
* Glycaemic control
* BP
* Hyperlipidaemia
* Stop smoking
* Weight loss
_Non-proliferative retinopathy_
* Regular observation (4-6/12 FU)
* If severe, pan retinal laser photocoagulation
_Proliferative_
* Laser therapy (focal/grid or panretinal photocoagulation)
* Vitrectomy (e.g. if vitreous haemorrhage or retinal detachment)
_Maculopathy_
* Intravitreal VEGF e.g. ranibizumab, becavizumab (central involving, \>400micron)
* Laser therapy (focal if focal disease or grid if diffuse disease)
48
There are two types of laser therapy that can be used in diabetic retinopathy; briefly describe each and state when may be used
* Focal: identify and target specific point of leakage with laser
* Grid:
* Pan-retinal: makes lots of burns in periphery of retina
49
What is the purpose of pan-retinal photocoagulation/how does it work in diabetic retinopathy?
Laser directed at many sites in periphery of retina; destroys some of the photoreceptors, reduces the oxygen consumption of the retina and re-establishes a balance between the oxygen supply and demand. Aim is to prevent deterioration/worsening of disease, not restore sight.
50
What is hypertensive retinopathy?
Systemic hypertension causes damage to small blood vessels in retina; may be develop progressively over time due to chronic hypertension in develop quickly in response to malignant hypertension
51
Hypertensive retinopathy is usually asymptomatic and diagnosed on routine screening; true or false?
True
52
What classification is used to stage hypertensive retinopathy?
State characteristic features present in stage 1, 2, 3 and 4 of hypertensive retinopathy
_Keith-Wagener-Barker Classification_
* Stage 1: slight arteriole narrowing, silver wiring
* Stage 2: focal narrowing of arterioles, arteriovenous nipping
* Stage 3: cotton wool spots, hard exudates, retinal haemorrhages
* Stage 4: Papilloedema
53
Explain why you get each of the following findings on fundoscopy of pt with hypertensive retinopathy:
* Silver wiring/copper wiring
* AV clipping
* Cotton wool spots
* Hard exudates
* Retinal haemorrhages
* Papilloedema
* **Silver wiring/copper wiring:** walls of arterioles are thickened & sclerosed so there is increased reflection of light
* **AV clipping:** arterioles compress veins where they cross (due to sclerosis of arterioles)
* **Cotton wool spots:** retinal ischaemia and infarction causing damage to nerve fibres (ischaemia of neuroretinal layer)
* **Hard exudates:** damage vessels leaking lipids
* **Retinal haemorrhages:** damaged vessels leaking blood into retina
* **Papilloedema:** ischaemia to optic nerve resulting in optic nerve swelling (oedema) and blurring of disc margins
54
Discuss the management of hypertensive retinopathy
Management centred around controlling BP and other cardiovascular disease risk factor e.g. smoking, lipids etc…
55
What is retinitis pigmentosa?
**Congenital, inherited** condition in which there is **degeneration of the rods and cones** in the retina (in most cases the rods degenerate more than the cones)
56
There are many different genetic causes of retinitis pigmentosa; true or false?
True
* Some causes result in isolated retinitis pigmentosa, others result in systemic diseases associated with the condition
* Age of presentation varies
* Prognosis varies
57
Describe typical presentation of retinitis pigmentosa (include symptoms and signs- including fundoscopy findings)
_Symptoms_ *_(explanation for order of symptoms is that rods tend to degenerate more than cones)_*
* Night blindness (often FIRST symptom)
* Peripheral vision loss
* … followed by central vision loss
_Signs_
* Bone spicule pigmentation that is most concentrated around mid-peripheral retina
* May be associated narrowing of arterioles
* May be associated waxy or pale appearance to optic disc
58
Discuss the management of retinitis pigmentosa
_General management:_
* Referral to ophthalmologist
* Vision aids
* Sunglasses (protect retina from accelerated damage)
* Driving limitations & informing DVLA
* Genetic counselling
* Regular follow up (assess vision and for other reversible conditions that may make symptoms worse)
_Treatments to slow disease progression (note: limited evidence)_
* **Gene therapy (approved by NICE)**
* Others:
* Vitamin & antioxidant supplements
* Oral acetazolamide
* Topical dorzolamide
* Steroid injections
* Anti-VEGF
59
What is herpes zoster ophthalmicus?
Reactivation of varicella-zoster virus in area supplied by ophthalmic division of trigeminal nerve (~10% of shingles)
*\*Basically shingles affecting the ophthalmic division of trigeminal nerve*
60
Describe typical presentation of herpes zoster ophthalmicus
* **Vesicular rash around eye** (may or may not involve the eye itself)
* **Hutchinson's sign** (rash on tip or side of nose; indicates nasociliary involvement and is strong risk factor for ocular involvement)
61
Discuss the management of herpes zoster ophthalmicus
NOTE: any ocular involvement requires urgent ophthalmology review
* **PO antiviral (e.g. Aciclovir)**
* Ideally start in first 72hrs
* IV if very severe or immunocompromised
* **Topical steroids (eye drops)** can be used if there is secondary inflammation of the eye
*\*Don't treat with topical antivirals*
62
State some potential complications of herpes zoster ophthalmicus
* Ocular
* Conjunctivitis
* Keratitis
* Episcleritis
* Anterior uveitis
* Ptosis
* Post-herpetic neuralgia
63
Which pts, with thyroid disease, may experience thyroid eye disease?
* Common in Graves' disease (25-50%)
* Hypothyroid
* Hashimoto's thyroiditis
* Euthyroid
64
Discuss who is more likely to get thyroid eye disease, men or women?
* Women more likely to have it
* However, severe cases of thyroid eye disease occur more often in men than in women
65
Describe the pathophysiology of thyroid eye disease
* **TSH receptors** are expressed on fibroblasts of retro-orbital and dermal tissues
* TSH autoantibodies bind to these receptors
* Causes immune response in the eye
* T cells produce cytokines and **stimulate fibroblasts to secrete GA**Gs (which increases osmotic load and so interstitial fluid content) and **differentiate into adipocytes**
* Increased interstitial fluid content along with infiltration of inflammatory cells causes **swelling of orbital tissues**
* **IGF-1 receptor** is also thought to play an important role in thyroid eye disease as there is aberrant expression of IGF-1 receptors on fibroblasts in pts with thyroid eye disease; thought that this promotes T cell recruitment
*IGF-1= insulin like growth factor 1*
66
What is the most important modifiable risk factor for thyroid eye disease?
Smoking
67
Describe typical presentation of thyroid eye disease (symptoms & signs)
_Symptoms_
* Gritty/watery eyes
* Puffy lids
* Bulging eyes
* Diplopia
* Ocular pain
_Signs_
* Proptosis
* Lid retraction *(with temporal flare and scleral show)*
* Lid lag on downgaze *(von Graefe sign)*
* Decreased retropulsion
68
Discuss the management of thyroid eye disease
* General
* Optimise **endocrine control**
* **Stop smoking**
* **Selenium** supplements
* **Topical lubricants**
* To treat inflammation
* **Steroids** +/- immunsparing agents
* **Immunosuppressive agents**
* AVOID RADIOACTIVE IODINE
* **Surgery** to decompress, correct strabismus, correct eyelids
69
State some signs/symptoms, in patients with thyroid eye disease, that indicate referral for urgent review by ophthalmologist
For patients with established thyroid eye disease the following symptoms/signs should indicate the need for urgent review by an ophthalmologist (see EUGOGO guidelines):
* unexplained deterioration in vision
* awareness of change in intensity or quality of colour vision in one or both eyes
* history of eye suddenly 'popping out' (globe subluxation)
* obvious corneal opacity
* cornea still visible when the eyelids are closed
* disc swelling
