Ophthalmology: Eye Conditions 3 Flashcards
What is the vitreous fluid/humor?
What is posterior vitreous detachment?
- 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
State 2 risk factors for posterior vitreous detachment- highlighting the key risk factor
- 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
Describe typical presentation of posterior vitreous detachment
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
What would you see on fundoscopy in posterior vitreous detachment?
Weiss ring (detachment of vitreous membrane around optic nerve forms a ring-shaped floater)
Do patients with suspected posterior vitreous detachment need to see an ophthalmologist?
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
Discuss the management of posterior vitreous detachment
- Reassurance: symptoms will improve over time as brain adjusts & PVD on it’s own does not lead to sight loss
What is a vitreous haemorrhage?
State some common causes
- Bleeding into the vitreous humour
- Common causes:
- Proliferative diabetic retinopathy (>50%)
- Posterior vitreous detachment
- Ocular trauma
State some risk factors for vitreous haemorrhage
Risk factors for vitreous haemorrhage include:
- Diabetes
- Trauma
- Anticoagulants
- Coagulation disorders
- Severe short sightedness
Discuss the presentation of vitreous haemorrhages
- 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
Discuss the management of vitreous haemorrhages
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)
State some potential complications of posterior vitreous detachment
Increased risk of:
- Retinal tear
- Retinal detachment
… which can both lead to vision loss
What is retinal detachment?
What usually causes the above?
Why is it a problem?
- 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
State some risk factors for retinal detachment
- Posterior vitreous detachment
- Diabetic retinopathy
- Trauma to the eye
- Retinal malignancy
- Older age
- Family history
- Previous surgery for cataracts
Describe typical presentation of retinal detachment (in adults)
- 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
Infants with retinal detachment often present late due to impaired ability to recognise and communicate symptoms; how may children with retinal detachment present?
- Squint
- White pupillary reflex (loss of red reflex)
What might you find on examination of pt with retinal detachment?
- Reduced peripheral visual fields
- Reduced central vision acuity (if macula involved)
- Loss of red reflex
- Relative afferent pupillary defect (if optic nerve involved)
Discuss the management of retinal detachment (include management of any associated retinal tears)
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)
What is a retinal vein occlusion?
State the two types of retinal vein occlusion
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)
Discuss pathophysiology of retinal vein occlusion
- 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
State some risk factors for retinal vein occlusion
- Hypertension
- Hypercholesterolaemia
- Diabetes
- Smoking
- Glaucoma
- Systemic inflammatory conditions e.g. SLE
How does retinal vein occlusion present?
- 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
What would you find on fundoscopy of pts with retinal vein occlusion?
- Flame haemorrhages
- Blot haemorrhages
- Optic disc oedema
- Macula oedema
- Cotton wool spots
In central retinal vein occlusion “blood & thunder”
What investigations would you do if you suspect retinal vein occlusion?
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
Discuss the management of retinal vein occlusion
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.
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)
Compare the following in terms of symptoms:
- Posterior vitreous detachment
- Retinal detachment
- Vitreous haemorrhage
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
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)
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
- Endothelial damage results in increased vascular permeability
- 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
What is IRMA?
- Intraretinal microvascular abnormalities
- Dilated & tortuous capillaries in retina
- Can act as shunt between arterial and venous vessels in retina
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)
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)!
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.
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
Discuss the management of hypertensive retinopathy
Management centred around controlling BP and other cardiovascular disease risk factor e.g. smoking, lipids etc…
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
State some potential complications of herpes zoster ophthalmicus
- Ocular
- Conjunctivitis
- Keratitis
- Episcleritis
- Anterior uveitis
- Ptosis
- Post-herpetic neuralgia
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 GAGs (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
