medical retina Flashcards
what does the viterous humour contain
volume of it?
water, hyaluronic acid and type II collagen.
4.0-4.4mL
retina role
derived embryologically from
- Blood tissue barrier
- Facilitate neural transmission
- Facilitate pathway of pathogens
layer responsible for converting light energy into neural signals.
Derived embryologically from the diencephalon.
The diencephalon gives rise to the optic vesicle and then the optic cup.
what are the two parts of the retina
● The outer retinal pigment epithelium (RPE) layer – From the outer optic cup of the diencephalon.
● The inner neurosensory retina (NSR) (composed of nine layers) – From the inner optic cup of the diencephalon.
why may retinal detachment occur
long distance between RPE and NSR
what are the 9 layers of the NSR
- Internal limiting membrane: Separates the retina from the vitreous.
- Nerve fibre layer (NFL): Contains ganglion cell axons that come together to form the optic nerve. Presents in the macular area and travels nasally to the
optic nerve directly through the papillomacular bundle. - Ganglion cell layer: Contains the cell bodies of the ganglion cells. Involved in
transmitting visual information to the brain including the stimulus required
for light pupillary response. - Inner plexiform layer: Synaptic layer between second and third order neurons.
- Inner nuclear layer: Contains cell bodies of bipolar cells and cell bodies of
Müller cells (principal glial cells of the retina). - Outer plexiform layer: Synaptic layer between photoreceptors and bipolar cells.
- Outer nuclear layer: Contains cell bodies of rods and cones.
- External limiting membrane (ELM): Connections between photoreceptors
and Muller cells create the ELM. - Photoreceptor layer: Composed of rods and cones.
what is the role of RPE and composed of
single layer of cuboidal epithelial cells containing melanosomes
- Absorbs light and prevents the scattering of light within the eye.
● Replenishes the molecules needed for phototransduction.
● Contains a blood-retinal barrier, which provides a selectively permeable
membrane to supply nutrients to the photoreceptors and maintain homeostasis.
The blood-retinal barrier is maintained by the zonulae occludentes.
● Phagocytosis of photoreceptor outer segment membranes.
● Transport and storage of metabolites and vitamins.
what is macula lutea ALSO KNOWN AS MACULA
pigmented, rounded area at the posterior pole of the retina, located temporal to the optic disc.
central, high-resolution, colour vision.
several layers of ganglion cells in contrast to the peripheral retina, which contains only one layer.
what is the fovea
depression at the centre of the macula
contains only cones and represents the retina’s highest visual acuity.
The centre of the fovea is avascular and is dependent on the underlying choriocapillaris for blood supply via diffusion across the RPE from the choroid
how many rods location pigment wavelength bipolar connection function
120 million
highest density in the mid-peripheral retina
rhodopsin
498nm
One bipolar cell can receive stimuli from multiple rods
• Night vision – low threshold to light
- Sensitive in dark-dim illumination
- Responsible for night and peripheral vision
how many cones location pigment wavelength bipolar connection function
6 million
Highest density at the
macula (especially the fovea)
Iodopsin
Three types:
Short (420),
medium (534)
long (564) wavelength cones which are sensitive to blue, green and red light, respectively
Forms a 1:1 ratio with bipolar cells
- Sensitive to bright light
- Responsible for central and colour vision
The outer third of retinal layers, including photoreceptors and RPE and choroid are supplied by
short posterior ciliary artery (choroid).
The inner two-thirds of retinal layers are supplied by
central retinal artery
pathogenesis of diabetic retinopathy
hyperglycaemia -> increased retinal blood flow-> damages endothelial walls and pericytes.
endothelial dysfunction-> vascular permeability + hard exudate formation
(lipoproteins in the outer plexiform layer).
microaneruysms formation?
Pericyte damage predisposes to the formation of microaneurysms,
which are leakages of blood from capillary walls
flame haemorrhages formation?
due to rupture of the capillary walls which track along the nerve
fibre layer.
cotton wool spot formation
Axonal debris at margins of ischaemic infarcts.
neovascularisation formation
occurs through angiogenic factors such as vascular
endothelial growth factor (VEGF) in response to ischaemia.
CMO which layer os mpst affected
outer plexiform layer
RFs of DR
● Duration of diabetes: Most important risk factor.
● Poor diabetic control
- Smoking
- hyperlipidaemia
- hypertension
- ethnicity
- pregnancy
Ix
- Fluoroscein angiography
- OCT
For type 2 diabetics, a 37% reduction in progression rate of microvascular complications (e.g. retinopathy) can be achieved with 1% reduction in HbA1c (1).
For insulin-dependent diabetics, intensive glycaemic therapy showed
a 76% reduction in progression of retinopathy when compared to the control group.
Note, however, intensive diabetic control may transiently worsen retinopathy in the first few months
● Pregnancy.
● Other factors:
(for type 2
diabetics, a tight blood pressure control with a mean of 144/82 mmHg caused a 37% reduction of microvascular complications
gradual onset of features of DR
- Any type of diabetic retinopathy.
- Diabetic macular oedema: Most common cause of visual impairment.
- Cataract.
acute onset of features of DR
- Painless: Similar to vitreous haemorrhage or tractional retinal detachment (flashes and floaters may precede visual loss).
- Painful: Similar to neovascular glaucoma (NVG) precipitated by rubeosis iridis.
classficiation of nonproliferative DR
MILD
MODERATE
SEVERE
● Mild
- At least one microaneurysm, intraretinal haemorrhages, exudates or cotton wool spots.
● Moderate
- Intraretinal haemorrhages (in 1–3 quadrants) or mild intraretinal microvascular abnormality (IRMA-shunt vessels that arise to supply hypoperfused areas).
- Venous beading (in 1 quadrant only).
● Severe Follows the 4-2-1 rule; one or more of: – Intraretinal haemorrhages in 4 quadrants – Venous beading ≥ 2 quadrants – Moderate IRMA ≥ 1 quadrant
Classification of proliferative DR
● Non-high risk
Neovascularization on disc (NVD) or elsewhere (NVE)
● High risk Fulfils one of the following: – NV >1/3 disc area – NVD plus vitreous haemorrhage – NVE >1/2 disc area plus vitreous haemorrhage
● Advanced
Tractional RD
what is diabetic maculopathy and its classification
presence of diabetic macular oedema
● Centre involving DMO or
● Extra-foveal DMO meeting clinically significant macular oedema (CSMO)
defined by the ETDRS
- Hard exudates + other ‘background’ changes on macula (< 1DD of fovea) • Microaneurysms + haemorrhage (< 1DD of fovea if VA is < 6/12)
- Retinal thickening
- ̄ Visual acuity
- Oedema
commoner in T2DM
ix for diabetic maculopathy
● Optical coherence tomography (OCT) for assessing and monitoring DMO.
● Fluorescence angiography (FA) mainly used to assess for retinal ischaemia.
Mx for diabetic retinopathy or maculopathy
Glycaemic and blood pressure control (use effective antihypertensives such as lisinopril).
Mx for non-proliferative DR
Monitoring in screening programmes or secondary care ranging from annual (for mild-moderate) to 4 monthly (severe).
Consider pan-retinal photocoagulation (PRP) for severe nonproliferative in elderly patients with type 2 diabetes or if poor attendance or prior to cataract surgery.
mx for proliferative DR
non-high risk
high risk
Non-high risk: Regular routine review ± PRP.
High risk: PRP within 2 weeks. Treat DMO, if coexists, at the same time or before.
Mx for viterous haemorrhage
Tractional RD or persistent vitreous haemorrhage
treat as high-risk PDR
pars plana vitrectomy
Mx for maculopathy
- Steroids
- Anti – VEGF
- Laser
Treated with intravitreal anti-VEGF (ranibizumab or aflibercept, note the latter has a higher molecular weight and is second line) if there is DMO on OCT and the vision is affected.
Consider using modified ETDRS laser if anti-VEGF is contraindicated (e.g. pregnancy).
Mx for diabetic retinopathy and cataract surgery
Treat CSMO and PDR or neovascularization of iris before cataract surgery. If there is no fundal view perform B scan ultrasound.
what is hypertensive retinopathy
Atherosclerotic changes and vasoconstriction of retinal arteries in response to chronic hypertension causes endothelial damage and can lead to retinopathy
Chronic hypertensive retinopathy can include similar signs to diabetic retinopathy.
Mx is usually with BP control.
clinical stages of hypertensive retinopathy
- Arteriolar narrowing.
- Arteriovenous nipping (Figure 14.3) or atherosclerosis with thickening of
retinal arterioles (‘copper/silver wiring’). - Stage 2 plus flame haemorrhages, cotton wool spots or exudates.
- Stage 3 plus papilloedema.
classification of retinal vein occlusion
complications
non-ischaemia
ischaemic
● Central (CRVO) versus branch (BRVO): An occlusion at or proximal to the lamina cribrosa where the retinal artery exits the eye leads to CRVO. An occlusion of one of the branches of central retinal vein leads to BRVO
● Ischaemic versus non-ischaemic.
- Non ischaemic CRVO: chronic macular oedema leading to permanent central scotoma.
- Ischaemic CRVO: neovascularization, neovascular glaucoma, vitreous haemaorrhage, macular degermation and optic atrophy.
RFs of retinal vein occlusion
● Age ● Microvascular: Hypertension, hyperlipidaemia - DM ● Combined oral contraceptive pill ● Glaucoma - polycythaemia
non-ischaemic CRVO features
fundoscopy findings
● Sudden, painless dVA (>6/60).
● Fundoscopy:
- Tortuosity and dilatation of all branches of central retinal vein
- dot/blot and flame haemorrhages of all four quadrants, prominent in the periphery
- with optic disc and macular swelling.
ischaemic CRVO features
fundoscopy findings
● Sudden, painless severe dVA (<6/60).
● Relative afferent pupillary defect (RAPD).
● Significant tortuosity and dilatation of all four quadrants - with severe flame haemorrhages - disc and macular oedema. - cotton wool spots - swollen optic nerve - risk of neovascularisation
● Rubeosis iridis in about 50% of patients, which can lead to NVG.
Mx of non ischaemic CRVO
If VA is 6/96 or better and there is evidence of macular oedema on OCT:
● Commence intravitreal anti-VEGF or Ozurdex (dexamethasone) implant).
● Both treatments are first line
-> although younger phakic patients or with history of glaucoma should be started on anti-VEGF.
->Patients with high
cardiovascular profile should be started on Ozurdex implant.
Mx for ischaemic CRVO
● No neovascularization and open angle: Monitor for neovascularization and glaucoma.
● Neovascularization present: Urgent Pan-Retinal Photocoagulation ± cyclodiode laser therapy if angle closure.
most common location
features
complication
of BRVO
● Most common location: Superotemporal, followed by inferotemporal.
● dVA, metamorphopsia, VF defect (altitudinal).
● Retinal haemorrhage in the affected quadrant.
● Complication: CMO and neovascularization.
