Lecture 13: Diabetic eye disease Flashcards
What are the types of diabetes mellitus?
Type 1
Type 2
Maturity onset diabetes of the young (MODY)
gestational
What is type 1 diabetes?
What is the percentage out of diabetes cases?
When is the onset?
What is the genetic risk?
-Body loses ability to produce insulin.
Around 10% of adults with DM.
Onset often in childhood.
Risk if mother has Type I ~risk 2%
if father has Type I ~8%.
What is type 2 diabetes?
What is the percentage out of diabetes cases?
what is it associated with?
What is the genetic risk?
Due to ineffective use of insulin (insulin resistance), or insufficient insulin production.
Controlled with diet, exercise, tablets, insulin.
Approximately 90% of diabetes cases worldwide.
Strongly associated with obesity, lack of physical activity, smoking.
Race: Prevalence increased ~6x in South Asian & ~3x in Afro-Caribbean people compared to Caucasian.
Risk increases with age.
Risk ~15% if 1 parent has type II DM, ~75% if both have.
As summary, what pathology can diabetes cause?
Cornea erosions, ulcers, persistent epithelial defects
cataract
rubeosis iridis
diabetic retinopathy
anterior ischaemic optic neuropathy (25 % of cases have DM)
retinal vein and artery occlusion
ocular motility abnormalities (II,IV, VI CNP)
What is diabetic retinopathy?
What is the prevalence of DR in people with DM?
what are the 2 types?
microvascular retinal disease
35%
peripheral (R)
Macular (M)
non-proliferative or proliferative
What pathology under diabetic retinopathy can cause sight loss?
-macular ischaemia
-macular oedema and exudate
-fibrous tissue formation from new blood vessels
-retinal detachment due to contraction of fibrous tissue from new blood vessels
-vitreous haemorrhage from new blood vessels
What is the risk of diabetic retinopathy related to?
duration of DM (76% risk if more than 20 years)
control of DM
Type of DM (75% type 1, 25% type 2)
Hypertension
High cholesterol (especially if associated with exudates)
What is the diabetic screening process called in the UK?
Who is screened?
NHS Diabetic Eye Screening Programme (DESP)
Everyone with diabetes aged over 12 years should be registered on the screening programme.
What type of pictures are taken for DESP?
Two 30 degree images graded in DESP– one centred on disc and one on macula.
R grade (periphery) and M grade (macula) given to each patient.
What is the DESP classification of peripheral DR?
R0: NO RETINOPATHY
R1: BACKGROUND DR (microaneurysms, retinal hemorrhage, exudate, venous loops, cotton wool spots)
R2: PRE-PROLIFERATIVE (multiple blot hemorrhages, venous beading, venous reduplication, IRMA)
refer to ophthalmologist
R3: PROLIFERATIVE (NVD (new vessels on disc), NVE (new vessels elsewhere), pre-retinal or vitreous hemorrhages, pre-retinal fibrosis +- tractional retinal detachment)
urgent referral
What are microaneurysms?
Single microaneurysm diagnoses DR
Dark red dots, sharp border
< 125μm in diameter
Smaller than vein diameter at ONH
Usually temporal to macula
in inner nuclear layer
What are dot haemorrhages?
-Capillaries in inner plexiform layer are ruptured
-Larger than microaneurysms but smaller than blot haemorrhages
-Not reliably differentiated from microaneurysms using ophthalmoscopy / fundus photography
What are blot hemorrhages?
How are they graded?
-Deeper capillaries between IPL and INL.
-Larger, darker than dot haemorrhage.
-Often sign of local ischaemia
If only a few = R1
if multiple (>8-10) and present in all 4 quadrants = R2.
What are flame shaped haemorrhages?
What is normally also present?
What other conditions can you get them in?
Superficial within nerve fibre layer
Often with cotton wool spots
Also seen in systemic hypertension, glaucoma, vein occlusion
What are exudates?
Lipid and lipoprotein leaked from capillaries in OPL or IPL (usually + oedema).
Can reabsorb spontaneously/ post laser treatment.
What is oedema?
How can you spot it?
-Accumulation of fluid within retina
-May see cysts and greying in association with haemorrhages and microaneurysms
presence of exudate or fluid on OCT image
What are cotton wool spots?
What are they caused by?
How are they graded?
Fluffy white lesions in RNFL.
Caused by focal or diffuse inner retinal ischaemia, disrupting RNFL axonal transport.
Reabsorb but can take 6+ months.
In presence of other features = R1 (DESP)
But, check for referable R2 features e.g. IRMA
What is venous loop?
What is it graded as?
Abrupt curving away from normal path of vessel
Has been moved recently from R2 to R1 (DESP).
BUT look carefully for other referable (R2) features.
What are the features of R1?
Haemorrhage
Oedema
Microanuerysms
Exudate
cotton wool spots
venous loops
What features of R2 require referral?
features that reflect retinal ischaemia
IRMA and venous beading
multiple blot haemorrhages
What does IRMA stand for?
What does it indicate?
What are the features?
intraretinal microvascular anomaly
Indicates retinal ischemia
-Mimic new vessels but represent dilated capillaries in area of occlusion
-Variable calibre, odd branching patterns and angles
-Appear to run from arterioles to venules
-No crossing of major vessels.
-Don’t leak.
What venous changes can you get in R2?
What are they a sign off?
-Veins variable calibre (thickness)
-Segmented, beaded, dilated
-Beading = localised areas increased calibre.
-Occluded vessels.
severe ischaemia
What happens in R3?
-New vessel growth in response to growth factors (e.g. VEGF) produced by RPE in ischaemic retina.
New vessels are fragile, and tend to leak and bleed.
-Often loop back on themselves and widen in diameter.
-Will cross major vessels (unlike IRMA).
-Often form ‘blossom’ of numerous vessels in a patch together.
-Obscure underlying lesions therefore on top of retina, not within it (unlike IRMA).
-Eventually grow into vitreous.
What is NVD?
New vessels on or within 1 DD from ONH
Retina usually R2 features
50% risk blindness in 5 years if untreated.
What is NVE?
Fine wispy vessels usually arising from large veins
Often temporal to macula, sometimes nasal
30% risk blindness in 5 years if left untreated
How can you get a vitreous haemorrhage?
What are the symptoms?
What is the treatment?
-Occur when new vessels grow forward from retina, cross the subhyaloid / preretinal space, and enter the vitreous.
-Px reports sudden visual loss or sudden onset of dark floaters.
-Appears dark, may completely block view of the retina.
-Takes long time to clear if erythrocytes break into vitreous body (months/years)
-Untreated, 30% of eyes will be blind within 1 year of first vitreous haemorrhage.
Vitrectomy carried out if unresolved in 6 months.
What is a pre-retinal haemorrhage?
Haemorrhage often has a flat top due to red blood cells settling down due to gravity.
What is pre-retinal fibrous traction?
What is the symptom?
WHat is the treatment?
-Fibrous tissue associated with new blood vessels and with previous vitreous / pre-retinal haemorrhage.
-Contraction of fibrous tissue can pull retina to cause tractional retinal detachment (TRD).
-Pale fibrous tissue may be visible.
-Retina may appear wrinkled (traction lines), bumped and folded, or tears may be visible.
TRD associated with sudden loss vision.
Vitrectomy carried out to prevent TRD.
What is rubeosis iridis?
-Severe retinal hypoxia (widespread proliferative DR) may lead to new vessel growth on iris or in angle.
-Can lead to neovascular glaucoma due to fibrovascular tissue blocking angle of drainage.
What is the DESP classification of maculopathy?
M0: NO MACULOPATHY
-microaneurysms or hemorrhages within 1DD of fovea but vision better than 0.3logMAR/ 6/12 snellen
M1: requires referral
-exudate within 1DD of fovea
-circinate within macula
-retinal thickening within 1DD of fovea
-microaneurysms or haemorrhage within 1DD of fovea ONLY if VA is worse than 6/12
Why can you get retinal thickening in M1?
macular oedema
cystoid in nature
What is the DESP classification of photocoagulation scars?
P0: NO PHOTOCOAGULATION
P1: PRESENCE OF PHOTOCOAGULATION SCARS
-evidence of focal/grid later to macula
-evidence of peripheral scatter laser
What are the referral f
guidelines for DR?
R1: annual review by optom, screening service
R2, M1: REFER to HES to be seen soon (within 4 weeks)
new vessel formation: Urgent referral (within 1 week)
sudden loss of vision, RD, pre-retinal/vitreous haemorrhage, rubeosis iridis: HES emergency
What are the modifiable risk factors for retinopathy?
-Blood sugar levels (control)
-Legacy effect’ whereby good glycaemic control in past protects against future DR progression.
-Lipid levels
Reducing lipid levels can reduce risk of progression, esp macular oedema and exudation.
-Blood pressure
-Smoking
Not a clearly defined risk factor
Some evidence that current smoking associated with early vascular complications in type I DM.
What are the signs of macular oedema that requires laser treatment?
Retinal thickening at or within 500µm of the centre of the macula
Hard exudates at or within 500µm of the centre of the macula, if associated with thickening of the adjacent retina
Retinal thickening of one disc area or larger any part of which is within one disc diameter of the centre of the macula
How is laser used in CSMO?
-If specific blood vessels are leaking (focal diabetic macular oedema), focal laser photocoagulation seals leaking blood vessels in small area of the retina.
-diffuse leakage from capillaries in macula (diffuse diabetic macular oedema) laser grid photocoagulation is used.
-Laser grid photocoagulation places numerous coagulations around the fovea in attempt to restore the blood–retinal barrier.
-Although this does not always improve visual acuity (VA), it often prevents additional deterioration.
What anti-VEGF therapy can you get for CSMO?
Lucentis
Aflibercept
both approved for treating DMO where macular thickness exceeds 400 microns
When may intravitreal steroid therapy be used in CSMO?
What are the side effects?
What does it involve?
-May be used for resistant cases.
raised IOP and cataract formation.
Triamcinolone injections or long-acting fluocinolone acetonide (FA).
What is the ophthalmologist management of proliferative DR?
When may a vitrectomy be considered?
pan-retinal photocoagulation
intravitreal anti-VEGF
vitrectomy for vitreous hemorrhage
Non clearing vitreous haemorrhage
Vitreous haemorrhage associated with retinal detachment or ghost cell glaucoma
Also used in patients with tractional retinal detachment, especially involving macula.
How does pan retinal photocoagulation work?
-Laser burns to peripheral retina.
-Light energy absorbed by melanin in RPE and melanosomes in choroid, converts to heat, which denatures proteins and causes necrosis.
-Reduced outer retinal oxygen consumption
- oxygen from the choroid can reach the inner retina.
Reduced hypoxia
- reduced VEGF production
- reduced neovascularisation.
May also work by killing ischaemic retina, so reducing VEGF production.
What are the outcomes of pan retinal photocoagulation?
What may be used as an alternative?
-Aims to stabilise vision.
-Causes collateral damage to retinal tissue.
-Can cause macular oedema (decrease in VA), colour vision defects, generalised field restriction, difficulty adjusting to changes in light levels.
-Can be painful.
-Repeated laser treatment may be needed.
-Cryotherapy may be used as alternative to laser photocoagulation.
What are the outcomes of pan retinal photocoagulation?
What may be used as an alternative?
-Aims to stabilise vision.
-Causes collateral damage to retinal tissue.
-Can cause macular oedema (decrease in VA), colour vision defects, generalised field restriction, difficulty adjusting to changes in light levels.
-Can be painful.
-Repeated laser treatment may be needed.
-Cryotherapy may be used as alternative to laser photocoagulation.
What type of glaucoma can you get due to diabetes?
neovascular glaucoma (caused by rubeosis iridis)
Open angle glaucoma (not conclusive association)
Narrow / Closed angle glaucoma
Secondary glaucoma
What is the treatment for neovascular glaucoma?
panretinal photocoagulation (to reduce hypoxia)
medical treatments e.g. atropine to reduce congestion, steroids to reduce inflammation, anti-glaucoma drugs + surgical treatment e.g. trabeculectomy in advanced cases.
Why can poor blood sugar control cause cataract?
What are the signs of osmotic stress?
What do diabetic lenses show?
Glucose is reduced to sorbitol which accumulates in the lens causing osmotic stress i.e. water drawn into lens
-transient hypermetropic
- myopic shift
-reduced amplitude of accomodation – px may report blurred vision.
Osmotic stress can cause cataract (lens fibres swell and rupture).
-Deposition of advanced glycation end products in lens may be linked to diabetic cataracts.
increased levels of free radicals, and reduced antioxidant activity
What are the signs of snowflake cataract?
Rare
Usually bilateral
Rapid onset
Related to very high serum glucose levels in young type I diabetic Px.
Multiple white anterior and posterior subcapsular and cortical opacities seen.
What are the signs of age-related diabetic cataract?
Usually posterior subcapsular or cortical, less commonly nuclear.
May appear ~10 years earlier than in non-diabetic Px.
What is anterior ischaemic optic neuropathy?
What are the signs and symptoms?
What is it associated with?
Acute vascular condition of ONH
Presents with rapid, painless, loss of vision, often on wakening.
VA from no perception of light to 6/6, but mostly better than 6/60. Stays stable over time.
Disc oedema and peripapillary flame shaped haemorrhages.
Disc pallor develops over time.
Most likely to occur in small optic disc with small optic cup (‘disc at risk’).
rarely associated with diabetic papillopathy (disc oedema, mild visual loss)
How can diabetes effect ocular motility?
Associated with III, IV, VI cranial nerve palsy.
Responsible for 25-30% of cases of acute extraocular muscle palsy in patients aged over 45 years.
Often recover within 3 months, but may recur.
How can diabetes effect the cornea?
What are the signs of diabetic epithliopathy?
When must you consider this?
Reduced corneal sensitivity due to corneal neuropathy
Aqueous tear deficiency - Dry Eye Syndrome
Corneal endothelial dysfunction
Recurrent erosions (see above)
Corneal abrasions
Persistent epithelial defects
-infection and trauma
CL fitting and refractive surgery
How can diabetes effect the cornea?
What are the signs of diabetic epithliopathy?
When must you consider this?
Reduced corneal sensitivity due to corneal neuropathy
Aqueous tear deficiency - Dry Eye Syndrome
Corneal endothelial dysfunction
Recurrent erosions (see above)
Corneal abrasions
Persistent epithelial defects
-infection and trauma
CL fitting and refractive surgery
When should you dilate a diabetic px?
What should the recall be for someone who someone who is not in the DESP?
You should dilate any patient with DM who has not been screened within the past 12 months.
12 months until they join
encourage to join DESP
What must you ask in the H+S of a diabetic px?
What type of DM?
What age of onset?
Ask about risk factors
When were you last seen by the DESP?
Any problems with vision at distance or near? Any flashers or floaters? Diplopia?
Plus usual detailed H&S.
What symptoms may px have with:
M1?
R3?
closed angle glaucoma?
cataract?
nerve palsy?
reduced VA
Haemorrhage: Sudden loss of vision, dark floaters
Tractional retinal detachment: flashing lights, sudden loss of vision, curtain/shadow/veil across vision.
Gradual worsening of vision and contrast sensitivity.
Nerve palsy will lead to diplopia.
What clinical assessment should you do for a DM px?
Functional:
Visual acuity
Contrast sensitivity
Colour vision
Visual fields
Intraocular pressure
Oculomotor status and pupils
Structural:
Fundus evaluation
Binocular indirect ophthalmoscopy
Fundus photography
OCT
Anterior eye / anterior chamber / vitreous
Retinal vasculature
Fluorescein angiography
How do diabetic signs show up on fluorescein angiography?
microaneurysms: little white spots
leaky new vessels: hyperfluorescent region
hemorrhage: dark area
