Diabetic Retinopathy

Presentations (Can still use the older classification)

Sir, this patient has:

(a)Type and location

1. Background diabetic retinopathy affecting the inferior/superior temporal/nasal

quadrants of the retina (usually seen in the posterior pole, ie area between the
superior and inferior temporal quadrants) as evidenced by
a. Microaneurysms
b. Dot, blot or flame shaped haemorrhages
c. Hard exudates
2. Pre-proliferative diabetic retinopathy affecting the inferior/superior
temporal/nasal quadrants of the retina
a. Cotton-wool spots
b. Venous dilatations, beading, looping or segmentation
3. Proliferative retinopathy diabetic retinopathy
a. Neovascularisation
i. At the disc
ii. Affecting the inferior/superior nasal/temporal quadrants of the
retina
4. Diabetic maculopathy
a. Circinate formation of hard exudates at or near the macula
b. Macular oedema (cannot be seen by direct ophthalmoscopy)

(b)Treatment for (3) and (4)

1. Focal photocoagulation scars

2. Panretinal or scatter photocoagulation scars
3. Macular photocoagulation scars

(c)Complications (for proliferative)

1. Vitreous haemorrhages
2. Fibrosis with traction retinal detachment
3. Optic atrophy (for all)

(d)Associations (mention if present)

1. Xanthelesma
2. Cataracts
3. Hypertensive changes
4. Robeosis irdis
Questions
What are microaneurysms?
 They are well-defined red dots seen in the superficial retinal layers which
represents outpouching of the retinal capillaries; earliest sign of diabetic
retinopathy
 Can also be seen in
o Hypertensive retinopathy
o Collagen vascular disease
o Severe anaemia
o Dysproteinaemia

What are flame-shaped haemorrhages?

 Superficial bleed shaped by nerve fibres into a fan shape which points towards the
disc

What are dot and blot haemorrhages?

 Formed as a result of rupture of microaneurysms with bleeding into the deep layer
of the retina

How do you differentiate between dot haemorrhages and microaneurysms?

 This is difficult and differences includes:
 Microaneurysms are well defined and last for months to years whereas dot
haemorrhages tend to be have an irregular outline and disappears within a few
days
 Fluoroscein angiography of which microaneurysms are hyperfluoroscent
whereas dot haemorrhages are hypofluoroscent

What are hard exudates?

 These are minute, yellow, well defined deposits of lipo-protein and lipid-laden
macrophages

What are cotton-wool spots?

 Build up of axoplasmic material due to interrupted flow caused by ischaemia from
capillary occlusion in the retinal nerve fibre layer

What are IRMAs?

 It stands for intraretinal microvascular abnormalities. They are remodelled
capillary beds without proliferative changes and are collateral vessels that do not
leak on fluoroscein angiography. Usually found on the borders of non-perfused
retina

What is neovascularisation?
  Formation of abnormal new vessels on the retinal surface and at the optic disc
because of ischaemia
 These are fragile and tend to bleed into the vitreous leading to vitreous
haemorrhages and fibrous tissue formation with resultant traction retinal
detachment

What is clinically significant macular edema?

 Thickening of the retina at or within 500 microns of the centre of the macula
 Areas of thickening 1disc area or larger, any part of which is within 1 disc
diameter of the centre of the macula
 Hard exudates at or within 500 microns of the center of the macula, if associated
with thickening of the adjacent retina

What is the pathogenesis of diabetic retinopathy?

 Earliest stages are characterised by increased vascular permeability, leading to
fluid accumulation in the retina (seen by leakage of fluoroscein dye into the
vitreous humor)
 Later there is vascular closure causing retinal ischaemia leading to
neovascularisation of the retina
 These new vessels are prone to complications of vitreous haemorrhages, fibro-
proliferative changes, retinal detachment and neovascular glaucoma

How can diabetes mellitus affect the eye?

 Eyelids – xanthelasma (association)
 Extraocular – mononeuritis multiplex, diabetic third (spares the pupils and
associated with headache; resolves within 3 months) or sixth nerve palsies
 Anterior chamber – neovascular/rubeotic glaucoma
 Iris – rubeosis irdis
 Pupils – Argyll Robertson pupil, RAPD
 Lens – cataracts(higher incidence and occurs at a younger age), refractor errors
(occurs due to fluctuation in the blood sugar level especially when starting
treatment; it is a benign condition)
 Vitreous body - haemorrhages
 Retina – DM eye changes, hypertensive, CRAO, lipaemia retinalis
 Optic nerve – optic atrophy, ischaemic papillitis
 Orbit – mucormycosis

How can patients present clinically?

 NPDR – asymptomatic
 PDR
o Asymptomatic
o Reduced VA or blindness as a result of complications
 CSME
o Asymptomatic
o Reduced in VA
 o Paracentral scotoma
o Decrease in central vision

What conditions can cause blindness in diabetic eye disease?

 Macular edema
 Retinal detachment
 Vitreous haemorrhages
 3.6% of type 1 and 1.6% of type 2 were legally blind according to the WESDR

When should we screen for diabetic eye disease?

 Type 1 DM – within 3-5 years of Dx of DM
 Type 2 DM – at diagnosis
 Pregnancy with pre-existing DM – prior conception and first trimester

How should we screen for diabetic eye disease?

 Fundal photography
 Indirect ophthalmoscopy with slit-lamp biomicroscopy
 Direct ophthalmoscopy through dilated pupils

How frequent should patients be followed up?

 No retinopathy – annually
 NPDR
o Mild and no retinal edema – 6 to 12 monthly
o Presence of retinal edema – 4 to 6 monthly
o Macula affected or severe – 1-4 monthly
 PDR – 1 to 4 monthly

How soon must you refer a patient with diabetic eye disease to the ophthalmologist?
 All patients with DM retinopathy needs a referral to an ophthalmologist
 Immediately (1 day)
o Sudden loss of vision
o Retinal detachment
 Urgently (within 1 week)
o Neovasculariastion
o Pre-retinal or vitreous haemorrhages
o Rubeosis irdis
 Soon (within 4 weeks)
o Pre-proliferative changes
o Macular diabetic changes
o Unexplained drop in VA

What are the risk factors for diabetic eye disease?

 Poor glucose control
o WESDR (Wisconsin Epidemiologic study of DR)
 o DCCT (Diabetes Control and Complications trial)
 Hypertension
o UKPDS (UK prospective diabetic study)
o Aim < 130/80 mmHg
 Hyperlidaemia
 Renal disease – aggressive treatment of renal disease may slow progression of
DM retinopathy and prevent neovascular glaucoma
 Cigarette smoking
 Duration of diabetes (non-modifiable)
o After 20yrs, nearly all patients with type 1 and 60% of type 2 will have
DR
 Pregnancy (non-modifiable)

How do you manage patients with diabetic eye disease?

 Management of the diabetic eye includes:
o Prompt referral to the ophthalmologist (see above)
o Macular oedema – focal or grid macular laser
o NPDR – none or consider scatter laser if severe
o PDR – scatter laser
o Vitreous surgery
 Non-resorbing vitreous opacities
 Traction retinal detachment threatening or involving the macula
 Progressive fibro-proliferative diabetic retinopathy
 Combined rhegmatogenous and traction retinal detachment
 Pay attention to
o Glycaemic control
o Blood pressure
o Quit smoking
o Screen for other DM complications especially DM renal disease
o Control hyperlidaemia
 Engage patient
o Education
o Importance of regular follow up

How would you manage a patient who requires laser therapy but has cataracts?
 If fundal visibility permits, laser treatment administered prior to cataract surgery
 If not, cataract surgery followed by prompt laser treatment

How effective is laser photocoagulation?

 For visual salvage in maculopathy
o Effective in 50-60% of cases
 For reduction of already formed abnormal new vessels on the retina
o It can abolish new vessels in up to 80% of patients with PDR and follow
up showed that disease had stabilised or cured
 o In pan-retinal photocoagulation, it reduces the ischaemic and hypoxic
retina, reducing angiogenic factors and neovascularisation
o It can alsobe used to treat microaneurysms
 There may be loss of peripheral vision