1. Ieuan Rees B.App.Sc.(Optom) (Hons)GradCertOcTher
Specialty Contact Lens Practitioner
Ophthalmic Medicines Prescriber
Orthokeratologist, Behavioural Optometrist

2. Diabetes and the Eye Diabetic Retinopathy Diabetic Macula Oedema
Diabetic retinopathy is the leading cause of new blindness in persons aged 25-74
Diabetic Macula Oedema
Glaucoma
Iris Neovascularisation
Neuropathies
Corneal Anomalies
Hyperopic /Myopic Prescription Changes
Extra-ocular Muscle Palsy
Dry Eye Disease (50%) (reduced corneal sensitivity)

3. >70% with diabetes will develop changes to their eyes…
within 15 years of diagnosis.

4. Optometry’s Role in Diabetic Eye Care
Optometrists screen for DR
appropriate skills
diagnostic equipment
accessible to the public.
capacity and responsibility to increase patient awareness about the condition.
Medicare item code (10915)

5. =>ischaemia and/or vessel leakage, causing swelling and bleeding.
Diabetic changes in the Eye
Diabetic retinopathy : Microvascular occlusion and leakage.
Capillaropathy-Degeneration and loss of pericytes, proliferation of endothelial cells thickening of basement membrane and occlusion
Haemotological changes=> Decreased blood flow
=>ischaemia and/or vessel leakage, causing swelling and bleeding.

6. Capillary non perfusion and retinal hypoxia which may cause:
Arteriovenous shunts (IRMA)
Neovascularization caused by angiogenic growth factors (VEGF)

7. Who is at risk?
All people with Type 1 or Type 2 diabetes are at risk of developing diabetic retinopathy.
Over the same duration, type 1 may result in worse diabetic retinopathy
The longer a person has diabetes, the greater the risk. (25% for 15 years)
Poor control of blood sugar levels can increase the risk
Access Economics Pty Ltd. Clear Insight – The Economic Impact and Cost of Vision Loss in Australia, 1.2 Diabetic Retinopathy, August 2004,

8. Other Risk Factors Systemic Hypertension Hyperlipidaemia Renal disease
Pregnancy (with prior Type 1 or Type 2 diabetes)
Family History of DR
Smoking

9. Controlling Diabetic Retinopathy Risk
Intensive glucose therapy
Reduces the onset of new DR by 75%
Reduces the progression of DR by 50%
HbA1c 6-7%
1% decrease in HbA1c associated with lowering the
risk of retinopathy %
progression to sight threatening DR 25%
risk for laser %
risk for blindness %

10. Controlling Diabetic Retinopathy Risk
Tight BP control associated with lower risk of
Retinopathy progression 35%
Need for laser 35%
Risk for vision loss %
Others: Hyperlipidemia(lipidil) / Smoking and Alcohol consumption / Pregnancy / Body Mass Index / Inflammation

11. Evidence indicates that early detection of Diabetic Retinopathy by regular eye examination, is key to reducing vision loss and blindness from diabetes.
It is estimated only ½ the Australians with diabetes have a regular eye exam and 1/3rd have never been checked.
Often there are no symptoms of diabetic retinopathy until serious damage has occurred.
Early diagnosis and treatment can prevent severe vision loss
Eye examination every Year is recommended for people with diabetes.

12. Visual Acuity Assessment: Baseline and every appointment.
Optometrical Evaluation of a Diabetic Patient
Case History: type and duration of diabetes, past glycaemic control, medications systemic history, frequency/ results of self-monitored blood glucose and recent laboratory tests for HbA1C, serum lipids and proteinuria.
Visual Acuity Assessment: Baseline and every appointment.
Fundus (Stereoscopic) Examination: :-Dilated fundus examination and Digital image of the retina.
Patient Education: Importance of regular eye examination /controlling systemic factors

13. Optometrical Evaluation of a Diabetic Patient
Pupil reactions: Direct/consensual and near pupillary responses.
Ocular motility: Extent, fluency and symmetry of ocular movements in all directions of gaze, ruling out eye movement anomalies.
:-Onset and direction of diplopia is necessary. Degree and direction of diplopia.
Visual field screening: Confrontation and/or visual field assessment as per Medicare guidelines.
Refraction: On indication where patient reports a change in vision or visual function or where a change in habitual visual acuity is measured.
Slit lamp biomicroscopy: Recommended at every visit to check for iris and corneal neovascularisation, diabetic cataract and corneal integrity.
Tonometry: Link between vasculopathic conditions and glaucoma.

14. ETDRS : Early Treatment Diabetic Retinopathy Study.
Mild
Non Proliferative Diabetic Retinopathy (NPDR)
Moderate
Severe
Very Severe
Proliferative Diabetic Retinopathy (PDR)
Early PDR
High Risk PDR

15. Optometry Australia:
Adopted the International Clinical Diabetic Retinopathy Disease Severity scale :-easily understandable scale to classify NPDR.

16. How to detect diabetic retinopathy?
Direct Ophthalmoscopy
Microaneurysms
Dot and blot hemorrhages
MA’s rupture in the deeper retinal layers
Flame-shaped hemorrhages occur in the more superficial layer
Retinal edema and hard exudates :-breakdown of the blood retinal barrier allowing leakage of serum protein and lipids
90D Un-dilated Slit Lamp Biomicroscopy

17. How to detect diabetic retinopathy?
90D Dilated Slit Lamp Biomicroscopy
NB: Stereoscopic Imaging
Cotton-wool spots are nerve fibre layer infarcts from occlusion of precapilary arteriole

18. How to detect diabetic retinopathy?
22D Full Field Binocular Indirect Ophthalmoscope:-Dilated
Venous loops and beading frequently occur adjacent to area of non perfusion and reflect increased retinal ischaemia
IRMA are collaterals without proliferation and can usually be found on the border of non perfused retina

19. How to detect diabetic retinopathy?
Neovascularization
Is the hall mark of PDR :- (NVD)
Or (NVE)
Standard Digital Retinal Photography
45 Degrees

20. ETDRS 7.
Early Treatment Diabetic Retinopathy Study.

21. How to detect diabetic retinopathy?
Optos: Optomap 200 Degree Digital Retinal Imaging
Optic disc edema occurs in patients with type I or II diabetes mellitus

23. Optos takes digital diabetic retinopathy screening further

25. Computer generated colour image

26. Green Laser Image

27. Red Laser Image

28. RED Laser Zoom.

29. What can we see with Optomap 2000 Digital Retinal Imaging ?

30. Primary aim is to diagnose, Report to GP…(BDR: Fenofibrate)
The Optometrist’s Role in Diabetic Retinopathy: Screening and Maintenance
Primary aim is to diagnose,
Report to GP…(BDR: Fenofibrate)
Refer to Ophthalomologist…
and consequently prevent / treat sight threatening DR retinopathy

31. How often should eye examinations occur?
Dictated primarily by the baseline stage of the retinopathy and its rate of progression to proliferative diabetic retinopathy
Only 5% patients with mild NPDR will progress to PDR in 1 year, monitoring every 6-12 months is appropriate
As many as 27% of patients with mod NPDR would progress to PDR in I year, review every 4-8 months
More than 50% of patients with severe NPDR would progress to PDR in one year, review 2-3 monthly
BDR to PDR

32. BDR to Macula Oedema

33. LIPIDIL
FIELD study
fenofibrate had a statistically significant relative risk reduction in the need for laser treatment for maculopathy and proliferative retinopathy.
ACCORD-Eye study :-statistically significant reduction in diabetic retinopathy progression in patients treated with fenofibrate and statin combination therapy compared to statin therapy alone.
Fenofibrate slows progression of diabetic retinopathy and the need for more invasive treatment modalities in patients with type 2 diabetes, when there is pre-existing retinopathy.
In October 2013, Australia became the first country in the world to approve the use of this medication for this specific indication.

34. The evidence indicates that only diabetic patients with some prior DR, whether mild or moderate may benefit at all from fenofibrate.
An argument can be made that fenofibrate is more clinically efficacious in patients:-
With moderately elevated
Low-density lipoprotein (LDL) (2.2 – 2.9 mmol/L) Triglyceride lipase (TGL) (3.3 – 5.2mmol/L).

35. First round assessment of risks
The risks of fenofibrate in the proposed usage are:
It can be considered ineffective polypharmacy to treat patients with diabetes that show no DR.
By delaying the use of fenofibrate to diabetic patients, the potentially unnecessary side effects, adverse drug reactions and drug interactions of fenofibrate are avoided.
This includes the waste of resources in providing fenofibrate in population where it is not effective (diabetics without prior DR).

36. Lipidil is indicated for the reduction in the progression of diabetic retinopathy in patients with Type 2 diabetes and existing diabetic retinopathy.
Lipidil does not replace the appropriate control of blood pressure, blood glucose and blood lipids in reducing the progression of diabetic retinopathy.

37. Diabetic Macula Oedema
Diabetic Macular Oedema is the most common cause of moderate visual loss.
Leaking micro-aneurysms, or diffusion from capillary incompetence results in intra-retinal fluid areas and can progress to cystoid macular oedema (CMO).
Diabetic macular oedema (DMO) is retinal thickening within two disc diameters of the centre of macula.

38. If they are left untreated, sight problems will develop.
Both proliferative diabetic retinopathy and diabetic macular oedema can be treated and managed if they are detected early enough.
If they are left untreated, sight problems will develop.

39. The International clinical diabetic macular edema severity scale has devised a simpler classification of DME.
Adopted by the Optometry Australia in 2014

40. DME and OCT:- Ocular Coherence Tomography
Identify eyes at risk of vision loss from DME and can be useful to guide decisions on the timing of treatment initiation or retreatment, as well as the timing of follow up care for eyes that are being managed with observation

41. Normal Macular Cross-Section OCT Scan

42. Cystoid Macula Oedema Due to Diabetic Retinopathy: OCT Images

46. Vitrectomy Retinal Laser
Photocoagulation has been the standard care for DME since the mid 1980.

47. Intravitreal Agents
Intravitreal therapy has radically changed the management of diabetic macular edema
Groups of drugs currently utilized are Corticosteroids (Triamcinolone) and Anti-Vascular Endothelial Growth Factor blockade (Anti-VEGF) (Lucentis and Avastin, Eylea))

48. Triamcinolone

49. EYLEA: Anti VEGF
The VIVID/VISTA clinical trials and early experience with aflibercept in DME
DME, diabetic macular oedema

50. Aflibercept: A specifically-designed anti-VEGF
Soluble decoy VEGF receptor1
Binds VEGF-A and PlGF with higher affinity than their natural receptors
Forms a stable, inert 1:1 complex with VEGF, binding both sides and preventing interaction with other molecules1
VEGFR-1 domain
Aflibercept molecule
VEGFR-2 domain
Aflibercept/VEGF complex
VEGF dimer
Fc fragment
PlGF, placental growth factor; VEGF, vascular endothelial growth factor; VEGFR, vascular endothelial growth factor receptor. 1. Heier JS et al. 2009; Available at Accessed July 2014.

51. Mean change in BCVA from baseline (ETDRS letters)
Initial rapid gains in visual acuity from baseline were maintained over 100 weeks
Mean change in BCVA from baseline (ETDRS letters) 2 10 12 14 6 4 8
VIVID week 100
10.7 2q8*
11.4 2q4*
9.4 2q8*
10.5 2q4*
1.2 Laser
0.7 Laser
100 92 80 68 64 56 52 40 36 28 20 12 4 8 16 24 32 44 48 60 72 76 84 88 96
12.5 2q4*
VISTA week 100
11.5 2q4*
11.1 2q8*
10.7 2q8*
0.2 Laser
0.9 Laser
100 92 80 68 64 56 52 40 36 28 20 12 4 8 16 24 32 44 48 60 72 76 84 88 96
BVCA is the primary endpoint. primary analysis was conducted at week 52, week 100 is exploratory only.
Week
Laser
2q4
2q8
*P< vs. laser. VIVID: Laser: n=132; 2q4: n=136; 2q8: n=135; VISTA: Laser: n=154; 2q4: n=154; 2q8: n=151.
Full analysis set (last observation carried forward). 2q4, 2 mg every 4 weeks; 2q8, 2 mg every 8 weeks after 5 initial monthly doses; BCVA, best corrected visual acuity; ETDRS, Early Treatment Diabetic Retinopathy Study.
Korobelnik J-F et al. Ophthalmology 2014; 121: ; Brown DM et al, Ophthalmology 2015; 122:

52. Proportion of patients gaining ≥15 letters from baseline was maintained over 100 weeks
VIVID
Week 52
VISTA
Week 100
≥15 letters 60 40
Patients (%) 20 50 30 10
Laser
2q4
2q8
9.1
32.4*
33.3*
7.8
41.6*
31.1*
13.0
38.3*
33.1*
12.1
38.2*
Secondary endpoint. primary analysis was conducted at week 52, week 100 is exploratory only .
*P< vs. laser. VIVID: Laser: n=132; 2q4: n=136; 2q8: n=135; VISTA: Laser: n=154; 2q4: n=154; 2q8: n=151. Full analysis set; last observation carried forward. 2q4, 2 mg every 4 weeks; 2q8, 2 mg every 8 weeks after 5 initial monthly doses.
Korobelnik J-F et al. Ophthalmology 2014; 121: ; Brown DM et al, Ophthalmology 2015; 122:

53. Proportion of patients losing ≥15 letters from baseline over 100 weeks20 15 10
Patients (%) 5
Laser
2q4
2q8
2.2
12.9
1.5
9.1
0.6
0.7
9.7
3.2
10.6
0.0
VIVID
Week 52
VISTA
Week 100
≥15 letters
Laser 9.1%. 2q4 0.6%. 2q8 0.7%. All compared to baseline (LOCF); last observation carried forward.
Laser 9.1%. 2q4 0.6%. 2q8 0.7%. All compared to baseline (LOCF); last observation carried forward.
(P = ) 2q4 vs laser. (P = ) 2q8 vs laser.
(P = ) 2q4 vs laser. (P = ) 2q8 vs laser.
primary analysis was conducted at week 52, week 100 is exploratory only. Proportion of patients losing ≥ 15 letters is an additional efficacy endpoint
VIVID: Laser: n=132; 2q4: n=136; 2q8: n=135; VISTA: Laser: n=154; 2q4: n=154; 2q8: n=151.
Full analysis set; last observation carried forward. 2q4, 2 mg every 4 weeks; 2q8, 2 mg every 8 weeks after 5 initial monthly doses.
Korobelnik J-F et al. Ophthalmology 2014; 121: ; Brown DM et al, Ophthalmology 2015; 122:

54. Reduction in CRT from baseline was maintained through week 100
-66
VIVID
-86
-196*
-212*
-195*
-192*
Mean change in CRT from baseline µm
*P< vs laser
-73
VISTA
-84
-191*
-186*
-183*
*P< vs laser
Laser
2q4
2q8

55. Summary
Optometry has the skills and equipment to diagnose diabetic retinopathy, diabetic macula oedema and other diabetes related eye conditions.
OCT and OPTOS have enhanced our ability.
(Both only Buck & Todd)
Treatments include PRP, Vitrectomy and Intravitreal Phamacological Agents.
Management by the GP for glycaemic control, lipid control, cholesterol and hypertension control is essential.
Fenofibrate should be considered at first sign of BDR.

56. Thank You Ieuan Rees B.App.Sc.(Optom) (Hons)GradCertOcTher
Specialty Contact Lens Practitioner
Ophthalmic Medicines Prescriber
Orthokeratologist, Behavioural Optometrist
Thank You
Special Thanks: Dr Andre Horak ..Vision Eye Institute