This document discusses diabetic retinopathy and its effects on the eye. It begins by outlining the various parts of the eye that can be affected by diabetes, including the lids, conjunctiva, cornea, iris, angle, lens, vitreous, retina, optic nerve, and sixth nerve. It then focuses on diabetic retinopathy, explaining that it has no initial symptoms, screening is important, and that intensive therapy and good blood glucose control can slow its progression. The document also describes treatments like laser therapy to preserve vision. It emphasizes that nearly all people with diabetes will develop some retinopathy and regular screening is needed to catch and treat it early.

1. DIABETIC RETINOPATHY
Dr. Riyad Banayot
St. John of Jerusalem Eye Hospital

3. Diabetic eye disease Lids
Recurrent styes, xanthalesma
& blepharitis

4. Diabetic eye disease
Conjunctiva & Cornea
Conjunctivitis & Keratitis

5. Diabetic eye disease Iris
 Rubeosis iridis (complication
of PDR)
 Spontaneous Hyphema
 Bleeding also occurs during
cataract surgery & iridectomy
 Diabetic iritis
 Pupillary dysfunction

6. Diabetic eye disease
 Angle Neovascularization
 IOP
 Secondary glaucoma (neovascular or
Hemorrhage)
 Hypotony in diabetic coma

7. Diabetic eye disease Lens
 True diabetic cataract below 30 years
 Pre-senile cataract above 40 years
 Hyperglycemia = index myopia
 Hypoglycemia = index hypermetropia

8. Diabetic eye disease
Vitreous
Hemorrhage

9. Diabetic eye disease Retina
 Diabetic retinopathy
 Lipemia retinalis due to high
blood level in uncontrolled
cases. Fundus appears pale
&retinal vessels are milky

10. Diabetic eye disease
Optic nerve
 Retrobulbar neuritis
 Acute papillitis

11. Diabetic eye disease
6th nerve
Paralytic squint

12. Diabetic eye disease
 Post operative complication
 Hemorrhage
 Infection
 Delayed wound Healing

13. Diabetic retinopathy
 A silent complication with no initial
symptoms (until they have a bleed in the
eye)
 When symptoms occur, treatment is more
complicated and often difficult with poorer
outcome
 Screening for retinopathy is of the utmost
importance

14. When to screen for
retinopathy
 Type 1 diabetes: within 5 years of
diagnosis
 Type 2 diabetes: at time of diagnosis
(30% already have complications)
Thereafter, every 1 to 2 years,
depending on the status of the retina

15. Diabetic eye disease
 Blurred vision: common symptom of
hyperglycaemia. Osmotic changes in the lens
due to fluctuating blood glucose levels (lens
changes shape)
 Blurred vision may also be due to other eye D
 Epidemiology:
 Some form of retinopathy: 21-36%
 vision-threatening retinopathy: 6-13%

16. Risk factors
 Poor glycemic
control
 Long duration
 Hypertension
 Dyslipidemia
 Nephropathy
 Pregnancy

17. Intensive therapy
DCCT – type 1 diabetes receiving intensive therapy:
 Patients without retinopathy:
reduced risk of developing retinopathy by
76%
 Patients with some retinopathy:
reduced risk of progression of retinopathy by
54%
DCCT 1993

18. Intensive therapy
UKPDS – type 2 diabetes:
 Good glyaemic control:
reduced progression of retinopathy by
20-30%
 Tight blood pressure control: reduced
progression of retinopathy by 34%
UKPDS 1998

19. Screening tests
 Visual acuity (OnceVA decreases to 6/24
the chance of saving the sight using laser
therapy is significantly reduced)
 Direct fundoscopy (through dilated
pupils)
 Retinal photography (FFA & OCT)
 Testing intra-ocular pressure

20.  Retina-5min video WMV
 Diabetic Retinopathy SWF
 DM Retina EXE

21. Diabetic retinopathy
 Non-proliferative diabetic retinopathy:
minimal, mild, moderate, severe
 Proliferative Diabetic Retinopathy
(PDR): high-risk PDR, advanced PDR
 Macular oedema, clinically significant
macular oedema

22. Normal retina
Macula
Optic disc

23. Non-proliferative diabetic
retinopathy
Hard exudates

24. Severe non-proliferative
retinopathy
Haemorrhage
Cotton wool
spot

25. Proliferative retinopathy
New vessels
Pre-retinal
haemorrhage

26. Advanced proliferative
retinopathy
Scar tissue

27. Vitreous haemorrhage
 See a black mark across the vision
 Some blood will be reabsorbed
 Vitrectomy may be necessary

28. Early macular oedema

29. Investigations
 Fluorescein angiogram:
provides more detailed information

30. Investigations: FFA
Dot
haemorrhage
Blot
haemorrhage

31. Fluorescein leakage

32. Treatment
 Laser therapy:
 Pan-retinal for proliferative
retinopathy
 Focal or grid for macular edema

33. Pan-bombing for proliferative
retinopathy

34. Grid laser for macular
oedema

35. Laser therapy
Side effects
 Loss of peripheral vision, tunnel vision,
night blindness
 Colour blindness
 Vision can get worse but “laser saves
sight” in long term

36. Treatment
 Blood pressure: reduces macular edema
 Blood glucose control: slows progression
 Control lipids
 Use of aspirin does not increase the risk
of retinal bleeding.

37. Pregnancy
 Pregnancy can cause transient
deterioration of diabetic retinopathy
but generally not permanent damage
 Baseline retinal assessment should be
performed before pregnancy
 Retinopathy is not a problem in
gestational diabetes

38. Summary
 100% of people with diabetes will
develop some retinopathy
 The higher the blood glucose level the
greater the risk
 Different grades of retinopathy
 Laser therapy saves sight
 Timely treatment is most effective
 Regular screening is a must