Diabetic eeye

1. DIABETES AND THE EYE
Monika Pradhan
Acute Eye Course
University of Auckland
NZNEC

2. LEARNING OBJECTIVES
Identify systemic risk factors
Differentiate clinical stages
Describe treatment strategies
Recognize importance of team approach
Introduction

3. Types
Type 1 (IDDM) – young, insulin deficiency
Types 2 (NIDDM) – older, related to obesity, lack
of response to endogenous insulin

4. U
S
:
E
P
I
D
E
M
I
O
L
O
G
Y
135 million people with diabetes worldwide
(90% type 2)
300 million people with diabetes projected by
2025
Introduction

5. DIABETES MELLITUS:
EPIDEMIOLOGY
NZ 200,000 diagnosed and approx 100,000
undiagnosed
http://www.moh.govt.nz/diabetes
Maori / Pacific (3x) and South Asians
www.diabetes.org.nz
www.diabetesyouth.org.nz
www.maoridiabetes.co.nz
www.letsbeatdiabetes.org.nz (Pacific)
Introduction

6. T
I
N
O
P
A
T
H
Y
Retinal complications of diabetes
Leading cause of blindness in working-age group
Introduction

7. Primary care physician
+
Ophthalmologist

Systemic control,
timely screening,
and early treatment
Introduction

8. DCCT: INTENSIVE GLUCOSE CONTROL, NO
BASELINE RETINOPATHY
27% reduction in developing retinopathy
76% reduction in risk of developing progressive
retinopathy
Systemic Controls

9. T
R
O
L
,
M
I
L
D
T
O
M
O
D
54% reduction in progression of retinopathy
47% reduction in development of severe NPDR or PDR
59% reduction in need for laser surgery
Pre-existing retinopathy may worsen in early stages of
treatment
Systemic Controls

10. UKPDS: TYPE 2 DIABETES
Increased glucose and BP control decreases
progression of retinopathy
Systemic Controls

11. UKPDS: RESULTS
Hemoglobin A1C reduced from 7.9 to 7.0 = 25%
decrease in microvascular complications
BP reduced to <150/85 mm Hg = 34% decrease
in retinopathy progression
Systemic Controls

12. N
S
I
O
N
C
O
N
T
R
O
L
As important as glucose control in lowering rate
of progression of diabetic retinopathy
ACE inhibitor or beta blocker decreases
microvascular complications
Systemic Controls

13. DIABETIC RETINOPATHY: PATHOGENESIS
Increased glucose

VEGF

Increased capillary permeability/
abnormal vasoproliferation
Pathogenesis

14. Pathogenesis
Normal Diabetic retinopathy

15. H
Y
:
C
L
I
N
I
C
A
L
S
T
A
G
Peripheral retinopathy
Nonproliferative diabetic retinopathy (NPDR) –
mild, moderate and severe
Proliferative diabetic retinopathy (PDR)
Macular oedema – CSMO
Clinical Stages of Retinopathy

16. E
R
A
T
E
N
P
D
R
Microaneurysms
Hard exudates
Intraretinal haemorrhages
Patients may be asymptomatic
Clinical Stages of Retinopathy

17. Severe NPDR
MAs and haemorrhages in 4 quadrants or
Venous beading 2 quadrants or
IRMA 1 quadrant

18. Clinical Stages of Retinopathy
Microaneurysms

19. Clinical Stages of Retinopathy
Intraretinal hemorrhages

20. Clinical stages of Retinopathy
Severe NPDR

21. DIABETIC MACULAR EDEMA
Diabetes ≤5 yrs = 5% prevalence
Diabetes ≥15 yrs = 15% prevalence
Clinical Stages of Retinopathy

22. CSMO
From centre of FAZ:
Oedema within 500μ
HE within 500μwith oedema
Oedema >1DD in size within 1DD
Clinical Stages of Retinopathy

23. Clinical Stages of Retinopathy
Healthy macula Edematous macula

24. Clinical Stages of Retinopathy
CSMO

25. Clinical Stages of Retinopathy
Cotton-wool spots

26. C
A
L
S
I
G
N
S
Neovascularisation – disc (NVD), elsewhere in
retina (NVE), iris (rubeosis / NVI) or angle (NVA)
Vitreous hemorrhage
Tractional retinal detachment
Neovascular glaucoma
Clinical Stages of Retinopathy

27. Clinical Stages of Retinopathy
New vessels at the disc New vessels elsewhere

28. Clinical Stages of Retinopathy
Pre retinal haemorrhage

29. H
A
G
E
:
S
Y
M
P
T
O
M
S
Floaters
Severe visual loss
Requires immediate ophthalmologic
consultation
Clinical Stages of Retinopathy

30. Clinical Stages of Retinopathy
Severely distorted retinal architecture

31. Clinical Stages of Retinopathy
New vessel growth - rubeosis

32. INSULIN USERS Dx <AGE 30
Duration (yrs) PDR
Prevalence
5 negligible
10 25%
15 55%
Clinical Stages of Retinopathy

33. INSULIN USERS Dx >AGE 30
Duration (yrs)
PDR Prevalence
20 20%
Clinical Stages of Retinopathy
PDR less common among noninsulin
users

34. REVIEW OF CLINICAL STAGES
NPDR: Patients may be asymptomatic
Severe NPDR: Laser therapy at this stage may
help prevent long-term visual loss
PDR: Major cause of severe visual loss
Clinical Stages of Retinopathy

35. Diagnosis
Slit-lamp biomicroscopy Indirect ophthalmoscopy

36. OCT

37. OCT – macular oedema

38. Diagnosis
Fundus photography Fluorescein angiography

39. Diagnosis
Dark, hypofluorescent patches indicative of ischemia
Late leak suggestive of new vessels

40. Treatment
Laser photocoagulation surgery

41. ETDRS
Macular laser for CSMO reduces risk of MVL
Panretinal laser for high risk PDR
Aspirin not useful for DR but also did not
increase vitreous haemorrhage
Treatment

42. Macular laser

43. Treatment
Acute panretinal laser photocoagulation burns

44. Treatment

45. C
O
A
G
U
L
A
T
I
O
N
(
P
R
P
Outpatient procedure
Approximately 1000 to 2000 burns per session
1 to 3 sessions
Treatment

46. PRP: SIDE EFFECTS
Decreased night vision
Decreased peripheral vision
Treatment

47. Intravitreal injections
Avastin or Lucentis – anti VEGF
Triamcinolone – steroid causes cataract and
glaucoma

48. Intravitreal triamcinolone

49. VITRECTOMY
Remove vitreous hemorrhage
Repair retinal detachment
Allow treatment with PRP
Treatment

50. Treatment

51. Treatment

52. I
O
N
S
:
S
U
M
M
A
R
Y
Laser photocoagulation surgery
Focal macular laser for CSME
Panretinal photocoagulation for PDR
Intravitreal injections
Avastin
Lucentis
Triamcinolone
Vitrectomy
May be necessary for vitreous hemorrhage or retinal
detachment
Treatment

53. T
I
E
N
T
S
W
I
T
H
T
Y
P
E
1
Annual ophthalmologic exams starting 5 years after
diagnosis and not before puberty
Screening Guidelines

54. PATIENTS WITH TYPE 2 DIABETES
Annual ophthalmologic exams starting at time
of Dx
Screening Guidelines

55. DIABETES AND PREGNANCY
Ophthalmologic exam before conception
Ophthalmologic exam during first trimester
Follow-up depends on baseline grade
Screening Guidelines

56. S
K
O
F
B
L
I
N
D
N
E
S
S
Team approach: primary care physician,
ophthalmologist, nutritionist, endocrinologist,
nephrologist
Access to eye care
Early treatment of DR
Systemic control
Conclusion