1. Diabetic retinopathy screening NSF-based training
Anatomy and physiology
Tunde Peto
Head of Reading Centre

2. Anatomy and physiology of the normal human eye
Key issues for discussion
Review the gross anatomical structures within and related to the eyeball and discuss their basic function
Review the basic physiology of refraction and vision
Learning outcome
Identify the different structures of the eye and discuss their basic function
Identify different anatomical structures on teaching slides

3. Basic Science in relation to eye disease: the normal retina and vision
Key issues for discussion
The normal anatomy of the retina
Photoreceptors and their biochemistry
Physiology of vision including colour vision
Learning outcome
Identify normal retinal structure on teaching slides

4. Vision Reflected light translated into mental image
Pupil limits light, lens focuses light
Retinal rods and cones are photoreceptors
Figure 10-36: Photoreceptors in the fovea

5. Photoreceptors
Rods – monochromatic, provide night vision: most numerous in periphery, sees all shades of grey and white; see in dark and around us
Peripheral changes might not affect the vision at all
Laser treatment and retinal detachment might result in visual field loss
Cones – red, green, & blue; color & details, most numerous in macula; you need very few for good vision!

6. Photoreception and Local Integration
Figure 10-35: ANATOMY SUMMARY: The Retina

7. Retina: More Detail
Figure 10-38: Photoreceptors: rods and cones

8. Vision: Integration of Signals to Perception
Bipolar
Ganglion
Movement
Color
Optic nerve
Optic chiasm
Optic tract
Thalamus
Visual cortex
Figure 10-29b, c: Neural pathways for vision and the papillary reflex

9. The aging retina: Age Related Maculopathy (ARM) and Macula Degeneration (AMD)
Key issues for discussion
Normal changes in the aging retina
Abnormal changes in the aging retina
The constituents of drusen
Geographic atrophy
Neovascular AMD
Learning outcome
Identify age related changes in the retina
Identify and discuss different types of drusen
Identify geographic atrophy
Identify and discuss the main features of neovascular AMD

10. Hard drusen (<63 mikron)

11. Normal SLO image

12. Hard and intermediate soft drusen (63-125 mikron)

13. Large soft Drusen on the posterior pole
Watch it developing over the years

14. 2 years later

15. 5 years later

16. 7 years later

17. 10 years later: some areas atrophied

18. Geographic Atrophy

19. Neovascular membrane at the fovea

20. Neovascular membrane at the fovea

21. FFA of the neovascular membranes: R eye: occult, L eye classic membrane

22. Right eye: occult membrane

23. Left eye: classic membrane

24. Fibrovascular scar and secondary atrophy

25. Neovascular membrane on SLO imaging

26. Pigment epithelial detachment: colour image

27. Pigment epithelial detachment on FFA

28. Pigment epithelial detachment: SLO image

29. Vascular occlusion Key issues for discussion
Learn normal vasculature of the eye
Discuss most common systemic causes of vascular problems in the eye
Discuss vein occlusion
Discuss arterial occlusion
Discuss clinical implications of these diseases
Learning outcome
Identify normal and abnormal vascular structures in the eye on teaching slides
Identify strategies to deal with these diseases

30. Central retinal vein occlusion: Introduction
dilated, tortuous veins & haems in all 4 quadrants
ischaemic (iCRVO) vs. non ischaemic (niCRVO)
ischaemic = non perfused, haemorrhagic
non-ischaemic = perfused, venous stasis retinopathy

31. Epidemiology (EDCCS)
2 per 1000 > 40 years, per 1000 > 64 years
33% ischaemic, 67% non ischaemic
13% < 45 years, 11% years, 76% > 55 years

32. Clinical features reduced visual acuity RAPD
retinal predictors of ischaemia
degree of intraretinal haemorrhage
venous dilatation
venous tortuosity
as chronicity develops
IRMA, microaneurysms, collateral vessels

34. Complications macular oedema, ischaemia NVE / NVD (6-7%)
iris neovascularisation (NVI), neovascular glaucoma (NVG) (21%)
cilioretinal artery occlusion
combined with CRAO

35. Large areas of ischaemia on FFA

36. Iris neovascularisation

37. Comined with CRAO: cherry red spot with white macula

38. Classification ischaemic vs non-ischaemic young vs old
two ends of a spectrum
elderly: if severe, retinal capillaries decompensate, iCRVO
young: if mild or moderate, retinal capillaries withstand increased venous pressure, niCRVO
young vs old
 40 yrs, 64% final VA  6/9
> 40 yrs, 40% iCRVO

39. Good perfusion on FFA

40. Poor peripheral perfusion on FFA

41. Differential diagnosis
Anterior ischaemic optic neuropathy / optic neuritis / optic nerve invasion
asymmetrical diabetic retinopathy
ocular ischaemic syndrome
severe anaemia, leukaemia
Waldenstroms macroglobulinaemia
carotico-cavernous fistula

42. Branch retinal vein occlusion
A cause should be found for it!
Most common caused: diabetes mellitus, hypertension and lipid abnormalities
Investigations need to be done by the referring physician, not in screening setting, however, you need to notify the physician
You will find asymptomatic old BRVO-s in screening setting

45. Embolic disease: local protocol, but requires GP notification so risk factors for stroke and sight threatening disease can be addressed

46. The normal optic nerve and its pathological changes
Key issues for discussion
Learn the normal anatomy of the optic nerve
Discuss the function of the optic nerve and its connection to the brain
Discuss major illnesses affecting the optic nerve
Discuss the main features of the glaucomatous changes of the optic nerve
Learning outcome
Identify the main features of the optic nerve and discuss the function
Identify normal optic nerve on teaching slides
Identify the main features of the diseases optic nerve

47. The Normal Optic Nerve Head
 The optic nerve head can be imagined as a ‘plug-hole’ down which over 1 million nerve fibres descend through a sieve-like sheet known as the lamina cribrosa. These fibres are then bundled together behind the eye as the optic nerve which continues towards the brain.
 The retinal nerve fibres are spread unevenly across the surface of the retina in a thin layer. As the nerve fibres converge on the edge of the disc they pour over the scleral ring and then down its inner surface. This dense packing of nerve fibres just inside the scleral ring is visualized as the neuroretinal rim.
 The inner (with respect to the centre of the optic nerve head) edge of this neuroretinal rim marks the most central of the nerve fibres. This edge is usually sloped, yet may be range from an overhang to vertical to a gentle slope towards the centre of the disc. This inner edge marks the cup edge.

48. Scleral Ring Cup Edge Neuro-retinal rim Outer edge
Inner edge (outer edge of disc or neuroretinal rim
Neuro-retinal rim
Cup Edge
Change in direction of blood vessel

49. The Scleral Ring
This ring is usually pale allowing it to be distinguished from the neuroretinal rim tissue which is pink. The ring may not be visible in a given disc image, or the visibility may vary in different areas of the circumference of the disc. It is often easier to see on the temporal side of the disc than on the nasal side.

50. Scleral ring Inner Outer
As vessels bridge the scleral ring, they often make a slight change in direction (black arrow) which may be a clue to its inner edge,
The change in colour is also evident in this case (arrows mark inner and outer edges)
Blurring of the image may occur due to media opacity or resolution of the image- this can make appreciation of the anatomy difficult.
Inner
Outer

51. The Cup edge
This is undoubtedly the most difficult contour to identify, and is subject to more variability than the disc edge.
The inner edge of the neuroretinal rim (=cup edge) may be sloped (especially on the temporal side of the disc) or vertical. In some cases the edge may be an overhang.
The most effective way of drawing this ring is to identify certain points on the cup edge where you are sure of its location, and then using a dot-to-dot procedure link up these points into a ring. First look for a blood vessel, preferably a small to medium-sized one (large vessels do not hug the surface and may not be tethered to the surface and therefore are unhelpful). Trace its path across the scleral ring and then over the rim tissue- at some point it will change direction as it bends inward towards the centre of the disc. If the slope is shallow this will be a gradual change in direction, however if vertical it will be an obvious bend, and in the case of an overhang it will suddenly disappear from view. It is the point of maximum change of direction of the vessel that marks the cup edge. When viewing the disc in stereo, the edge of the cup can often be clearly seen in areas where there are no vessels as a guide.
There can be a temptation to mark the cup edge where the colour changes from the pink of the rim to the pallor of the cup. In many situations this would be correct, yet in some situations the edge of pallor is not necessarily the edge of the cup, and hence it is better to rely on vessels and stereo cues as described above.
The following images illustrate these points.

52. The cup edge The Cup Edge:
3 blood vessels here show the edge of the cup:
The points of maximum inflection (bend) are marked by arrows.

53. The cup edge
Cup Edge:
In this very clear image, the arrows mark the cup edge. This illustrates that occasionally large vessels may obscure the edge from view, and in this case one should mark points of certainty either side of the vessel and link these up.

54. Optic nerve head assessment
Dr. Patricio Schlottmann
Research Fellow
Glaucoma Research Unit

55. Overview
Glaucoma definition
Anatomy
Risk factors
Cup/disc

56. Definition
Glaucoma is a chronic, progressive optic neuropathy that manifests by a characteristic Visual Field loss and distinctive structural changes recognizable at the level of the Optic nerve head or the Retinal Nerve Fibre Layer (RNFL)

57. Definition Chronic: having a progressive course of indefinite duration
Progressive: tending to become more severe
Optic neuropathy: disease of the of the optic nerve

58. Definition Optic neuropathy
The ganglion cells and their axons are the damaged structures
Other cells within the retina are also affected

59. Anatomy

60. Anatomy

61. Risk Factors Major risk factors for developing glaucoma are:
1. elevated intraocular pressure
2. African descent
3. family history of glaucoma
4. increased age

62. Risk factors
Elevated intraocular pressure

63. Risk factors African derived individuals
Glaucoma is 4 times more prevalent
Is usually more severe
Starts at earlier age
Progresses more rapidly

64. Risk Factors Family history of glaucoma
A first degree relative affected by glaucoma increases the risk of developing the disease in the future
Patients should be questioned about the severity of glaucoma in the affected relative

65. Risk Factors Increased age Prevalence increases with age
It is 10% of subjects over 80 years

66. Cup/disc Definition Relationship between cup area and disc area Disc

68. Cup/disc
Examples
0.3
0.5
0.1
0.7
0.8
0.95

69. What to look for? Large cup/disc Asymmetry Haemorrhages >0.7-0.8
> between eyes
Haemorrhages

70. What to look for? Notches Areas of thinning Focal loss of fibres
Diffuse thinning of the rim

71. Screening for glaucoma
Too many false positives
2% subjects over 40
Advanced condition is easier to diagnose

72. What to do with a suspect?
They will need referral to eye department
Phenotyping
Decision on treatment or observation

73. Phenotyping Complete evaluation of the patient Medical history
Risk factors
Medications
Scans VF
Clinical examination w/dilation
3 hours visit

74. Examples

75. Examples

76. Examples

77. Examples