ophthalmology guidelines

1. Dr/Reyad Abo-Yossif
Ophthalmology specialist

5. Screening of diabetic patients:
* type 1 diabetes:
- all individuals ≥ 15 age,
-5 years after diagnosis,
*type 2 diabetes at diagnosis.
If retinopathy is detected, then sight-threatening DR treatment
should be introduced.
Monitoring of the disease progress to be continued at least once per
year.
If DR is not present, then re-screening rhythm should be assigned,
annually in all type 1 diabetes and type 2 diabetes every 1-2 years

6. AAO recommends follow up of DME progression at annual
basis, irrespectively to type of mellitus

7. In diabetes, vision loss is most commonly the result of:
-diabetic retinopathy (DR) (neovessels)
-diabetic macular edema (DME)

9. DME
Structural changes of DME are characterized by the
accumulation of liquid and hard exudates in the outer
plexiform and inner nuclear layers of the macula and
formation of fluid-filled cystoid spaces.

10. (WESDR) in the USA found that 20% of patients with type
1 diabetes and 14%-25% of patients with type 2 diabetes
developed DME over a 10-year follow up period.

15. RT values are classified as:
1. normal
2. borderline
3. edema (definite thickening)

17. 1. Fixation Point:
thickness at the point of fixation, as reported in the
Table “Eye Information” of the Retinal Map.
Normal: 150 ± 20m
Borderline: 170–210m
Edema: ≥ 210m

18. 2. Central Zone:
Normal: 170 ± 20m
Borderline: 190–230m
Edema: ≥230m

19. 3. Perifoveal and peripheral areas:
Normal: 230 ± 20m
Borderline: 250–290m
Edema: ≥290m

24. On the authority of Wilkinson et al. Diabetic Macular
Edema
is classified to:
mild – where some retinal thickening or hard
exudates in posterior pole but outlying from the
center of the macula,
moderate where retinal thickening or hard
exudates approaching the center of the macula but
not involving the center and
severe, where retinal thickening or hard exudates
involving the center of the macula

25. Diabetic macular edema develops and progresses as a
result of the interaction of different non-modifiable and
modifiable risk factors

26. Diabetes duration is the most important ( non-
modifiable) risk factor directly associated with the
incidence and prevalence of DME in patients with both
types of diabetes.

27. Hyperglycemia is the strongest (modifiable risk
factor) for the development and progression of DR and
DME.
The Diabetes Control and Complications Trial (DCCT) in
type 1 diabetes and the United Kingdom Prospective
Diabetes Study (UKPDS) in type 2 diabetes found that
tighter control of glycemia (HbA1c ≤7%) significantly
reduced the risk of development and progression of DR,
DME, vitreal hemorrhage and need for laser treatment, as
well as the risk of blindness.

28. The DCCT also found that intensive glycemic control was
associated with 46% reduction in the incidence of DME
at the end of the trial and 58% reduction 4 years later
compared with those in the conventional group.

29. Hypertension is also an important modifiable risk
factor for DME.
Each 10-mm Hg increase in systolic blood pressure was
associated with an approximately 15% additional risk
of DME.
In the UKPDS, patients with hypertension with tight
blood pressure control had a 34% reduction in the rate
of progression of DME and 47% reduction in
deterioration of visual acuity (VA).

30. Some clinical trials also showed that specific blood pressure-
lowering medications that target the renin-angiotensin
system had additional beneficial effects on DR and DME,
independently of their hypotensive actions.

31. Dyslipidemia has a significant role in the
pathogenesis of DME;
some studies report that serum lipids were
independently associated with DME.
The Fenofibrate Intervention and Event Lowering in
Diabetes (FIELD) study showed that fenofibrate
reduced the frequency of laser treatment for DME by
31% in type 2 diabetes

32. Other non-modifiable and modifiable risk factors are
puberty, pregnancy, genetic factors, nephropathy,
obesity and smoking

34. RCO identifies four main therapeutic options of the DME
treatment.
These are :
-laser photocoagulation,
-intravitreal steroid treatment,
- intravitreal VEGF inhibitors
-polytherapy of laser photocoagulation + anti-VEGF or +
intravitreal steroid treatment

35. Traditional Treatment of DME

36. Ideal metabolic control of diabetes, assuming strict
control of well-known modifiable risk factors of
hyperglycemia, hypertension, dyslipidemia and others, is
the primary goal of treatment and the basic way of
preventing and stopping the progression of DME.

37. Laser photocoagulation has been the primary treatment for
DME since the early 1980s.
The role of laser in preventing visual loss and blindness due to
DME was established in 1970s-1980s by two large studies, the
Diabetic Retinopathy Study (DRS) and the Early Treatment
Diabetic Retinopathy Study (ETDRS)

38. The ETDRS demonstrated that photocoagulation reduced
the risk of moderate vision loss caused by DME in about
50% of the eyes, in only 3% of eyes this therapy led to
improvement of VA, and in the rest VA unfortunately
remained poor due to persistence of macular edema

39. According to the studies referred by Canadian experts,
laser treatment reduces loss of vision by 90% in severe
DR proliferative on non-proliferative retinopathy and by
50% the incidence of visual loss in clinically significant
macular edema (CSDME)

43. The potential complications of macular laser include :
laser scar expansion, paracentral scotomata, elevation of
central visual field thresholds, secondary choroidal
neovascularization and subretinal fibrosis.

44. Novel Treatment Options for DME

45. DRCR Network group recommends a modified ETDRS
focal/grid laser regimen(MLT) as follows:
all leaking microaneurysms 500 to 3000 μm from fovea
should be treated directly with 50 μm spot size,
duration 0.05-0.1 s and intensity to achieve grayish
reaction; grid treatment should be performed to areas
of retinal thickening from 500 to 3000 μm superiorly
and inferiorly and to 3500 μm temporally with a
space of two burns width apart

48. Corticosteroids
Corticosteroids are potent anti-infl ammatory agents
that can counteract many of the pathological processes
thought to play a role in the development of macular
edema.
They prevent leukocyte migration, reduce fibrin
deposition, stabilize endothelial cell tight junctions,
and inhibit synthesis of vascular endothelial growth factor
(VEGF), prostaglandins and pro-inflammatory cytokines

51. Recently, the DRCR.net found that IVTA had best effect on
VA improvement within 4 months of the application and
that this effect was transient.
A longer-lasting and doubling effect on VA was achieved
only by using the IVTA plus focal/grid laser treatment

52. Anti-VEGFs
Four VEGF-binding agents are currently used for
ocular diseases:
pegaptanib, bevacizumab (off -label), ranibizumab
and afl ibercept.

53. DRCR.net Protocol T showed that intravitreal aflibercept,
bevacizumab and ranibizumab improved vision in eyes
with center-involved DME, but the relative effect depended
on baseline VA.
When the initial VA loss was mild, there were no
differences among study groups.
At worse levels of initial VA, aflibercept was more effective
in improving vision

55. The ICO classifies diabetic eyes as having :
-no Diabetic Macular Edema,
-non-central involved DME and
-central-involved DME

56. For non-central involved DME, ICO experts recommend
the disease progress assessment every 3 months,
for central involved DME every 1 month

58. ICO guidelines pay special attention to OCT, describing
this method as the most sensitive in DME identification,
that allows quantitative disease assessment

59. laser photocoagulation persists preferred treatment for
noncenter-involving macular edema

60. Patients with high levels of sub-retinal hard exudates and
increased serum lipids might be at higher risk of sub-
retinal fibrosis development after the photocoagulation

61. ICO guidelines consider laser photocoagulation for both
non-central involved and central involved DME.
For non-central involved DME focal laser is advised to
leaking microaneurysms‚ if thickening is threatening the
fovea’.
No treatment is recommended to lesions closer than 300-
500 μm from the center of the macula

62. For central involved Diabetic Macular Edema, ICO
proposes laser photocoagulation as therapeutical option
for eyes with good or without good visual acuity, but
always as secondary choice, especially in eyes with
persistent retinal thickening despite anti-VEGF treatment,
when anti-VEGF treatment is not available or monthly
follow up is not possible

63. AAO guidelines recognize intravitreal injections of VEGF
inhibitors as effective treatment and based on the many
studies showing visual acuity improvement in DME
patients,
these should be considered as first choice therapy for
center-involving DME

64. In the first year of treatment 8-10 injections are
considered, in the second year 2-3 injections, in the third
year 1-2 injections and in the fourth and fifth year
of treatment 0-1 injections

66. As per ICO guidelines for eyes with persistent retinal
thickening complementary treatment of laser
photocoagulation is considered

67. International Council of Ophthalmology guidelines
identify precisely five indications for vitrectomy in DME
(13):
1. Severe vitreous hemorrhage of minimum 1-3 months
duration that does not disappear automatically.
2. Advanced active proliferative DR that persists despite
extensive pan retinal photocoagulation.
3. Recent traction macular detachment.
4. Combined traction-rhegmatogenous retinal
detachment.
5. Tractional macular edema or epiretinal membrane
involving the macula.