brief idea about eye disease in diabetes and its treatment according to recent guidelines in 2016

2. INTRODUCTION
• Diabetic retinopathy is one of the leading cause of blindness.
• Duration of diabetes is a major risk factor associated with the
development of diabetic retinopathy. After 5 years,
approximately 25% of Type 1 patients will have retinopathy.
After 10 years, almost 60% have retinopathy, and after 15
years, 80% have retinopathy.
• In type 2 DM, it depends on
• Duration of disease
• Accompnying hypertension
• And smoking

3. CLASSIFICATION OF DIABETIC
RETINOPATHY
1. Non –proliferative diabetic retinopathy (NPDR)
• Mild
• Moderate to severe
2. Proliferative diabetic retinopathy(PDR)
3. Maculopathy
• Diffuse or focal
• CSME
• Ischemic maculopathy

5. DEFINITION OF DME
• It is the retinal thickening caused by intraretinal leakage of fluid
primarily in inner and outer plexiform layer due to increased
capillary permiability
• It can be present with any level of DR
• RISK FACTORS
• Duration of Diabetes Mellitus (DM)
• Poor control of DM with chronically elevated hemoglobin
A1c (HbA1c)
• Hypertension
• Hyperlipidemia

7. PATHGENESIS
Normal retinal capillaries are non fenestrated and has blood
retinal barrier that does not allow leakage of fluid
Retina also does not have lymphatic system, so leaked fluid is
accumulated and cause edema
Chronic hyperglycemia-related accumulation of advanced
glycated end products (AGEs) causes disruption of the blood
retinal barrier (BRB) and an altered vitreo-retinal interface.
Altered BRB leads to interstitial fluid accumulation within the retina
and, in some cases, cyst formation, particularly in the perifoveal
retina.

8. Histopathological examination of the eyes with
diabetic retinopathy shows
• loss of intramural pericytes,
• thickening of the basement membrane and
• progressive closure of the retinal capillaries.
• The initial loss of pericytes leads to dilatation of the vessels
(microaneurysm, the first sign seen on fuduscopy) and
breakdown of BRB
In addition there is increased aggregation of platelets,
causing capillary non perfusion
• Extensive closure of capillaries leads to ischaemia
that leads to opening of shunt vessels “IRMA” and
neovascularisation by elaborating VEGF

9. CSME
It is defined as edema or hard exudates within 500 micrometer of
the foveal centre or
Edema of more than one disc area in extent, any part of which is
within 1 DD of the foveal centre

10. DIFFRENTIAL DIAGNOSIS
• ARMD (Exudative)
• BRVO
• CRVO
• Hypertension maculopathy
• Irvine-Gass syndrome
• Uveitis
• Epinephrine use in aphakia
• Hypotonic retinopathy
• Ruptured microaneurysm
• Radiation retinopathy
• Subfoveal choroidal neovascularization

11. DIAGNOSTIC PROCEDURES
• Optical coherence tomography (OCT)
OCT shows three basic structural changes:
1. retinal swelling,
2. cystoid macular edema, and
3. subretinal fluid.

12. OCT is a more sensitive method for objective evaluation of vitreo-macular traction
and
for measurement of macular thickness.
OCT is more sensitive at detecting retinal thickening than is biomicroscopy.
Experienced examiners generally cannot detect retinal thickening until retinal
thickness is ≥ 300 µm.
OCT is not required to establish the diagnosis according to current guidelines but its
an additional modality that allow identification and evaluation of macular pathology
And it also allow presice and reproducible way to monitor macular edema

13. FFA
Fluorescein Angiography (FA) FA is performed to identify leaking
microaneurysms or capillaries and areas of retinal ischemia.
Leakage on the angiogram is not synonymous with retinal
edema.
Focal CSME is characterized by focal leakage from
microaneurysms or capillaries
whereas diffuse DME is diagnosed when poorly demarcated
areas of leakage are present on the FA.

15. MANAGEMENT
• DIET
• LIFESTYLE CHANGES
PREVENTION
• People with Type 1 diabetes should have annual screenings for diabetic
retinopathy beginning 5 years after the onset of their disease,
• whereas those with Type 2 diabetes should have a prompt examination at
the time of diagnosis and at least yearly examinations thereafter.
• Women who develop gestational diabetes do not require an eye
examination during pregnancy
• However, patients with diabetes who become pregnant should be examined
early in the course of the pregnancy.

16. TREATMENT
MEDICAL CARE
Control of diabetis
Life style modification
Diet
OCCULAR TREATMENT
LASER
Anti VEGF
Steroids

17. LASER Photocoagulation (Focal or Grid)
GOALS
• To reduce progression
• It reduces the risk of moderate visual loss from diabetic macular
edema by 50%, from 24% to 12% 3 years after initiation of
treatment.
TIMING
• It is most effective when initiated before visual acuity is lost from
diabetic macular edema
• LASER treatment of DME should precede PRP by at least 2-6
weeks because PRP before this has been known to worsen
DME.
• PRP should not be delayed in very severe NPDR or high risk
PDR.
Multiple sessions over many months are frequently necessary for
resolution of DME

18. Side effects and complications of focal
LASER
• Paracentral scotomata
• Transient increased edema/decreased
vision
• Choroidal neovascularization
• Subretinal fibrosis
• Inadvertent foveolar burns

19. Normal or Minimal NPDR
• The patient with a normal retinal examination or
minimal NPDR (i.e., with rare microaneurysms)
should be re-examined annually, because within
1 year 5% to 10% of patients without
retinopathy will develop diabetic retinopathy.
• Laser, color fundus photography, and FA are not
necessarily indicated.

20. Mild to Moderate NPDR without Macular Edema
• Patients should be re-examined within 6 to 12 months, because
disease progression is common.
• Laser and FA are not indicated for this group of patients.
• Color fundus photography and OCT imaging of the macula may
occasionally be helpful to establish a baseline for future
comparison and for patient education.
• Patients with macular edema that is not clinically significant
should be re-examined within 3 to 4 months, because they are
at significant risk of developing CSME.

21. Mild to Moderate NPDR with CSME
• Fluorescein angiography prior to laser surgery for CSME is
often helpful for identifying treatable lesions.
• Fluorescein angiography is less relevant when there are
circinate lipid exudates and the leaking lesions are clearly
detected within the lipid ring.
• Fluorescein angiography is also useful for detecting capillary
dropout and pathologic enlargement of the foveal avascular
zone, a feature that may be useful when planning treatment
The traditional treatment for CSME has been laser.
However, current data from multiple well-designed studies
demonstrate that intravitreal anti-VEGF agents provide a more
effective treatment for center-involved CSME than monotherapy
with laser.

22. Anti-VEGF Therapy
• At the present time, anti-VEGF therapy is the initial treatment
choice for center-involving macular edema, with possible
subsequent or deferred focal laser treatment.
• The Ranibizumab for Edema of the mAcula in Diabetes (READ-
2) study involved 126 patients randomized to either anti-VEGF
therapy (in this case ranibizumab alone), laser alone, or
focal/grid laser combined with anti-VEGF therapy.
• The group that received anti-VEGF therapy alone or with laser
treatment did better than the group treated with laser alone.
• The Diabetic Retinopathy Clinical Research Network
(DRCR.net) also showed that anti-VEGF with either prompt or
deferred laser photocoagulation was better than either laser
alone or laser combined with triamcinolone acetonide.

23. • Bevacizumab or Laser Treatment (BOLT) study also showed
favorable outcomes for bevacizumab use over macular laser
treatment in eyes with ci-CSME.
• The DME and VEGF Trap-Eye: Investigation of Clinical Impact
(DA VINCI) study demonstrated better outcomes using
aflibercept over laser treatment for ci-CSME.
• Most recently, the DRCR.net protocol T demonstrated that
anti-VEGF therapy using bevacizumab, ranibizumab, or
aflibercept is an effective treatment for center-involving CSME.
However, at worse levels of initial visual acuity (20/50 or
worse), aflibercept was more effective at improving visual
acuity than the other anti-VEGF agents tested.

24. • With the advent of anti-VEGF therapy for macular edema, many
retina specialists prefer to use a modified ETDRS(Early
Treatment Diabetic Retinopathy Study) treatment approach.
• This includes a less intense laser treatment, greater spacing,
directly targeting microaneurysms, and avoiding foveal
vasculature within at least 500 µm of the center of the macula.

25. Severe NPDR and Non-High-Risk PDR
• Severe NPDR and non-high-risk PDR are discussed together
because the ETDRS data showed that they have a similar
clinical course and subsequent recommendations for treatment
are similar.
• the ETDRS suggested that panretinal photocoagulation should
not be recommended for eyes with mild or moderate NPDR,
provided that follow-up could be maintained. When retinopathy
is more severe, panretinal photocoagulation should be
considered

26. • Careful follow-up at 3 to 4 months is important:
• if the patient will not or cannot be followed closely or if there are
associated medical conditions such as impending cataract
surgery or pregnancy, early laser panretinal photocoagulation
may be warranted
• Currently, the role of anti-VEGF therapy in the management of
severe NPDR and non-high-risk PDR is under investigation.

27. High-Risk PDR
• New vessels within one disc diameter of the optic nerve head
that are larger than one-quarter to one-third disc area in size
• New vessels elsewhere that are at least one-half disc area in
size
• Vitreous or preretinal hemorrhage
• Very recently, the DRCR.net study protocol S has demonstrated
that alternative use of anti-VEGF agents (ranibizumab was used
in this protocol), may be an alternative to PRP.
• However, many feel that PRP remains the first choice for
management of PDR. The anti-VEGF alternative could be
considered for patients who can follow-up regularly.
• Further studies are required to determine the long-term
implications of using anti-VEGF agents alone.

28. Additional panretinal photocoagulation, anti-VEGF therapy, or
vitrectomy surgery may be necessary for the following
situations:
• Failure of the neovascularization to regress
• Increasing neovascularization of the retina or iris
• New vitreous hemorrhage
• New areas of neovascularization