3. Criteria for the Diagnosis of Diabetes Mellitus
• Symptoms of diabetes plus random blood
glucose concentration 11.1 mmol/L (200
mg/dL)or
• Fasting plasma glucose 7.0 mmol/L (126
mg/dL)or
• Two-hour plasma glucose 11.1 mmol/L (200
mg/dL) during an oral glucose tolerance test
4. Risk Factors for Type 2 Diabetes
Mellitus
•Family history of diabetes (i.e., parent
or sibling with type 2 diabetes)
•Obesity (BMI 25 kg/m2)
•Habitual physical inactivity
•Race/ethnicity (e.g.,African American,
Latino, Native American,Asian
American, Pacific Islander)
•Previously identified IFG or IGT
5. •History of GDM or delivery of baby >4
kg (>9 lb)
•Hypertension (blood pressure 140/90
mmHg)
•HDL cholesterol level <35 mg/dL (0.90
mmol/L) and/or a triglyceride level
>250 mg/dL (2.82 mmol/L)
•Polycystic ovary syndrome or
acanthosis nigricans
•History of vascular disease
7. DIABETIC RETINOPATHY
Diabetes – sustained hyperglycemia secondary to
lack, or diminished efficacy of endogenous insulin
2 main types of diabetes
• Insulin dependent diabetes (IDD)
• 10 -20 years of age
• Non-insulin dependent diabetes (NIDD)
• 50 – 70 years old
8. Diabetic retinopathy
• Leading cause of legal blindness in individuals between
the ages of 20 and 65 years
Risk factors for diabetic retinopathy
1.Duration of diabetes – most important factor
2.Poor metabolic control
3.Other factors – pregnancy, hypertension, renal
disease, anemia
9. Pathogenesis of DR
DR is a microangiopathy affecting the retinal
precapillary arterioles, capillaries and venules.
Large vessels may also be involved. Retinopathy
has features of both microvascular occlusion
and leakage.
10. Microvascular occlusion:
• Thickening of basement membrane
• Capillary endothelial cell damage and
proliferation
• Changes in red blood cells leading to defective
oxygen transport
• Increased stickiness and aggregation of
platelets
11. Pathogenesis of DR
Microvascular occlusion
↓
Retinal capillary non-perfusion
↓
Retinal ischemia
↓
Retinal hypoxia
↓
AV shunts (IRMA) & neovascularization
15. The hard exudates are composed of lipid
and proteinaceous material, such as
fibrinogen and albumin that leak from the
impaired blood–retinal barrier. They are
deposited primarily in the outer plexiform
layer of the retina.
16.
17. Microvascular leakage
Pathogenesis
The cellular elements of retinal capillaries consists
of endothelial cells and pericytes.These elements
are responsible for the structural integrity of the
vessel wall.
In DM there is reduction of pericytes which causes
distention of capillary walls and breakdown of
blood retinal barrier, leading to leakage of plasma
constituents into the retina (increased vascular
permeability) leading to retinal edema.
18. Reduction in number of pericytes
↓
Distended capillary walls
& breakdown of blood retinal barrier
↓
Leakage of plasma constituents into the retina
↓
Retinal edema
↓
Exudates
PATHOGENESIS OF DIABETIC RETINOPATHY
20. SIMPLE BACKGROUND DR
1. Microaneurysms (saccular pouches due to capillary
distention)
- First clinically detectable lesion of DR
- Small round dots usually temporal to the macula
2. Hemorrhages
3. Hard exudates – yellow waxy appearance with
distinct margins
4. Retinal edema
21.
22.
23. Signs of background diabetic retinopathy
Microaneurysms usually
temporal to fovea
Intraretinal dot and
blot haemorrhages
Hard exudates
frequently
arranged in clumps or
rings
Retinal oedema seen as
thickening on biomicroscopy
24. PREPROLIFERATIVE DR
- Lesions are caused by retinal ischemia
1. Vascular changes
2. Dark blot hemorrhages (hemorrhagic retinal infarcts)
3. Cotton wool spots caused by capillary occlusion
4. Intraretinal microvascular abnormalities
25. Preproliferative diabetic retinopathy
Treatment - not required but watch for proliferative disease
• Cotton-wool spots
• Venous irregularities
• Dark blot haemorrhages
• Intraretinal microvascular
abnormalities (IRMA)
Signs
27. Indications for treatment of proliferative
diabetic retinopathy
NVD > 1/3 disc in area Less extensive NVD
+ haemorrhage
NVE > 1/2 disc in area
+ haemorrhage
28. TREATMENT
1. Medicine
anti-VEGF medicine: aflibercept, bevacizumab, or ranibizumab.
These medicines block the growth of abnormal blood vessels in the eye.
These can stop further vision loss and may improve vision in some people.
2. Laser photocoagulation
aim: to induce involution of new vessels and prevent recurrent vitreous
hemorrhage
COMPLICATIONS
1. Persistent intragel vitreous hemorrhage
2. Retinal detachment
3. Opaque membranes
4. Burnt-out stage – increase in fibrous component and decrease in vascular
component
5. Rubeosis iridis
29. • Spot size (200-500 m)
depends
on contact lens magnification
• Gentle intensity burn (0.10-0.05 sec)
• Follow-up 4 to 8 weeks
• Area covered by complete PRP
• Initial treatment is 2000-3000 burns
Laser panretinal photocoagulation
30. Indications for vitreoretinal surgery
Retinal detachment involving
macula
Severe persistent vitreous
haemorrhage
Dense, persistent premacular
haemorrhage
Progressive proliferation
despite laser therapy