Diabetic Retinopathy

Waseem Al-Zamil, MD.

 the two main types of diabetes :
 Insulin-dependent diabetes (IDD):
- known as type 1 .
- develops most frequently between 10 and 20
years of age .
 Non-insulin-dependent diabetes (NIDD):
- also known as type 2.
- develops most frequently between the ages
of 50 and 70 years.
 Prevalence
 Diabetic retinopathy is a leading cause of new
cases of blindness in people aged 20 to 74 years .

 It has a considerable impact on both the patient

and the society because it typically affects
individuals in their most productive years .
 Prevalence
 Blindness is 25 more common in diabetics than
non diabetics.
 Prevalence of PDR is much more in type I than
type II.
 Diabetic retinopathy more sever in type I than
type II.
 Prevalence
 Macular edema :
NPDR : 2 -6 %
PDR : 20-63 %
 Macular edema :
20.1 % in younger onset group.
25.4 % in older onset group taking insulin
13.9 % in older onset group not taking insulin
 Prevalence
 The 25-year cumulative rate of progression of
DR in Type I was:
- progression of DR was 83%.
- progression to PDR was 42%.
- macular edema was 26%.

( WESDR Ophthalmology. 2008 Nov;115(11):1859-68 (

 RISK FACTORS
 The duration of diabetes :
 is the most important factor.
 In patients diagnosed as having diabetes before
the age of 30 years, the incidence of DR :
- after 10 years is 50%
- after 30 years is 90%
 RISK FACTORS
 It is extremely rare for DR to develop within 5
years of the onset of diabetes.

 about 5% of Type II have NPDR at

presentation perhaps due to the lag between
onset and diagnosis.
 RISK FACTORS
2 . Glycemic control :
 Good metabolic control of diabetes will not prevent
DR, although it may delay its development by a few
years.
 increased severity of diabetic retinopathy is associated
with poorer glucose control.
 insulin treatment is associated with a decreased risk of
either the development or progression of diabetic
retinopathy in patients with type 1 diabetes.
 RISK FACTORS
 With strict control of DM:
- risk of developing retinopathy was
reduced by 75% .
- 50% reduction in the rate of progression of
retinopathy in existing retinopathy
- early worsening of retinopathy is unlikely to
threaten vision .

Diabetes Control and Complications Trial Research Group N Engl J Med 1993; 329:977-986.
 RISK FACTORS
3 . Miscellaneous factors :
- pregnancy. (Hormonal changes )
- systemic hypertension.
- renal disease .
- anaemia.( ↓oxygen )
- elevated serum lipid.
- carotid artery occlusive disease.
- Alcohol. ( ? )
- Obesity.
 Ocular Risk Factors
 PVD :
• due to degenerative changes in the vitreous.
• significantly more common in diabetic subjects.
• complete PVD may prevent the development of
PDR because the hyaloid is needed as a scaffold
for retinal neovascularization.
• attached posterior hyaloid has also been
associated with an increased risk for DME
 Ocular Risk Factors
 High myopia :
• choroidal degeneration and extensive old
chorioretinopathy protect against DR.
• believed to act in the same manner as pan retinal
photocoagulation by reducing the metabolic
needs of the retina
 Ocular Risk Factors
 Removal of cataract :
• DR may progress after cataract surgery.
• Patient who have CSME, SNPDR or PDR
should undergo photocoagulation if the media is
sufficiently clear.
• If the cataract preclude retina evaluation and
treatment, prompt postoperative retinal
evaluation and treatment should considered.
 PATHOGENESIS
 Diabetic retinopathy is a microangiopathy
affecting the retinal precapillary arterioles,
capillaries and venules .
 Retinopathy has features of both:
- microvascular leakage. (mild- mod NPDR)
- microvascular occlusion .(sever NPDR-PDR)
 PATHOGENESIS
 Microvascular occlusion :
 thickening of the capillary basement
membrane.
 capillary endothelial cell damage and
proliferation.
 changes in red blood cells leading to
defective oxygen transport, and increased
stickiness and aggregation of platelets
 PATHOGENESIS

Microvascular occlusion

retinal ischaemia

retinal hypoxia

Arteriovenous shunts Fibrous glial cell Neovascularization

( IRMA ) proliferation
 IRMA

Fibrous glial tissue New vessel proliferation

proliferaion

Tractional RD
RD
 PATHOGENESIS
 Microvascular leakage :
- due to reduction in the number of pericytes .
- The pericytes are wrapped around the
capillaries and are thought to be responsible for
the structural integrity of the vessel wall.
- Development of retinal edema requires
accumulation of fluid which occurs if :

Leakage : Absorption :
- Microanurerysms. - Uptake from adjusent capillaries
- Incompetent capillaries - Healthy RPE cells
 PATHOGENESIS
Loss pericytes

Microvascular leakage

haemorrhage retinal oedema

Localized
Diffuse
Microanurysm” ”
 CLINICAL FEATURES
 Microaneurysms :
- located in the inner nuclear layer .
- the first clinically detectable lesions .
- small round dots .(20-200 μ)
- mostly located near and temporal to the macula.
- When coated with blood they may be
indistinguishable from dot haemorrhages.
 CLINICAL FEATURES
 Haemorrhages :
The clinical appearance depending on location
- 'dot' and 'blot' :
* originating from the venous end of the capillaries.
*located in the compact middle layers of the
retina .
- Flame-shaped :
* originate from the more superficial precapillary
arterioles, follow the course of the retinal nerve
fibre layer. (liner disribution)
 CLINICAL FEATURES
Hard exudates :
- located between the inner plexiform and inner
nuclear layers of the retina. (OPL)
- They are often distributed in a (circinate
pattern) .
- The centres of rings of hard exudates usually
contain microaneurysms .
- Made up of accumulated lipoproteins .
 CLINICAL FEATURES
 Retinal oedema :
- located between the outer plexiform and inner
nuclear layers.
- Later it may involve the inner plexiform and
nerve fibre layers, until eventually the entire
thickness of the retina may become oedematous.
- with further accumulation of fluid, the fovea
assumes a cystoid appearance .
 Macular edema types: (FFA + Clinical)
n Focal ME :which has identifiable leakage source.
n Diffuse ME: which has multiple unidentifiable
source of leakage.
n Cystoid ME: in which fluid accumulate in OPL
and INL to form cystoid spaces.
 Optical coherence tomographic
patterns of diabetic macular edema
 (1) spongelike retinal
swelling.

 (2) cystoid macular edema

(CME).

 (3) serous retinal

detachment (SRD).

Kim BY, Smith SD, Kaiser PK: Optical coherence tomographic patterns of diabetic macular edema. Am J
Ophthalmol 142(3):405-412, 2006
 CLINICAL FEATURES
 Vascular changes :
- venous changes :in the form of 'beading',
'looping' and 'sausage-like' segmentation.
- It represent endothelial cell proliferation.
- arterioles may also be narrowed and even
obliterated, resembling a BRAO .
- The most powerful predictors for
development of PDR.
 CLINICAL FEATURES
 Cotton-wool spots : (Soft exudates )
- Nerve fiber layer infarction.
- caused by capillary occlusion in the retinal
nerve fibre layer.
- The interruption of axoplasmic flow caused by
the ischaemia, and subsequent build-up of
transported material within the nerve axons, is
responsible for the white and opaque
appearance of these lesions.
- Disappear within weeks to months.
 CLINICAL FEATURES
 Intraretinal microvascular abnormalities (lRMA) :
- Dilated, tortous retinal capillaries that act as a shunt
between arterioles and venules.
- frequently seen adjacent to areas of capillary closure.
- IRMA may resemble focal areas of flat NVE . But in
IRMA :
5. intraretinal location.
6. absence of profuse leakage on fluorescein
angiography.
7. failure to cross over major retinal blood vessels.
 CLINICAL FEATURES
 New Vessels:
- Unlike IRMA, they arise on the retinal surface
and may extend or be pulled into the vitreous
cavity.
- NVD : NV appears on or within one DD of
disc margin .
- NVE : any other location .
 CLINICAL FEATURES
 Fibrous Glial proliferation :
- Accompained growth of new vessels.
- It is proliferation between the posterior vitreous
gel and the ILM.
- Derived from retinal glial cells and fibrocytes.
 Classification of severity of diabetic
retinopathy

 Nonproliferative DRP :
Mild NPDR Microaneurysms, retinal hemorrhage and hard
exudate
Moderate Mild NPDR plus cotton wool spots .
NPDR
Severe NPDR Moderate NPDR plus one of :
4:2:1 2. Intraretinal Hges in four quadrants .
3. marked venous beading in two or more quadrants
Rule 4. IRMA one or more quadrants.
Very severe Two or more of the above features described in severe
NPDR NPDR
 Classification of severity of diabetic
retinopathy
 Proliferative DRP :

Early PDR New vessels and/or fibrous proliferations; or

preretinal and/or vitreous hemorrhage
PDR with HRC 1. NVD ≥ 1/3 of DD.
2. less extensive NVD, if vitreous or preretinal
hemorrhage is present .
3. NVE ≥ half disc area, if vitreous or preretinal
hemorrhage is present
Advanced PDR 1. Extensive vitreous hemorrhage precluding
grading.
2. retinal detachment involving the macula.
3. phthisis bulbi .
 Diagnostic Testing

 Fluorescein Angiography :
- Not needed to identify CSME or PDR.
- But :
4. As a guide during CSME treatment.
5. Identify macular capillary nonperfusion.
6. Identify subtle areas of NV causing recurrent
vitreous hemorrhage despite full PRP.
 Diagnostic Testing
 Color Fundus photography :
- For Documentation purpose .

 Ultrasonography :
- When opaque media preclude retinal
examination.
- Useful in ruling out :
7. RD.
8. Traction threatening macular detachment.
 Diagnostic Testing
 Color vision assessment:
- DM associated with acquired blue-Yellow defect
caused by diabetes it self and macular edema.
(patients unable accurately match in self –
monitored color-dependant urine or blood-
glucose tests)
 Diagnostic Testing
 Visual Felid:
- Diabetic individuals often complaining of night
vision loss and felid constriction due to:
3. Retinopathy.
4. Retinal non perfusion.
5. Laser surgery.
- Higher risk of developing glaucoma.
 Complications of proliferative
diabetic retinopathy
1. Persistent vitreous haemorrhage .
2. Retinal detachment .
3. Opaque membranes .
4. Rubeosis iridis .
 MANAGEMENT OF
DIABETIC RETINOPATHY
 Medical Therapy :
• Glycemic control :
DCCT , Tight control decrease risk of
progression of retinopathy , nephropathy and
neuropathy.
• Blood pressure control.
• Blood lipids control.
 MANAGEMENT OF DIABETIC
RETINOPATHY
 Laser surgery :
The treatment of depends on the severity of
retinopathy and the presence or absence of
CSME, which may be present at any stage .
 Macular oedema
 defined as the presence of any retinal thickening
or hard exudates within one disc diameter (i.e.
1500 µm) of the centre of the fovea.
 clinically insignificant macular oedema do not
require treatment, only should be followed up at
6 monthly intervals.
 Clinically significant macular
oedema (CSMO)
 defined as the presence of one or more of the
following features:
 Retinal oedema within 500 µm of the centre of the
fovea .
 Hard exudates within 500 µm of the fovea, if
associated with adjacent retinal thickening (which may
be outside the 500 µm limit) .
 Retinal oedema that is one disc area (1500 µm) or
larger, any part of which is within one disc diameter
of the centre of the fovea.
 Focal laser photocoagulation
 All eyes with CSMO should be considered for
treatment with laser photocoagulation
irrespective of the level of visual acuity because
treatment reduces the risk of visual loss by 50%.
 Focal laser photocoagulation
 Poor visual outcome after focal laser
associated with :
2. Macular ischemia .
3. Hard exudates deposit in the fovea.
4. Marked cystoid macular edema.
5. Diffuse fluorescin leakage .
 Direct treatment
 involves applying laser burns to microaneurysms and
microvascular lesions in the centre of rings of hard
exudates located between 500 and 3000 µm (two disc
diameters) from the centre of the fovea.
 - The spot size is : 50-100 µm .

- The duration of : 0.10 second or less.

- The power : sufficient power to obtain a gentle
whitening or darkening of the microaneurysm.
- Wave length : green – yallow Argon
 1500 mirco
3000 micro

500 micro
 Direct treatment
 Treatment of lesions between 300 and 500 µm
from the centre of the fovea should be
considered if CSMO persists, in spite of
previous treatment and, if visual acuity is less
than 6/12.
 Grid treatment
 used for areas of diffuse retinal thickening
located more than 500 µm from the centre of
the fovea and 500 µm from the temporal margin
of the optic disc.
 - The spot size is : 50 - 100µm .
- The exposure time : 0.10 second.
- The burns should be of very light intensity and
one burn width apart.
- Wave length : green – yallow Argon .
 Macular oedema treatment
 It should be emphasized that the main aim of
treatment is to preserve the patient's current
visual level.
 Only about 15% of eyes show improvement.
 It may take up to 4 months for the oedema to
resolve, re-treatment should not be considered
prematurely .
 Focal Laser Side Effects
1. Paracentral scotoma.
2. Transient increased edema and decresed
vision.
3. Choroidal neovascularization.
4. Subretinal fibrosis.
5. Scar expansion.
6. Foveolar burns.
Anti-VGEF & Macular Edema
Anti-VGEF & Macular Edema
Algorithm for panretinal scatter coagulation of
the retina
 laser photocoagulation
The following are the clinical features of eyes at high risk
PDR:
 NVD or neovascularization within one disc diameter of
the optic disc more than one-quarter disc in area .
 Less extensive NVD associated with vitreous or
preretinal haemorrhage.
 NVE more than one-half disc in area in association
with vitreous or preretinal haemorrhage.
 laser photocoagulation
 The aim of treatment is to:
2. induce involution of new vessels .
3. prevent vitreous haemorrhage.
 Initial treatment involves the placement of
about 2000-3000 burns in a scatter pattern,
extending from the posterior fundus to cover
the peripheral retina in one or more sessions.
 laser photocoagulation
 The technique of PRP is as follows:
 Topical corneal anaesthesia is adequate in most
patients.
 - The spot size :depends on which contact
lens is being used. (500 - 200 µm).
- The duration : between 0.10 and 0.05 second
- The power level : produces a gentle burn
 laser photocoagulation
3. burns spaced about one half burn apart.
4. the power is increased by 50 mW increments until a
grey-white burn of gentle intensity is produced .
Follow-up :
- is after an interval of 4-8 weeks.
- In eyes with severe NVD, several treatment sessions
with 5000 or more burns may be required.
- the most important cause of persistent
neovascularization is inadequate treatment.
 laser photocoagulation
 Signs of involution :
2. regression of neovascularization leaving only 'ghost'
vessels or fibrous tissue.
3. decrease in venous dilatation.
4. absorption of retinal haemorrhages .
5. disc pallor .
 Treatment of recurrence :
Further argon laser PRP filling in any gaps between
previous laser scars.
 PARS PLANA VITRECTOMY
INDICATIONS
 Severe persistent vitreous haemorrhage .
 Tractional retinal detachment involving
the macula.
 Combined tractional and rhegmatogenous
retinal detachment .
 Progressive fibrovascular proliferation .
 Rubeosis iridis associated with vitreous
haemorrhage.
 PARS PLANA VITRECTOMY
INDICATIONS
6. Dense, persistent, premacular, subhyaloid
haemorrhage .
7. Red Blood Cell-induced glaucoma.
8. Bilateral vitreous haemorrhage .
9. Dense cataract associated with vitreous
haemorrhage .
 Follow up
Retinal Finding Suggested follow-up
Normal Annually
Mild NPDR Every 9 months
Moderate NPDR Every 6 months
Sever NPDR Every 4 months
CSME Every 2- 4 months
CNSME Every 6 months
PDR Every 2-3 months
 Aspirin & DRP
 Is Aspirin effective in preventing progression of
diabetic retinopathy ?
2. Aspirin use did not alter progression of diabetic
retinopathy .
3. Aspirin use did not increase the risk of vitreous
hemorrhage .
4. Aspirin use did not effect visual acuity.
5. Aspirin use reduce the cardiovascular morbidity
and mortality .
 Sorbinil & DRP
 Sorbinil is an aldose reductase inhibitor.
 Sorbinil does not affect the progression of DRP
or Diabetic neuropathy.
 Practical Points
 Pregnancy :
• DR accelerate during pregnancy and improve
postpartum.
• Do not hesitate to treat with laser when
indicated.
• FFA should be avoided in all but the most
difficult cases of macular edema.
 Practical Points
 PRP:
• Three-mirror lens can be used for both focal
laser and PRP.
• Do not forget lens magnification , in most lenses
use 200μm to produce 500 μm spot in the
retina.
• Do not count the spots but fill up an
appropriate region of retina .
 Practical Points
• Usually PRP performed in 2 sessions spaced 2-4
weeks apart.
• If possible start with inferior retina.
• If patient discomfortable during PRP:
- Reassure the patient it is expected and the
treatment going well.
- Decrease the duration to about 0.05 s.
- Do it in more but shorter sessions.
- Retrobulbar anesthetic can be used.
 Practical Points
• Major reason for under treatment is not well
dilated pupil.
• If NV recur after complete PRP :
- Add more PRP in the periphery or between
previous laser burns.
- Vitrectomy .
 Practical Points
 CSME + Capillary non perfusion :
• Some recommend doing grid laser for area with
capillary non perfusion (decrease possibility of
NV )
 Lowering serum lipid and ME :
• Clofibrate (in several British study)
• Reduce amount of hard exudate but macular
edema edema persist with only modest
improvement in VA .
 Remember
 Argon blue : 488 nm.
 Argon green : 514 nm.
 Dye yellow : 577 nm.
 Krypton red : 647 nm.