1. Diabetic Retinopathy &
Hypertensive Retinopathy
By:
Ch.Vineela,

2. Diabetic Retinopathy
• Diabetic retinopathy is
retinopathy (damage to
the retina) caused by
complications of
diabetes
mellitus, which can
eventually lead to
blindness
• It is an ocular
manifestation of
systematic disease
which affects up to 80%
of all diabetic patients

3. DR - Pathogenesis
• Damage to capillaries –
– formation of microaneurysm (MA) and
– leakage leading to
• dot & blot haemorrhage,
• exudates and
• oedema
• Changes in blood constituents leading
– to decreased blood flow
• Micro-vascular or small blood vessel occlusion leading to
– capillary non-perfusion
• Consequences of ischaemia are
– formation of new blood vessels (neo-vascularisation) as retina
responds by secreting vascular endothelial growth factor VeGF

5. Diabetic Retinopathy (DR) –
Risk factors
• Duration of diabetes
• Poor control of Diabetes
• Pregnancy
• Hypertension
• Nephropathy
• Obesity and hyperlipidemia
• Smoking

6. Classification
1 ) Non –proliferative -Mild
- Moderate
- Severe
- Very Severe
2) Proliferative
3)Diabetic Maculopathy-- focal exudative
-diffuse exudative
- ischemic
- mixed

7. Non-proliferative changesclinical
• Microaneurysms (MA) – appear as tiny red dots
• Oedema – clinically causes thickness
»Localised due to leakage from MAs’
»Diffuse due to capillary leakage
»Initially located between the OPL and INL
»Later involves the INL and NFL
»eventually the entire thickness of the
retina becomes oedematous
»At the fovea, it is cystic in nature

9. Non-proliferative changes –
Clinical Features contd
 Exudates:
formed at the
junction of normal
and oedematous
retina
composed of
lipoprotein and
lipid-filled
macrophages
located mainly
within the outer
plexiform layer

10. Non-proliferative Clinical
Features contd
Haemorrhage
• ‘Dot and blot’ –
in the compact
middle
layers, from
venous end of
capillaries
• ‘flame shaped’ as
they are placed
superiorly in
nerve fibre layer
(RNFL)

11. Non-proliferative DR
Treatment
• Usually not required
• Only when exudates/oedema in macula
(clinically significant macular oedema)
• Pt followed up every 6-12 months

12. Diabetic Maculopathy
• Involvement of the fovea by oedema, hard exudates or
ischaemia
• Most common cause of visual impairment in diabetic
patients, with type 2 diabetes.
1.Focal maculopathy
• well-circumscribed retinal thickening associated with
• complete or incomplete rings of hard exudates
2. Diffuse maculopathy
• diffuse retinal thickening, which may be associated
with cystoid changes.
• landmarks are obliterated by severe oedema which
may render localization of the fovea impossible

13. Focal maculopathy

14. Diffuse maculopathy

15. Maculopathy
3. Ischaemic maculopathy
• The signs are variable and the macula may look
relatively normal despite reduced visual acuity.
• In other cases pre-proliferative diabetic
retinopathy
• FA shows capillary non-perfusion at the fovea
and frequently other
• Areas of capillary non-perfusion at the posterior
pole

16. Ischaemic Maculopathy

17. Clinically significant
macular oedema
4. CSMO
• Retinal oedema within
500μm of the centre of the
macula
• Hard exudates within
500μm of the centre of the
macula, if associated with
retinal thickening (which
may be outside the 500μm)
• Retinal oedema one disc
area (1500μm) or larger, any
part of which is within one
disc diameter of the centre
of the macula

18. Maculopathy Treatment
• All cases of CSMO are treated
• Aim of treatment is to maintain current level of
vision
• Argon laser photocoagulation
»Focal application
»Grid application
• Intravitreal Triamcinalone – effect lasts 6/12

19. Maculopathy – Focal
Treatment
Focal Treatment
Grid Laser Treatment

20. Non-proliferative Preproliferative changes in DR
• DR that exhibits signs of imminent proliferative disease
• Clinical signs indicate progressive retinal ischaemi
 Cotton-wool spots - composed of accumulations of
neuronal debris within the nerve fibre layer.
• Signs. Small, whitish, fluffy superficial lesions which
obscure underlying blood vessels
 Intraretinal microvascular abnormalities (IRMA) are
arteriolar-venular shunts that run from retinal arterioles to
venules, thus by-passing the capillary bed.
Signs. Fine, irregular, red lines that run from arterioles to
venules

21. Non-proliferative Preproliferative changes in DR
 Other features
a. Venous changes
consist of dilatation and
tortuosity,
looping beading and
‘sausage-like’
segmentation
b. Arterial changes
include peripheral
narrowing
c. Dark blot
haemorrhages represent
haemorrhagic retinal
infarcts and are located
within the middle retinal
layers

22. NPDR

23. Proliferative
DR (PDR)
PDR affects 5–
10% of the
diabetic
population.
Type 1
diabetics are at
particular risk
with an
incidence of
about 60% after
30 years.

24. PDR
• Pathogenesis - Primary feature is
neovascularization caused by angiogenic
growth factors elaborated by hypoxic retinal
tissue in an attempt to re-vascularize hypoxic
retina.
• Clinically
»New vessels at the disc (NVD)
»New vessels elsewhere (NVE)
• Leaks in FA

25. PDR
NVD
NVE

26. PDR
• Treatment
• Laser therapy is aimed at inducing involution
of new vessels and preventing visual loss
• Pan retinal laser photocoagulation PRP –
delivery at slit lamp or via Indirect
Ophthalmoscope
• About 2500 burns over 2 sessions

27. PDR - treatment

28. PDR - consequences
• Vitreous Haemorrhage
– retrohyaloid, intragel
or both
• Tractional RD
• Rubeosis Iridis and
Neovascular Glaucoma
(NVG)

29. Treatment of Complications
of PDR
• Persistent Vit Haem
» Vitrectomy
» Endophotocoagulation
• Tractional RD
» Vitrectomy
» +/- Oil
• Rubeosis Iridis / NVG
»
»
»
»
Adequate PRP +/- Intravitreal Avastin (anti-angiogenic factor)
Medical management of glaucoma
Surgical management of glaucoma
Cyclodestructive laser

30. Screening
•
All diabetic patients aged over 12 years and/or entering puberty should be
screened
General screening and referral to Specialist
• 1. Annual review
􀁍 Normal fundus. 􀁍 Mild NPDR with small haemorrhages and/or small hard
exudates more than one disc diameter from the fovea.
• 2. Routine referral (weeks)
􀁍 NPDR with large exudates within the major temporal arcades but not
threatening the fovea.
􀁍 NPDR without maculopathy but with reduced visual acuity impairment.
• 3. Early referral (days)
􀁍 CSMO
􀁍 Severe and very severe NPDR.
• 4. Urgent referral (same day)
􀁍 PDR.
􀁍 Preretinal or vitreous haemorrhage.
􀁍 Rubeosis iridis.
􀁍 Retinal detachment
Screening in pregnancy Diabetic retinopathy can significantly worsen during
pregnancy.

31. HT Retinopathy
• Untreated systemic hypertension is associated with
– retinopathy,
– optic neuropathy, and
– choroidopathy.
• Retinopathy consists of a spectrum of retinal vascular
changes that are pathologically related to
microvascular damage from elevated blood pressure.

32. Pathogenesis
Arteriolar narrowing
• Arteriolar narrowing may be focal or
generalized;
• Ophthalmoscopic diagnosis of generalized
narrowing is difficult, although the presence
of focal narrowing makes it highly probable
that blood pressure is raised.
• Severe hypertension may lead to the
development of cotton-wool spots

33. Vascular leakage
• Vascular leakage leads to flame-shaped retinal
haemorrhages and retinal oedema
• Chronic retinal oedema may result in the
deposition of hard exudates around the fovea
with a macular star configuration
• Swelling of the optic nerve head is the
hallmark of accelerated hypertension

34. Grades of HT Retinopathy
• Grade 1 consists of ‘mild’ generalized retinal
arteriolar narrowing;
• Grade 2 consists of ‘more severe’ generalized
narrowing, focal areas of arteriolar narrowing and
arterio-venous (AV) nicking;
• Grade 3 consists of grade 1 and 2 signs plus the
presence of retinal
haemorrhages, microaneurysms, hard exudates
and cotton-wool spots;
• Grade 4, also called accelerated (malignant)
hypertensive retinopathy, consists of signs in the
preceding three grades plus optic disc swelling

37. Treatment
• Major aim of treatment is to prevent,limit
patient ‘s high blood pressure and reduce high
risk of cardiovascular disease and death.
• Anti –hypertensive drug treatment required to
control the high blood pressure