Hypertensive Retinopathy

1. HYPERTENSIVE
RETINOPATHY
ANGEL DAS

2. Hypertensive Retinopathy
• Fundus changes that occur in patients with severe hypertension
• Clinical presentation includes changes of
-Retinopathy
-Choroidopathy
-Optic neuropathy

3. pathogenesis
• 3 factors play role in pathogenesis
1. Vasoconstriction
2. Arteriosclerotic changes
3. Increased vascular permeability

4. Pathophysiology
Systemic chronic
hypertension
Arteriosclerosis
Narrowing of
retinal arterioles
Retinal
Ischaemia
Hypoxia
Increased
capillary
permeability
Focal Retinal Oedema, retinal
haemorrhage,cotton wool spots, hard
exudates

5. Clinical types
Clinically hypertensive fundus changes can be described as
• Chronic hypertensive retinopathy
• Malignant/acute hypertensive retinopathy

6. Chronic hypertensive retinopathy
• Usually asypmtomatic
• Clinical situations include
1. Hypertension with involutinary ( senile)
sclerosis:
elderly patients (> 50 yrs ),fundus changes comprise augmented arteriosclerotic retinopathy.

7. 2.Chronic hypertension with compensatory
arteriolar sclerosis
• Seen in young individuals
• young arterioles respond to HTN by prolifrative and
fibrous changes in media
• In the kidneys there will be chronic
glomerulonephritis
• so known as albuminuric or renal retinopathy

8. Normal Fundus

9. Fundus Changes
• Generalized arteriolar narrowing
• Focal arteriolar narrowing
• A-V nicking
-hallmark of HR

10. • Salu’s sign – deflection of veins at A-V crossing
• Bonnet sign – banking of veins distal to A-V crossing
• Gunn sign – tapering of veins on either side of crossing

11. • Arteriolar Reflex Changes
-bright, thin, linear reflex –Normal
-diffuse, less bright reflex –Grade I/II
-Copper wiring
-Silver wiring

12. • Superficial retinal haemorrhages
• Hard exudates
• Cotton wool spots

13. Malignant hypertension
• rapid progression of the hypertensive state in a patient with relatively young
arterioles undefended by sclerosis
• There will be retinopathy , choroidopathy & optic neuropathy
• It is asso. With renal insufficiency

15. Choroidopathy
• Elschnig’s spots- focal areas infarcted retinal pigment
epithelium
• Siegrist streaks- due to fibrinoid necrosis in malignant
hypertension

16.  Grade I
 Mild generalised arteriolar
attenuation
 Broadening of arteriolar
light reflex
 Vein concealment

17.  Grade II
 Marked generalised narrowing
and focal attenuation of
artertioles
 Salus’ Sign (deflection of veins
at AV crossings)

18.  Grade III
 Copper wiring of arterioles
 Bonnet Sign (banking of
veins distal to av crossings)
 Gunn Sign (tapering of vein
on either side of av crossings)
 Flame shaped haemorrhages,
 Cotton wool spots
 Hard exudates
Gunn SignBonnet sign

19.  Grade IV
 Grade III changes
 Silver wiring of
arterioles
 Papilloedema

20. • Scheie classification

21. Management
Mild HR BP control only
Moderate HR BP control
+
Assess cholesterol levels & if indicated cholesterol
lowering agents
Accelerated HR Urgent anti hypertensive management by stepwise
control of BP over a few hours

22.  BP >160/100mm Hg- >
200/130mm Hg
 Narrowing of nasal arterioles-
generalised
 Cotton wool spots; retinal
hemmorhages- retinal hypoxia
 ‘Macular star’ – ‘flat macular
detachment’

23. Management
• Changes are reversible , disappear after delivery
• In preorganic stage : conservative treatment , pregnancy is continued under
close observation
• Advent of hypoxic retinopathy( cotton wool spots,hemorrhages,retinal
edema): indication for termination of pregnancy ,otherwise permanent visual
loss or even loss of life may occur.