2. • Ocular fundus is of paramount importance in evaluation
of systemic vascular disease.
• It is the only region of the body in which physician can
directly visualize manifestation of vascular
pathophysiology.
• Hypertensive Retinopathy is the retinal vascular
damage caused by systemic hypertension.
3. • Ocular involvement in the setting of malignant
hypertension was first described by Liebriech
in 1859.
• Hayreh, over the course of the 1970s and
1980s, elucidated pathophysiologic
mechanisms for ocular involvement and
described clinical findings through direct
patient management observations and animal
models.
8. RISK FACTORS
• Age
• Family History
• Obesity
• Smoking
• Stress
• Alcohol consumption
• Lack of exercise
9. CLINICAL FEATURES
• Most patients are asymptomatic
• Some complain of headache and blurring of vision (Bilateral)
• On Ophthalmoscopy
• Generalized arteriolar narrowing
• Changes of the arterovenous crossings
• Flame haemorrhage
• Aneurysms
• Exudates
• Cotton-wool spots
• Optic disc swelling
10. Arteriolar narrowing
(vasoconstriction)
• Generalized narrowing is
difficult to see but focal
narrowing is well appreciated
• Focal narrowing occurs from
spasm of local areas of the
vascular musculature. Spencer
speculated that either edema in
and around the vessel wall or
vascular spasm leads to focal
narrowing, which can become
permanent with fibrosis.
15. Hard Exudates
• Extravasated fluid is rich in
fibrin and protein which readily
coagulates.
• These hyaline or lipid deposits
are seen as cluster around
leaking microaneurysms
16. Cotton wool spots
cystoid bodies
soft exudates
• White plaques with a hazy,
irregular outline.
• They are usually ovoid in shape,
variable in size and number.
• Seen in posterior fundus
• Occur in nerve fiber layer of
retina – result of capillary
infarction
17. Optic disc swelling
• Optic disc edema is a primary
manifestation of hypertensive
optic neuropathy.
• Vasoconstriction and choroidal
ischemia in the setting of
malignant hypertension result in
optic disc edema and axoplasmic
flow stasis
18. Keith,Wagner and Baker (1939)
• Grade 1
• generalized arteriolar attenuation
• broadening of arteriolar light
reflex
• concealment of vein at a-v
crossings
20. • GRADE 3
• copper wiring of arterioles
• venous banking distal to a-v crossing
(bonnet’s sign)
• venous tapering on either side of crossing
(gunn’s sign)
• right angle deflection of veins.
• flame shaped hemorrhages cotton wool spots,
hard exudates.
21. • GRADE 4
• All changes of grade 3
• Silver wiring of arterioles
• Disc edema
22.
23. 1. Hypertension with senile (involutionary) sclerosis
•Fundus changes comprise augmented atheriosclerotic retinopathy.
2.Hypertension without sclerosis
•There are few retinal signs.
•The arterioles are constricted,pale and straight with acute angled
branching.
•Exudates and papilloedema are never seen.
CLINICAL TYPES
24. 3.Hypertension with compensatory arteriolar sclerosis
•Advanced fundus changes have been described as “albuminuric or
renal retinopathy”.
4.Malignant hypertension
•Marked arteriolar narrowing
•Papilledema
•Retinal edema over posterior pole
•Cotton wool spots
25. Management
• The aim of treatment is to prevent, limit, or reverse target
organ damage by lowering the patient's high blood pressure.
• Lifestyle changes Promote Healthy lifestyle; exercise,
healthy foods
• Advice patient to reduce the Blood Pressure
• Take the medication accordingly
