2. INTRODUCTION
Systolic BP> 140 mm Hg, diastolic BP>90mm Hg.
• Hypertensive Retinopathy refers to fundus
changes in patients suffering from systemic
hypertension
• 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
3.
4. EPIDEMIOLOGY
• Hypertension affects around 26% of adult
population worldwide
• Prevalence of hypertensive retinopathy is
approx 30% among the hypertensives
• Afro-carribeans have a double relative risk
compared to other population
• Major risk factors include Age, Family history,
Obesity, Smoking, Stress, Alcohol , lifestyle
5. PATHOGENESIS
3 major factors have role:
I .VASOCONSTRICTION:
Primary response to raised blood pressure is
Arterial narrowing, leading to following changes:
(a)Vasoconstriction of retinal arterioles
(b)Vasoconstriction of choroidal vessels: Leads to choroidal
and RPE ischaemia, manifests as Hypertensive
Choroidopathy
(c)Vasoconstriction of Peripapillary choroid: leads to Optic
nerve head ischaemia, manifests as Hypertensive Optic
Neuropathy
6. 2. ARTERIOSCLEROTIC CHANGES:
due to thickening of vessel wall,
(a)Changes in arteriolar reflex
(b)AV nipping
Reflect the duration of Hypertension
3. INCREASED VASCULAR PERMEABILITY:
- Results from hypoxia
- Leads to Haemorrhages, exudates, macular
edema, focal retinal edema, disc edema
11. Chronic Hypertensive Retinopathy
FUNDUS CHANGES:
I .ARTERIOLAR NARROWING:
• Generalized narrowing is difficult to see but
focal narrowing is well appreciated
• Focal narrowing occurs from spasm of local
areas of the vascular musculature
16. ARTERIOLAR REFLEX CHANGES
• Bright and thin, linear blood reflex:
-seen over the surface of arteriole in young.
-due to blood column in arteriole (vessel wall
is almost transparent)
• More diffuse and less bright reflex: - due to
thickening of vessel wall
17. FLAME SHAPED HEMORRHAGES -lll
• Superficial
• occur at posterior pole
• Disruption of capillaries in retinal nerve fibre
layer
18. HARD EXUDATES
• Lipid deposits in outer plexiform layer of
retina
• Usually follows leaky capillaries in severe
disease
• Appear as 'yellow waxy spots' with sharp
margin
• Generally seen in posterior pole
19. COTTON WOOL SPOTS
• Also called 'Soft Exudates'
• White plaques with a hazy, irregular outline.
• They are usually ovoid in shape, variable in
size and number
• Occur in nerve fibre layer of retina result of
capillary infarction
20.
21. OPTIC DISC SWELLING/
PAPILLOEDEMA
• Optic disc edema is a primary manifestation of
hypertensive optic neuropath
• Vasoconstriction and choroidal ischemia in the
setting of malignant hypertension result in
optic disc edema and axoplasmic flow stasis
25. Grade ll
• Marked generalised narrowing and focal
attenuation of artertioles
• 'Salus' Sign (deflection of veins at AV
crossings)
26.
27. Grade lll
• Retinal arteriolar narrowing + focal constriction
• Prominent AV crossing changes
• Bonnet Sign (banking of veins distal to AV c)
• Gunn Sign (tapering of vein on either side of AV
crossings)
• Flame shaped haemorrhages
• Cotton wool spots
• Hard exudates
33. OTHER CLASSIFICATION
Scheie classification
• Stage 0: No visible retinal abnormalities
• Stage 1: Diffuse arteriolar narrowing; no focal
constriction
• Stage 2: More pronounced arteriolar narrowing
with focal constriction
• Stage 3: Focal and diffuse narrowing, with retinal
haemorrhages S
• Stage 4: Retinal oedema, hard exudates, optic
disc edema
34. Wong and Mcintosh classification
• Mild retinopathy: one or more of the following signs:
generalised arteriolar narrowing, focal arteriolar
narrowing, AV nicking, arteriolar wall reflex
broadening.
• Moderated retinopathy: consists of mild retinopathy
with one or more of the following signs: Retinal
haemorrhages (blot and dot or flame shaped),
microaneurysms, cotton-wool spots, and hard exudates
• Accelerated retinopathy: consists of moderate
retinopathy signs plus optic disc swelling
-may be associated with visual loss
35. MALIGNANT HYPERTENSIVE
RETINOPATHY
• Cause: Rapid progression to a serious degree
in young patient with relatively young
arterioles undefended by fibrosis
• Changes include:
1 . Hypertensive Retinopathy
2.Hypertensive Choroidopathy
3 . Hypertensive Optic Neuropathy
38. • Acute focal retinal pigment epitheliopathy
characterized by focal white spots
• Serous neurosensory retinal detachment
39. MANAGEMENT
• MILD: BP control only
• MODERATE: BP control +assessment of risk factors
( eg. cholesterol)
BP monitoring every 3-6 months
If indicated, risk reduction therapy ( cholesterol
reducing agents)
• ACCELERATED: small step wise control of BP, avoid
sudden reduction ( risk of Optic nerve head
hypoperfusion, Stroke)
40.
41. PREGNANCY INDUCED HTN
• Previously called 'Toxemia of Pregnancy’
• Raised BP , proteinuria , generalised edema
• Retinal changes liable to occur when
BP >160/ 100 mm Hg,
marked when BP> 200/130 mm Hg
42. • Earliest changes: narrowing of nasal arterioles
-generalised narrowing
• Persistent spasm of vessels - cotton wool
spots, hemorrhages
• Retinal edema and exudation
43. MANAGEMENT
• Changes are reversible , disappear after delivery
(unless organic cause established)
• Pre- Organic Stage: patient responds well to
conservative treatment, pregnancy continued
under close observation
• Hypoxic Retinopathy: cotton wool spots,
haemorrhages, retinal edema
terminate pregnancy ??