RETINA 2

Dr Monika Mahat
Resident
Department of Ophthalmology
HYPERTENSIVE RETINOPATHY
INTRODUCTION
• Hypertensive retinopathy refers to fundus
changes occurring in patients suffering
from systemic hypertension
• Ocular effects can be observed in the
retina, choroid and optic nerve
• Primary response of the retinal arterioles
to systemic hypertension
 PATHOGENESIS
3 factors which play role in the pathogenesis of hypertensive retinopathy

1. Vasoconstriction - Primary response of the retinal arterioles to systemic

hypertension is vasoconstriction, which is less marked in older
individuals because of involutional sclerosis conferring increased rigidity
2. Arteriosclerotic Changes -Arteriolosclerosis refers to hardening and loss
of elasticity of small vessel walls, manifested most obviously by
arteriovenous (AV) nipping (nicking) at crossing points.
3. Increased Vascular Permeability - In sustained hypertension the inner
blood–retinal barrier is disrupted, increased vascular permeability
leading to flame-shaped retinal haemorrhages and oedema
CLINICAL TYPES
Clinically, the hypertensive fundus changes can be described as:
1. Chronic Hypertensive Retinopathy
2. Malignant or Acute Hypertensive Retinopathy
CHRONIC HYPERTENSIVE
RETINOPATHY
• Usually asymptomatic
• Includes:
• Hypertension with involutionary (senile) sclerosis
• Chronic hypertension with compensatory arteriolar sclerosis – Seen in
prolonged benign hypertension usually associated with benign
nephrosclerosis
• Fundus Changes:
1. Generalized arterial narrowing – Vasoconstrictive Phase (Vasospasm)
and Sclerotic Phase (intimal thickening, hypoplasia of tunica media, and
hyaline degeneration, leads to arteriolar narrowing with tortuosity)

2. Focal arteriolar narrowing - localized vasoconstriction

3. Arteriovenous nicking (AV Crossing) - hallmark of hypertensive retinopathy,
occurs where arteriole crosses and compresses the vein, as the vessels share a
common adventitious sheath
• Salu’s sign - deflection of veins at the arteriovenous crossings
• Bonnet sign - banking of veins distal to arteriovenous crossings
• Gunn sign - tapering of veins on either side of the crossings
4. Arteriolar Reflex Changes - The normal light reflex of the
retinal vasculature is formed by the reflection from the
interface between the blood column and vessel wall:
• Bright and thin, linear blood reflex – Normally seen
• More diffuse and less bright reflex - Due to thickening of vessel wall
• Copper Wiring - reddish-brown reflex of the arterioles occurs due to
progressive sclerosis and hyalinization
• Silver Wiring - opaque–white reflex of the arterioles occurs
ultimately due to the continued sclerosis

5. Superficial Retinal Haemorrhages (Flame Shaped) : Due to

disruption of the capillaries in the retinal nerve fibre layer
5. Hard Exudates: Lipid deposits in the outer
plexiform layer of retina which occur
following leaky capillaries in severe
hypertensive retinopathy, May be
arranged as macular-fan or macular-star

6. Cotton Wool Spots : fluffy white lesions

and represent the areas of infarcts in the
nerve fibre layer, due to ischaemia caused
by capillary obliterations
MALIGNANT HYPERTENSIVE RETINOPATHY

Rapid progression to a serious degree in a young patient with arterioles

undefended by fibrosis

1. Acute hypertensive retinopathy

• Marked arteriolar narrowing
• Superficial retinal haemorrhages
• Focal intraretinal periarteriolar transudates (FIPTs)
• Cotton wool spots
• Microaneurysms, shunt vessels and collaterals
2. Acute hypertensive choroidopathy
• Acute focal retinal pigment epitheliopathy
• Elschnig’s spots - small black spots surrounded by yellow
halos, these are formed due to clumping and atrophy of the
infarcted pigment epithelium
• Siegrist streaks - linear configuration of the pigment along
the choroidal arterioles
• Serous neurosensory retinal detachment

3. Acute hypertensive optic neuropathy

• Disc oedema and hemorrhages on the disc and peripapillary
retina
• Disc pallor
Siegrist streaks

Elschnig’s spots
STAGING OF HYPERTENSIVE
RETINOPATHY
Keith and Wagner classification
MANAGEMENT
• Mild: Blood pressure control only
• Moderate: (characterized by retinal hemorrhages, microaneurysms,
and cotton-wool spots)
• Blood pressure control benefit from further assessment of vascular risk
factors (e.g., cholesterol levels) and if indicated, risk reduction therapy (e.g.,
cholesterol lowering agents)
• Accelerated (Bilateral disc swelling): Control of blood pressure over a
few hours [NOT SUDDEN - reduce perfusion of optic nerve head and
central nervous system (causing stroke)]
EALE’S DISEASE
• Retinal vasulitis
• Idiopathic inflammation of the peripheral retinal vein
• Characterized by recurrent vitreous hemorrhage

ETIOLOGY:
• Not known
• Hypersensitivity reaction to tubercular protein
CLINICAL FEATURES:
• B/L, common in male
• Floaters, painless blurring of vision

STAGES:
1. Stage of inflammation:
• peripheral veins are congested and exudates and sheathing seen
• Superficial hemorrhages seen

2. Stage of ischaemia:
• Avascular area seen in periphery due to obliteration of vessels
3. Stage of neovascularization:
• New vessel formation seen in the area between the perfused and non
perfused area
• These vessels bleed leading to vitreous hemorrhage

4. Stage of sequelae:
• Complications like tractional RD, vitreoretinopathy, neovascularization iris
and neovascular glaucoma
TREATMENT:

• Medical T/T: oral corticosteroid

• Laser photocoagulation
• Vitreoretinal surgery