HYPERTENSIVE RETINOPATHY

ROLL NO-75
INTRODUCTION
• It refers to fundus changes occurring in patients suffering from
systemic hypertension.
• Clinical presentation includes changes of
Retinopathy
Choroidopathy
Optic neuropathy
PATHOGENESIS
• 3 Factors play role in pathogenesis-
• 1)Vasospasm. Arteriolar narrowing due to vasospasm is the primary
response to raised blood pressure and is related to the severity of
hypertension (acute hypertensions).
• 2) Arteriosclerotic changes which manifest as changes in the
arteriolar reflex and A-V nipping result from thickening of the vessel
wall and are a reflection of the duration of hypertension (chronic
hypertension).
• 3)Increased vascular permeability results from hypoxia causing
breakdown of inner blood retinal barrier and occurs in severs
hypertension and is responsible for haemorrhages, exudates, focal
retinal oedema, macular oedema
 CLINICAL TYPES
• Clinically hypertensive retinopathy can be divided into-

1) Chronic hypertensive retinopathy

2)Malignant/Acute hypertensive retinopathy

 Benign or Chronic Hypertensive
retinopathy
• Patients with chronic hypertensive retinopathy are usually asymptomatic.

Clinical situations in which chronic hypertensive retinopathy occurs include:

1. Hypertension with involuntary (senile) sclerosis

When hypertension occurs in elderly patients (after the age of 50 years) in

the presence of involuntary sclerosis the fundus changes comprise
augmented arteriosclerotic retinopathy.
 2.Chronic hypertension with compensatory
arteriolar sclerosis
• This condition is seen in young patients with prolonged benign
hypertension usually associated with benign nephrosclerosis.
• The young arterioles respond by proliferative and fibrous changes in
the media (compensatory arteriolar sclerosis).
• Advanced fundus changes in these patients earlier have been
described as 'albuminuric or renal retinopathy'.
 Fundus changes of chronic hypertensive
retinopathy-
• 1. Generalized arterial narrowing or attenuation,
depending upon the severity of hypertension may
be mild or marked, and consists of vasoconstrictive
and sclerotic phases.
• 2. Focal arteriolar narrowing is seen as areas of
localized vasoconstriction on the disc and within ½
disc diameter of its margin zone
• 3.Arteriovenous nicking is the hallmark of
hypertensive retinopathy and occurs where
arteriole crosses and corn presses the vein, as the
vessels share a common adventitious sheath.
• Also known as A-V crossing changes, these include:
• Salu's sign, i.e. deflection of veins at the arteriovenous crossings,
• Bonnet sign, i.e. banking of veins distal to arteriovenous crossings, and
• Gunn sign, i.e. tapering of veins on either side of the crossings.
4. Arteriolar reflex changes.-
• Bright and thin, linear blood reflex is seen normally
• More diffuse and less bright reflex is seen due to thickening of vessel wall
shows grade I and ll hypertensive retinopathy.
• Copper wiring, i.e. reddish-brown reflex of the arterioles occurs due to
progressive sclerosis and hyalinization, and is a sign of grade Ill retinopathy.
• Silver wiring, i. e. opaque- white reflex of the arterioles occurs ultimately due
to the continued sclerosis, and is seen in grade IV hypertensive retinopathy.
• 5. Superficial retinal haemorrhages (flame-
shaped)
• 6.Hard exudates are lipid deposits in the outer
plexiform layer of retina which occur following
leaky capillaries in severe hypertensive
retinopathy.
• 7. Cotton wool spots are fluffy white lesions and
represent the areas of infarcts in the nerve fibre
layer. These occur due to ischaemia caused by
capillary obliterations in severe hypertensive
retinopathy.
 Malignant hypertensive
retinopathy
• Malignant hypertension is not a separate variety of hypertension, but
is an expression of its rapid progression to a serious degree in a
patient with relatively young arterioles undefended by fibrosis.
• It is characterised by changes of
1 acute hypertensive retinopathy,
2 choroidopathy and
3 optic neuropathy.
 Acute hypertensive retinopathy
• Fundus changes include:
• Marked arteriolar narrowing due to spasm of the arteriolar wall, in response
to sudden rise in blood pressure.
• Superficial retinal haemorhages, flame shaped, appear in the posterior pole.
• Focal intraretinal periarteriolar transudates (FlPTs) are small, white, focal
oval lesions occurring due to the deposition of macromolecules along the
major arterioles.
• Cotton wool spots are also more marked in malign ant hypertensive
retinopathy.
• Microaneurysms, shunt vessels and collaterals may also develop as a result
of capillary obliterations.
 Acute hypertensive
choroidopathy
Various fundus changes include:
• Acute focal retinal pigment epitheliopathy
• Elschnig's spots are small black spots surrounded by yellow halos, these are
formed due to clumping and atrophy of the infarcted pigment epithelium
• Siegrist streaks are formed due to linear configuration of the pigment along
the choroidal arterioles.
• Serous neurosensory retinal detachment, which preferentially affects the
macular area, may occur due to accumulation of fluid beneath the retina
following breakdown of outer blood-retinal barrier owing to ischemic
damage to the retinal pigment epithelium.
 Acute hypertensive optic
neuropathy
• Changes include:

• Disc oedema and haemorhages on the disc and peripapillary retina which
occur due to vasoconstriction of peripapillaiy choroidal vessels supplying
the optic nerve head. The ischemia of the optic nerve head leads to stasis
of axoplasmic flow, thus the lesion is a form of anterior ischaemic optic
neuropathy.
• Disc pallor, of variable degree, may occur late in the course of disease.
 Keith and Wagner classification
• Grade I. Mild generalized arteriolar attenuation, particularly of small
branches, with broadening of the arteriolar light reflex and vein
concealment
• Grade II. Marked generalized narrowing and focal attenuation of arterioles
associated with deflection of veins at arteriovenous crossings (Salus' sign)
• Grade lll. Grade II changes plus copper-wiring of arterioles, banking of veins
distal to arteriovenous crossings (Bonnet sign), tapering of veins on either
side of the crossings (Gunn sign) and right-angle deflection of veins (Salu's
sign). Flame-shaped haemorrhages, cotton-wool spots an d hard exudates
are also present.
• Grade IV. All changes of grade Ill plus silver-vviring of arterioles and
papilloedema
RETINOPATHY IN PREGNANCY-
INDUCED HYPERTENSION
• Retinal changes are liable to occur in this condition when blood pressure
rises above 160/ 100 mm of Hg and are marked when blood pressure rises
above 200/ 130 mm of Hg.
• Earliest changes consist of narrowing of foveal and nasal arterioles, followed
by generalised narrowing.
• Appearance of 'cotton wool spots' and superficial haemorrhages.
• Further progression of retinopathy occurs rapidly if pregnancy is allowed to
continue and changes of hypertensive optic neuropathy and acute
choroidopathy (Elschnig spots and other RPE lesions) can occur. • Retinal
oedema and exudation is usually marked and may be associated with 'macular
star' or 'flat macular detachment'.
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