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HYPERTENSIVE

RETINOPATHY
Chikita Artia Sari / I 11109014
Definition
Hypertensive retinopathy represents the
ophthalmic findings of end-organ damage
secondary to systemic arterial hypertension.
The appearance of the fundus in hypertensive
retinopathy is determined by the degree of
elevation of the blood pressure and the state of
the retinal arterioles.
In mild to moderate systemic hypertension, the
retinal signs may be subtle. Focal attenuation of
a major retinal arteriole is one of the earliest
signs. Diffuse arteriolar attenuation, broadening
of the arteriolar light reflex, and arteriovenous
crossing changes also occur.
Definition
In young patients with accelerated malignant
hypertension, an extensive retinopathy is seen,
with hemorrhages, retinal infarcts (cotton-wool
spots), choroidal infarcts (Elschnig's spots), and
occasionally serous detachment of the retina.
Severe disk edema is a prominent feature and
may be accompanied by a macular star of hard
exudate. Vision may be impaired and may
deteriorate further if blood pressure is reduced
too quickly.

Incidence
In the Beaver Dam Eye Study, which evaluated
hypertensive patients without coexisting,
confounding vascular diseases, the overall
incidence of hypertensive retinopathy was about
15%; specifically, 8% showed retinopathy, 13%
showed arteriolar narrowing, and 2% showed
arteriovenous nicking.
The Stage of Hypertensive
Retinopathy
Hemorrhag
e
Exudate Disc
Edema
Grade 1 - - -
Grade 2 - - -
Grade 3 + + -
Grade 4 + + +
Normal Retina and Hypertensive
Retinopathy
Normal Retina Hypertensive
Retinopathy
A: Hemorrhages
B: Exudates
(Fatty
Deposits)
C: Cotton Wool
Spots (Micro
Strokes)
A B
C
GRADE I
Generalized
arteriolar
attenuation
Broadening of
arteriolar light
reflex
Concealment of
vein at a-v
crossings
Arteriolar
Narrowing
GRADE II
Severe
generalized
and focal
arteriolar
constriction
A-v crossing
changes (salus
sign)

Grade II (AV Nicking)
Arteriovenous nicking is a highly specific finding
and the hallmark of chronic hypertensive
retinopathy. At the arteriovenous crossings in the
retina, the vessels share a common adventitial
sheath.
Arteriovenous nicking is diagnosed when the
crossing retinal vein becomes less apparent or
even disappears on either side of the artery.
The course of the vein may change to a more
perpendicular direction as well. If there is
impedance to flow, the segment of the vein distal
to the constriction appears larger, darker, and
more tortuous.
GRADE III
Copper wiring of arterioles
Venous banking distal to A-
V crossing (bonnets sign)
Venous tapering on either
side of crossing (gunns
sign)
Right angle deflection of
veins.
Flame shaped hemorrhages
cotton wool spots, hard
exudates.
GRADE IV
All changes of grade 3
Silver wiring of
arterioles
Disc edema
Papilledema from
malignant
hypertension. There is
blurring of the borders
of the optic disk with
hemorrhages (yellow
arrows) and exudates
(white arrow)
Clinical Signs
Patients with hypertensive retinopathy are
usually asymptomatic. Common clinical findings
include focal constriction and dilatation of the
retinal arterioles, tortuosity of the retinal
arterioles, an increase in the arteriolar light
reflex, and loss of transparency of the intra-
arterial blood column.
Additional signs of impedance to flow are retinal
hemorrhages, macular edema, and cotton-wool
spots. In areas of frank obstruction, the presence
of venous-venous collaterals may be long
standing.

Clinical Signs
Secondary ocular complications of chronic
systemic arterial hypertension include retinal
vascular occlusive disease, macroaneurysm
formation, and nonarteritic anterior ischemic
optic neuropathy.
The appearance of the ocular fundus in
hypertension is related directly to the status of
the retinal arteries and the rate of rise and
degree of systemic blood pressure.
Visual disturbances are common in malignant
hypertension. Symptoms include headache,
scotoma, diplopia, dimness in vision and
photopsia
Clinical Signs
Ocular findings in malignant arterial hypertension
are divided into three distinct categories:
hypertensive retinopathy, hypertensive
choroidopathy, and hypertensive optic
neuropathy.
The causes of these clinical findings includes
constriction of vascular beds from circulating
catecholamines, obstruction of arterioles, and
breakdown in the blood-retina barrier.
Clinical Signs
In acute malignant hypertensive retinopathy
include focal arteriolar narrowing, cotton-wool
spots, intraretinal transudates, macular edema,
and retinal hemorrhages.
Retinal hemorrhages are linear, occurring in the
nerve fiber layer in the peripapillary region.
Cystoid macular edema, lipid deposits, and
arteriolar changes are signs of more chronic
malignant hypertensive retinopathy.
Clinical Signs
Arteriolar narrowing observed on
ophthalmoscopy has been challenged by
Hayreh, who refers to this clinical finding as
pseudonarrowing secondary to retinal edema
creating a visual effect of narrowing of the retinal
arteriole.
Cotton-wool spots are fluffy, elevated, tanwhite
areas of retinal opacity occurring within a few
disc diameters of the optic nerve, caused by
occlusion of terminal retinal arterioles. Capillary
nonperfusion is present on angiography. Cotton-
wool spots typically resolve in 36weeks and are
associated with permanent nerve fiber layer loss
in the vicinity of the lesion.
Clinical Signs
Periarteriolar intraretinal transudates are tan
white retinal lesions occurring in the vicinity of an
arteriole. The lesions measure about one quarter
of the disc area but are clinically larger, as they
coalesce with adjacent lesions.
Intraretinal transudates occur secondary to focal
areas of arteriolar leakage identified on
angiography and resolve without residual retinal
damage in 23weeks.
Macular edema and subretinal fluid are retinal
findings related to hypertensive choroidal
changes affecting the retinal pigment epithelium
(RPE), with alterations in the blood-retina barrier.
Clinical Signs
Several classification schemes have been used
to stage hypertensive retinal changes. The two
most widely accepted are the Keith-Wagener-
Barker classification and the Scheie
classification.
The Keith-Wagener-Barker scheme combines
the clinical findings of hypertension and
atherosclerosis.
The Scheie classification keeps the two disease
processes separate.
KEITH-WAGENER-BARKER CLASSIFICATION
Group
I
Mild-to-moderate narrowing or sclerosis of
the arterioles
Group
II
Moderate to marked narrowing of the
arterioles
Local and/or generalized narrowing of
arterioles
Exaggeration of the light reflex
Arteriovenous crossing changes
Group
III
Retinal arteriolar narrowing and focal
constriction
Retinal edema Cotton-wool patches
Hemorrhage
SCHEIE CLASSIFICATION
HYPERTENSION
Grade
0
No change
Grade
I
Barely detectable arteriolar narrowing
Grade
2
Obvious arteriolar narrowing with focal
irregularities
Grade
3
Grade 2 plus retinal hemorrhages
and/or exudates
Grade
4
Grade 3 plus papilledema
SCHEIE CLASSIFICATION
ARTERIOLAR SCLEROSIS
Grade
0
Normal
Grade
1
Barely detectable light reflex changes
Grade
2
Obvious increased light reflex changes
Grade
3
Copper-wire arterioles
Grade
4
Silver-wire arterioles
Pathology
Microscopically, early changes from hypertension
demonstrate sclerosis and thickening of the
arteriolar walls with luminal narrowing. These
findings become more prominent with long-
standing systemic hypertension.
Arteriole thickening in the choroidal vessels is
typically more severe than in the retinal arterioles
and more closely resembles systemic arterial
changes.
Pathology
In malignant hypertension, the arterioles are
similarly thickened, but necrosis and fibrinoid
deposition in the vessel wall occur.
Electron micrographs of retinal arterioles in
malignant hypertension eventually demonstrate
dilatation of the lumen, with focal breaks in the
endothelium surrounded by lipid and fibrin, as
the autoregulatory mechanisms of the arterioles
are exceeded.
Other pathological findings include optic nerve
edema, cotton-wool spots, microaneurysms, and
focal infarcts

Treatment
Treatment of the underlying systemic condition
can halt the progress of the retinal changes, but
arteriolar narrowing and arteriovenous nicking
usually are permanent.
Treatment of malignant hypertensive retinopathy,
choroidopathy, and optic neuropathy consists of
lowering blood pressure in a controlled fashion to
a level that minimizes end-organ damage. The
actual level of blood pressure is less important in
gauging the urgency of the situation than is the
ongoing end-organ damage.
Treatment
In hypertensive patients, the autoregulatory
mechanism that maintains constant blood flow to
tissues is elevated to a higher level. This allows
for the tolerance of higher blood pressures, and
lowering blood pressure below the regulatory
range can prevent adequate blood flow from
reaching vital organs.
Therefore, blood pressure should be lowered in a
slow, deliberate, controlled fashion to prevent
end-organ damage. Too rapid a decline can lead
to ischemia of the optic nerve head, brain, and
other vital organs, resulting in permanent
damage.

Treatment
Medications used to treat hypertensive
emergencies include sodium nitroprusside,
nitroglycerin, calcium channel blockers, beta
blockers, and angiotensin-converting enzyme
inhibitors.
Treatment should be initiated in a controlled,
monitored setting under the auspices of a
physician skilled in the use of antihypertensive
medications.


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