HYPERTENSIVE RETINOPATHY

It refers to fundus changes occurring in patients
suffering from systemic hypertension.
Pathogenesis
Three factors which play role in the pathogenesis of
hypertensive retinopathy are vasoconstriction,
arteriosclerosis and increased vascular permeability.
1. Vasoconstriction. Primary response of the retinal
arterioles to raised blood pressure is narrowing
(vasoconstriction) and is related to the severity of
hypertension. It occurs in pure form in young
individuals, but is affected by the pre-existing
involutional sclerosis in older patients.2. Arteriosclerotic changes which manifest as
changes in arteriolar reflex and A-V nipping result
from thickening of the vessel wall and are a reflection
of the duration of hypertension. In older patients
arteriosclerotic changes may preexist due to
involutional sclerosis.
3. Increased vascular permeability results from
hypoxia and is responsible for haemorrhages, exudates
and focal retinal oedema.
Grading of hypertensive retinopathy
Keith and Wegner (1939) have classified
hypertensive retinopathy changes into following four
grades:
Grade I (Fig. 11.12A). It consists of mild
generalized arteriolar attenuation, particularly of
small branches, with broadening of the arteriolar
light reflex and vein concealment.
Grade II (Fig. 11.12B). It comprises marked
generalized narrowing and focal attenuation of
arterioles associated with deflection of veins at
arteriovenous crossings (Salus’ sign).
Grade III (Fig. 11.12C). This consists of 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 and hard
exudates are also present.
Grade IV (Fig. 11.12D). This consists of all
changes of Grade III plus silver-wiring of arterioles
and papilloedema.Clinical types
Clinically, hypertensive retinopathy may occur in four
circumstances:
1. Hypertension with involutionary (senile) sclerosis.
When hypertension occurs in elderly patients (after
the age of 50 years) in the presence of involutionary
sclerosis the fundus changes comprise augmented
arteriosclerotic retinopathy.
2. Hypertension without sclerosis. It occurs in young
people, where elastic retinal arterioles are exposed to
raised blood pressure for a short duration. There are
few retinal signs. The arterioles are constricted, pale
and straight with acute-angled branching. There are
minimal signs of arteriovenous crossing. Occasionally
small haemorrhages may be found. Exudates and
papilloedema are never seen.
3. 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 have been described as ‘albuminuric or renal
retinopathy’.
4. Malignant hypertension. It 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. The fundus picture is characterised by
marked arteriolar narrowing, papilloedema (an
essential feature of malignant hypertension), retinal
oedema over the posterior pole, clusters of superficial
flame-shaped haemorrhages and an abundance of
cotton wool patches.
RETINOPATHY IN PREGNANCY-INDUCED
HYPERTENSION
Pregnancy-induced hypertension (PIH), previously
known as ‘toxaemia of pregnancy’, is a disease of
unknown etiology characterised by raised blood
pressure, proteinuria and generalised oedema. 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 nasal
arterioles, followed by generalised narrowing. Severe
persistent spasm of vessels causes retinal hypoxia
characterised by appearance of ‘cotton wool spots’
and superficial haemorrhages. If pregnancy is allowed
to continue, further progression of retinopathy occurs
rapidly. Retinal oedema and exudation is usually
marked and may be associated with ‘macular star’ or
‘flat macular detachment’. Rarely it may be
complicated by bilateral exudative retinal detachment.
Prognosis for retinal reattachment is good, as it
occurs spontaneously within a few days of
termination of pregnancy.
Management. Changes of retinopathy are reversible
and disappear after the delivery, unless organic
vascular disease is established. Therefore, in preorganic
stage when patient responds well to
conservative treatment, the pregnancy may justifiably
be continued under close observation. However, the
advent of hypoxic retinopathy (soft exudates, retinal
oedema and haemorrhages) should be considered an
indication for termination of pregnancy; otherwise,
permanent visual loss or even loss of life (of both
mother and foetus) may occur.