Etiology
Occlusive disorders of retinal vessels are more
common in patients suffering from hypertension and
other cardiovascular diseases. Common causes of
retinal artery occlusion are:
Atherosclerosis-related thrombosis at the level
of lamina cribrosa is the most common cause
(75%) of CRAO.
Emboli from the carotid artery and those of
cardiac origin account for about 20% cases of
CRAO.
Retinal arteritis with obliteration (associated
with giant cell arteritis) and periarteritis (associated
with polyarteritis nodosa, systemic lupus erythematosus,
Wegner’s granulomatosis and scleroderma)
are other causes of CRAO.
Angiospasm is a rare cause of retinal artery
occlusion. It is commonly associated with
amaurosis.
Raised intraocular pressure may occasionally be
associated with obstruction of retinal arteries for
example due to tight encirclage in retinal
detachment surgery.
Thrombophilic disorders such as inherited
defects of anticoagulants may occasionally be
associated with CRAO in young individuals.
Clinical features
Clinically retinal artery occlusion may present as
central retinal artery occlusion or branch artery
occlusion. It is more common in males than females.
It is usually unilateral but rarely may be bilateral (1 to
2% cases).
1. Central retinal artery occlusion (CRAO). It occurs
due to obstruction at the level of lamina cribrosa.
Symptoms. Patient complains of sudden painless loss
of vision.
Signs. Direct pupillary light reflex is absent. On
ophthalmoscopic examination retinal arteries are
markedly narrowed but retinal veins look almost
normal. Retina becomes milky white due to oedema.
Central part of the macular area shows cherry-red
spot due to vascular choroid shining through the thin
retina of this region. In eyes with a cilioretinal artery,
part of the macular will remain normal (Fig. 11.7). Blood
column within the retinal veins is segmented (cattletrucking).
After a few weeks the oedema subsides,
and atrophic changes occur which include grossly
attenuated thread-like arteries and consecutive optic
atrophy (see page 302, 303 Fig 12.12B).
2. Branch retinal artery occlusion (BRAO). It usually
occurs following lodgement of embolus at a
bifurcation. Retina distal to occlusion becomes
oedematous with narrowed arterioles (Fig. 11.8). Later
on the involved area is atrophied leading to permanent
sectoral visual field defect.Management
Treatment of central retinal artery occlusion is
unsatisfactory, as retinal tissue cannot survive
ischaemia for more than a few hours. The emergency
treatment should include:
1. Immediate lowering of intraocular pressure by
intravenous mannitol and intermittent ocular
massage. It may aid the arterial perfusion and
also help in dislodging the embolus. Even
paracentesis of anterior chamber has been
recommended for this purpose.
2. Vasodilators and inhalation of a mixture of 5
percent carbon dioxide and 95 percent oxygen
(practically patient should be asked to breathe in
a polythene bag) may help by relieving element
of angiospasm.
3. Anticoagulants may be helpful in some cases.
4. Intravenous steroids are indicated in patients
with giant cell arteritis.
Complications
In some cases ‘neovascular glaucoma’ with incidence
varying from 1% to 5%, may occur as a delayed
complication of central retinal artery occlusion.
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