ARTERIAL INEFFICIENCIES: CENTRAL RETINAL ARTERY OCCLUSION
Background
Central retinal artery occlusion
is a relatively rare emergent condition of the eye resulting in sudden painless
vision loss. This vision loss is usually dramatic and permanent and the
prognosis is poor. Patients particularly at risk include those with giant cell
arteritis, atherosclerosis, and thromboembolic disease, a wide variety of
treatment modalities have been tried over the last one hundred years with
little to no success, with the exception of hyperbaric oxygen therapy.
Rationale
For Hyperbaric Oxygen Therapy (HBO) In The Management Of Central Retinal Artery
Occlusion (CRAO)
The
arterial blood supply to the eye is provided by the ophthalmic artery, one of
the branches of cavernous portion of the internal carotid artery. Some of the
branches of the ophthalmic artery (lacrimal, supraorbital, ethmoidals, medial
palpebral, frontal, dorsal nasal) supply orbital structures, while others
(central artery of the retina, short and long posterior ciliaries, anterior
ciliaries) supply the tissues of the globe.(1) The central retinal artery enters the globe
within the substance of the optic nerve and serves the inner layers of the
retina through its many branches. The long posterior ciliary arteries provide
blood to the choroid and the outer layers of the retina. There are
approximately twenty short posterior ciliary arteries and usually two long
posterior ciliary arteries. The posterior ciliary vessels originate from the
ophthalmic artery and supply the entire uveal tract, cilioretinal arteries, the
sclera, the margin of the cornea, and the adjacent conjunctiva. The anterior
ciliary arteries also arise from the ophthalmic artery, supply the extraocular
muscles, and anastamose with the posterior ciliary vessels to form the major
arterial circle of the iris, which supplies the iris and ciliary body.
The
visual signs and symptoms of vascular occlusive diseases of the retina are
dependent on both the particular vessel occluded, the degree of occlusion, the
location of the occlusion, and the presence or absence of a cilioretinal
artery. In approximately 15%-30% of individuals, a cilioretinal artery is
present. This artery is part of the ciliary (not retinal) arterial supply but
supplies the area of the retina around the macula (central vision area.) If a
cilioretinal artery is present, central vision may be preserved in central
retinal artery occlusion (CRAO). The outcome of these disorders also depends on
the vessel occluded and the degree of occlusion, but also on the time interval
until therapy is initiated and the presence of alternate sources of oxygen to
the ocular tissues.
In
CRAO, the inner retinal layers (ganglion cell layer and inner nuclear layer),
which are normally served by the retinal circulation, may obtain enough oxygen
via diffusion from the choroidal circulation to function normally if the
individual is exposed to elevated partial pressures of oxygen. Animal models
have shown the choroidal supply of oxygen to the inner layers of the retina may
be sufficient to maintain ganglion cell viability even when the retinal vessels
have been completely obliterated.(2)
Normally, the choroidal circulation supplies the majority of the oxygen
to the retina. Under
normoxic conditions, approximately 60% of the retina’s oxygen comes from the
choroidal circulation. Under hyperoxic conditions, the choroid is capable of
supplying 100% of the oxygen needed by the retina.(3)
In
considering the effect of treating CRAO with supplemental oxygen, four key
factors determine success: 1) therapy must be initiated before the retinal
tissue is irreparably damaged; 2) the degree of occlusion of the blocked vessel
may vary - this may account for why some patients respond to oxygen at lower
partial pressures than others; 3) some patients may not respond to oxygen
therapy, even if it is initiated promptly, if the level of occlusion is at the
ophthalmic artery because in this event, the blood supply to the posterior
ciliary vessels is blocked as well and there is no alternate choroidal blood
supply to provide oxygenation of the inner layers of the retina; and 4) an
adequate partial pressure of oxygen must be maintained to keep the retina
viable until circulation is restored.
The etiology
of the arterial occlusion (thrombosis, embolus, arteritis, vasospasm) has also
been described as affecting outcome.(4,5) Careful classification of the factors
involved in an individual case of CRAO is crucial to understanding the natural
outcome and results of therapy. In the
largest published series of CRAO patients, Hayreh describes the natural
progression of this condition without hyperbaric oxygen therapy. He found that
patients with transient CRAO (resolution of symptoms in minutes to hours) and
those with cilioretinal arteries had much better outcomes than those who did
not. In those patients without cilioretinal arteries, 80% had a final outcome
of counting fingers or less and only 1.5% of them obtained a final vision of
20/40 or better.(5)
Recanalization occurs in
retinal vessels after CRAO.(6,7)
In relatively few cases, however, does this angiographic reperfusion
lead to an improvement of vision.(7) The retina has the highest rate of oxygen
consumption of any organ in the body at 13ml/100g/min.(8,9) Therefore, it is very sensitive to ischemia.
In order to be effective, the administration of supplemental oxygen must be
continued until such time as flow through the retinal artery has resumed to a
level sufficient to maintain inner retinal viability under normoxic conditions.
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More Information and References can be found
in the 12th Edition of the Hyperbaric Oxygen Therapy Indications
Book. For Sale on
the UHMS
Publications page.