Central
Retinal Vein Occlusion
Management of CRVO(continued)
A. MEDICAL TREATMENTS
- Anticoagulants and antiplatelet agents:
The required treatment for many of the major systemic venous thromboembolic
disorders (e.g., deep vein thrombosis) is anticoagulants or agents
which reduce platelet aggregation. Because of that, unfortunately,
there is a common impression among ophthalmologists and hematologists
that these therapeutic agents should also help patients with CRVO.
My studies of CRVO have shown anticoagulant therapy to be harmful
because it increases the amount of retinal hemorrhages, with devastating
results - often converting a benign form of CRVO into blinding CRVO11.
Not only that, but I also have many patients who developed CRVO while
on anticoagulants for various systemic diseases, clearly indicating
lack of therapeutic benefit by anticoagulants. I have found that patients
on antiplatelet agent, such as aspirin, are also liable to develop
excessive retinal hemorrhages which adversely affect the outcome.11
Conclusion: Available evidence and our experience of managing more than 700 cases of CRVO over more than three decades indicate that anticoagulants and antiplatelet agents are contraindicated in CRVO11; they are not only of no therapeutic value but are definitely harmful. Therefore, they should never be used unless there are other more important life-threatening systemic indications.
- Hemodilution: A few studies
have suggested the presence of abnormal blood viscosity in CRVO patients.
Based on that assumption, some authors have advocated the use of hemodilution
in CRVO. I recently reviewed6
all the available reports on hemodilution in the literature and found
that there is little scientifically valid evidence of beneficial effects
of this therapy.
Conclusion: There is no convincing evidence that hemodilution benefits patients with CRVO. Therefore, I do not advocate this therapy.
- Systemic corticosteroids:
In non-ischemic CRVO, as discussed above, the primary cause of visual
disability is the presence of macular edema. Therefore, in these cases
the most important management consideration is controlling macular
edema. There is no definite therapy available to treat macular edema.
In our prospective studies on the subject for about 30 years, I have
found that there is a small group of patients with non-ischemic CRVO
who respond to systemic corticosteroids when given in high doses (80
mg Prednisone daily), with resolution of macular edema and visual
improvement while they are on therapy. Unfortunately, when the steroids
therapy is lowered below a certain level (usually 40 mg Prednisone),
the macular edema returns and the vision starts to deteriorate. It
is not at all uncommon for those who respond to treatment to require
a maintenance dose of about 40 mg Prednisone or so for many months.
For example, in one young man with non-ischemic CRVO in his only eye
and a visual acuity of 20/200 (6/60) initially, visual acuity immediately
improved to 20/30-20/40 (6/9-6/12) with 80 mg prednisone. To maintain
that visual acuity he required a maintenance dose of 30-40 mg Prednisone
for almost 3 years, and every attempt to go any lower immediately
produced worsening of macular edema and deterioration of visual acuity.
He finally ended up with a visual acuity of 20/20 (6/6) and no visual
or systemic disability. Of course, a maintenance therapy for a long
period produces side-effects of corticosteroids and the patient needs
a close follow-up by both the ophthalmologist and the internist.
The most critical thing to remember in systemic corticosteroid therapy for macular edema is that it does not work in every patient. If a patient shows no improvement within two weeks, I stop the treatment. It is also important to stress to the patient that the treatment is simply helping to reduce or eliminate macular edema to prevent long term permanent macular changes, and that it is NOT a cure for the CRVO which has to take its own natural course.
- Intravitreal corticosteroids:
Recently improvement of macular edema and visual acuity has been reported
in a few eyes with non-ischemic CRVO and macular edema with intravitreal
injection of triamcinolone acetonide. I have discussed this regimen
of treatment in my recent review6.
Intravitreal injection of triamcinolone acetonide temporarily improved
visual acuity but on a long-term follow up there was no
significant difference between the initial pre-injection visual acuity
and the final visual acuity (personal communication
from Professor Jost Jonas). Among the reported side-effects of intravitreal
injection of triamcinolone acetonide (most of the studies are in diabetic
macular edema) are development of ocular hypertension (requiring anti-glaucoma
therapy) in about 33% to 50% of eyes after about one to two months,
progression of cataract in some, and, rarely, endophthalmitis. Repeated
intravitreal injections of triamcinolone acetonide can result in primary
open angle glaucoma; this is particularly important in CRVO since
in these patients there is already a significantly high incidence
of glaucoma and ocular hypertension12.
In contrast to this, in my experience of treating these patients with
systemic steroids (see above), the incidence of developing ocular
hypertension is very low.
Conclusion: Available evidence indicates that oral or intravitreal corticosteroids may help to reduce macular edema associated with non-ischemic CRVO and improve visual acuity in some patients, but only as long as they are on the treatment. I have found steroid therapy of no help in ischemic CRVO in spite of the presence of macular edema, most probably because of irreversible ischemic damage to the retinal ganglion cell in the macular region.
- Systemic acetazolamide (Diamox):
I have found that some patients (but not all)
with non-ischemic CRVO and macular edema respond to this therapy;
but once again the macular edema is under control only so long as
the patient is taking the drug. I usually give sustained release acetazolamide
(Diamox Sequels) 500 mg twice daily. Unfortunately this drug can also
produce severe systemic side-effects in some patients. If a patient
does not respond within 2 weeks, there is high likelihood that he/she
is not going to respond. I have not found this helpful in ischemic
CRVO.
Conclusion: Available evidence indicates that Diamox may help to reduce macular edema associated with non-ischemic CRVO and improve visual acuity for some patients, but only as long as they continue the treatment.
- Ocular hypotensive therapy:
Ophthalmologists often start the eye with CRVO on ocular hypotensive
therapy, e.g., topical beta blockers, etc. or even systemic carbonic
anhydrase inhibitors, under the erroneous impression that lowering
the intraocular pressure in the involved eye improves the retinal
blood flow. With venous outflow obstruction, lowering the intraocular
pressure does not influence the retinal blood flow. Moreover, our
clinical and experimental studies have clearly shown that development
of CRVO, by some unknown mechanism, actually lowers the intraocular
pressure, usually more than any of the ocular hypotensive agents do.
We have discussed the whole subject in detail elsewhere12.
I jokingly tell my residents and fellows that CRVO is the most effective
treatment available to lower intraocular pressure! Thus, eyes with
CRVO usually have normal intraocular pressure unless they develop
neovascular glaucoma. In eyes with normal intraocular pressure, ocular
hypotensive therapies seldom lower the pressure appreciably. Furthermore,
lowering the IOP to very low levels could enhance macular edema.
Since there is a high incidence of ocular hypertension or glaucoma in patients with CRVO, development of CRVO in one eye mandates treatment of ocular hypertension in the fellow uninvolved eye to reduce the risk of development of CRVO in thateye12.
Conclusion: There is no scientific rationale for the use of ocular hypotensive therapy in CRVO eyes with normal IOP. However, the fellow uninvolved eye MUST be treated to reduce the chances of its developing CRVO if it has ocular hypertension or glaucoma.
© text and images,
2003, Sohan Singh Hayreh.
Reproduction of any part of this material is not permitted without express
permission from Dr. Hayreh.
